easy emg. a guide to performing nerve conduction studies and electromyography
TRANSCRIPT
Thank you to my mentors, Avital Fast, MD and Jay Weiss, MD, for
sparking my interest in EMG.
I have been fortunate to have a supportive and loving family, without
whom this book would not have been possible. Special thanks to my
husband, Jay and my children – Ari, Helene, Stefan and Richard for
giving purpose and focus to my life.
Lyn Weiss, MD
This book is dedicated to all of the physicians who are committed to
teaching electrodiagnostic medicine. And, with special gratitude to my
EMG instructor, Nicholas Spellman, MD, who was part of a terrific
team at Walter Reed Army Medical Center led by
Dr Praxedes Belanderes. I also give thanks to my
mentor, friend and Chairman at Harvard, Walter Frontera, MD,
PhD, who is unfailingly supportive of my academic endeavors.
Julie Silver, MD
To my parents, who taught the importance
of learning. Avital Fast, MD, who,
while teaching EMG, would constantly remind residents that
we are clinicians, not technicians. He taught that a good
electromyographer must be a clinician first.
Mostly however, I dedicate this book to Lyn Weiss, MD.
I have been blessed that my Chairman, my partner,
my best friend and my wife are one and the same person.
It has been a privilege and pleasure to learn with you,
learn from you, teach you and teach with you.
Ari, Helene, Stefan, Richard and Lyn – you give meaning to life.
Jay Weiss, MD
Commissioning Editor: Rolla CouchmanProject Development Manager: Hilary HewittProject Manager: Rory MacDonaldDesign Manager: Andy Chapman
BUTTERWORTH-HEINEMANNAn imprint of Elsevier Inc
© 2004, Elsevier Inc. All rights reserved.
The right of Lyn Weiss, Julie K Silver, Jay Weiss to be identified as editors of this work has been asserted by them in accordance with the Copyright, Designs and Patents Act 1988.
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First published 2004
ISBN 0750674318
British Library Cataloguing in Publication DataA catalogue record for this book is available from the British Library
Library of Congress Cataloging in Publication DataA catalog record for this book is available from the Library of Congress
NoticeMedical knowledge is constantly changing. Standard safety precautions must be followed, but as new research and clinical experience broaden our knowledge, changes in treatment and drug therapy may become necessary or appropriate. Readers are advised to check the most current product information provided by the manufacturer of each drug to be administered to verify the recommended dose, the method and duration of administration, and contraindications. It is the responsibility of the practitioner, relying on experience and knowledge of the patient, to determine dosages and the best treatment for each individual patient. Neither the Publisher nor the editors/contributors assumes any liability for any injury and/or damage to persons or property arising from this publication.
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Contributors
Dennis Dowling DOChairman and ProfessorThe Stanley Schiowitz Department ofOsteopathic Manipulative MedicineNew York College of OsteopathicMedicineNew York Institute of TechnologyOld Westbury, NY, USA
Carlo Esteves MD DOFellow, Pain MedicinePacific Pain Treatment CenterSan Francisco, CA, USA
Rebecca Fishman DOChief of Physical Medicine andRehabilitationNew York College of OsteopathicMedicineNew York Institute of TechnologyOld Westbury, NY, USA
Nancy Fung MDAssistant Attending Physician New York Weill Cornell CenterNew York Presbyterian HospitalNew York, NY, USA
Walter Gaudino MDAssociate Professor of Clinical PhysicalMedicine and RehabilitationAssociate Chairman, Department ofPhysical Medicine and RehabilitationNassau University Medical CenterEast Meadow, NY, USA
Kristin Gustafson DOChief Resident, Department of PhysicalMedicine and Rehabilitation
Nassau University Medical CenterEast Meadow, NY, USA
Victor Isaac MDResident, Department of PhysicalMedicine and RehabilitationNassau University Medical CenterEast Meadow, NY, USA
Arthur Kalman DOSHANDS at the University of FloridaGainesville, FL, USA
David Khanan MDPrivate Practice Long Island, NY
Thomas Pobre MDAssistant Professor of Clinical Physical Medicine and RehabilitationDirector of Outpatient PhysicalMedicine and RehabilitationNassau University Medical CenterEast Meadow, NY, USA
Chaim Shtock MD DOResident, Department of PhysicalMedicine and RehabilitationNassau University Medical CenterEast Meadow, NY, USA
Julie K Silver MDAssistant ProfessorDepartment of Physical Medicine andRehabilitationHarvard Medical SchoolBoston, MA, USA
Contributorsviii
Limeng Wang MDResident, Department of PhysicalMedicine and RehabilitationNassau University Medical CenterEast Meadow, NY, USA
Lyn Weiss MD Chairman and Director of ResidencyTraining;Professor of Clinical Physical Medicineand Rehabilitation;Director of Electrodiagnostic ServicesDepartment of Physical Medicine andRehabilitationNassau University Medical CenterEast Meadow, NY, USA
Jay Weiss MDMedical DirectorLong Island Physical Medicine andRehabilitationLevittown, NY, USA
Jie Zhu MDInterventional Pain FellowComprehensive Pain CenterAllentown, PA, USA
Preface
This book is the brainchild of a Physical Medicine and Rehabilitation resident who,early in her training, was frustrated by the lack of understandable electrodiagnosticmedicine textbooks. There are many excellent texts that describe the theory and practiceof electrodiagnostic medicine. However, this book is intended to be used by physicianswho are just starting their training. This is not meant to be a comprehensive text. It ismeant, rather, to serve as a bridge to more in-depth textbooks.
The first three chapters are introductory in nature. They briefly review what EMGtesting is and why we do it. Chapter 4 assesses nerve conduction studies. The needleportion of the examination is discussed in Chapter 5. Chapter 6 reviews the effect of injuryon peripheral nerves. Suggestions on how to plan out the examination are reviewed inChapter 7. Chapter 8 examines some of the pitfalls that may befall both the novice and themore experienced electromyographer.
Chapters 9 through 20 review some of the commonly encountered clinical entities thatthe beginning electromyographer might encounter. Chapter 21 gives suggestions on howto write a complete electrodiagnostic report. Chapter 22 details the commonly acceptednormal values for electrodiagnostic labs. It should be stressed however, that each labshould develop its own set of normals based on its own particular patient population andelectrodiagnostic equipment. Reimbursement issues are discussed in Chapter 23.
It should be noted that this does not represent the complete spectrum of electro-diagnostic testing. Since this book is specifically targeted at novices in the field, some ofthe more complex testing, including somatosensory evoked potentials, blink reflex, andsingle fiber EMG, is not discussed.
Although this text does review a great deal of technical information, the mostimportant lesson one can learn, which is stressed repeatedly throughout the text, is that theelectrodiagnostic test is an extension of the history and physical examination. We are, firstand foremost, physicians, with an obligation to provide our patients with compassionateand quality care.
Lyn Weiss, MD
Acknowledgments
Thank you, Sheila Slezak for your dedication, intelligence and good nature. You are aneditor, investigator and computer whiz, all rolled into one super-secretary.Thank you, Lisa Krivickas, MD, for your assistance in editing this book.Jie Zhu deserves recognition for his work on the many tables in this text.Special appreciation to Rebecca Fishman, DO, who was the impetus for this book. Youhave intellectual curiosity, the drive to get things accomplished and the personality to getpeople to cooperate.
Lyn Weiss, MD
1What is an EMG?
Julie Silver
Electrodiagnostic studies seem very confusing at first. Remember this: the entirepurpose of electrodiagnostic studies is to help you figure out whether there is a problemin the nervous system and if so, where the problem is occurring (Fig. 1.1). Easy to say,but we all recognize that the nervous system is a complicated part of our anatomy.Indeed, many medical students and residents find their initial exposure to these tests andthe courses in which they are taught overwhelming. But the truth is that they are fairlystraightforward and easy to understand.
If you don’t believe this, think back to when you were a small child learning to read.At first all of the letters in the alphabet didn’t make sense. Some had loops, some hadstraight lines, some had angled lines and some had all of these. But once you figured outall the letters, suddenly you could look at them anywhere and they made sense to you. Ofcourse, you still couldn’t read. That came later. But, even after you learned the alphabet,the higher-level task of reading (at some point not too long after you learned thealphabet) eventually became a breeze. So, too, will electrodiagnostic studies.
Think of the first half of this book as learning the alphabet. You will need to simplymemorize some terms and try to understand when to use them and in what context theyare meaningful – just like the alphabet letters. The second half of this book is the partwhere you learn to read or to put the things you have memorized to use in a logical wayso that when electrodiagnostic studies are ordered, you can understand what informationis being conveyed and how to perform the study. Keeping with the alphabet/readingexample, more advanced electrodiagnostic textbooks will teach you the equivalent ofgrammar and higher level skills that are extremely important. However, you don’t needto know all that at first. Go through every chapter in this book, and just like you learnedthe alphabet and then learned to read, you will become an expert at electrodiagnosticstudies – only it will happen much faster this time!
The term electrodiagnostic studies really encompasses a lot of different tests. Themost common tests done (and the ones that will be presented in this book) are nerveconduction studies (NCS) and electromyography (EMG). Often people refer to both NCSand EMG as just EMG because these two tests are nearly always done together. But, whenyou are talking with people who are familiar with electrodiagnostic testing, to avoidconfusion it is best to speak of these components separately. The tests can provide differentinformation, however, both tests assess the electrical functioning of nerves and/or muscles.
It is interesting to note that electrodiagnostic studies originated in the 19th centurybut have only been consistently used within the past 30–40 years. This is because themachines became more sophisticated with computerization, and at the same time, easierto use. Highly refined techniques enhanced diagnostic applications and encouragedpeople to use these tests.
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One of the things that will make it much easier for you to learn both EMG and NCSis to understand that they are really an extension of the neurological and musculoskeletalexamination. The more you know about the basic anatomy of the nerves and muscles,the easier it will be to learn about electrodiagnostic studies. If you are just beginning tolearn about what nerves supply what muscles and such, this will be a slightly morecomplicated subject, but still very manageable. Just keep reading.
Table 1.1 is a summary of the process of performing electrodiagnostic studies. Therest of this chapter is devoted to explaining the two basic tests: EMG and NCS. Some ofthis you will simply need to memorize, but hopefully as you read, it will start to makesense.
Nerve Conduction Studies
NCS are done by placing electrodes on the skin and stimulating the nerves throughelectrical impulses (Fig. 1.2). To study motor nerves, electrodes are placed over a muscle
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Sensory nerve root
Dorsal root ganglion
Motorneuron
Motor nerve root
Peripheral nerve
Motor nerve
Neuromuscular junction
Muscle
Sensorynerve
Figure 1.1 The goal of electrodiagnostic studies is to determine whether there is aproblem along the peripheral nervous system pathway and if so, where the problemis. Examples of locations of possible lesions and associated diagnoses include:Motor nerve cell body (anterior horn cell) – amyotrophic lateral sclerosisRoot – cervical or lumbar radiculopathyAxon – toxic neuropathyMyelin – Guillain–Barré syndromeNeuromuscular junction – myasthenia gravisMuscle – muscular dystrophy
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that receives its innervation from the nerve you want to test (stimulate). The electricalresponse of the muscle is then recorded and you can determine both how fast and howwell the nerve responded. This is very valuable information and can help you todetermine whether the patient’s condition is stemming from a problem with the nerve orthe muscle.
NCS are broken down into two categories: motor and sensory nerve conductiontesting. The autonomic nervous system can be tested, but rarely has clinical applicationsand is beyond the scope of this text. NCS can be performed on any accessible nerveincluding peripheral nerves and cranial nerves. The basic findings are generally two-fold: 1. how fast is the impulse traveling? (e.g., how well is the electrical impulseconducting?); and, 2. what does the electrical representation of the nerve stimulation(action potential morphology) look like on the screen? (e.g., does there appear to be aproblem with the shape or height that might suggest an injury to some portion of thenerve such as the axons or the myelin?).
1 What is an EMG? 3
1. Evaluate the patient by doing a history and physical examination with thegoal of developing a differential diagnoses list.
2. Select the appropriate electrodiagnostic tests you want to perform in order torule in or out diagnoses on your list.
3. Explain to the patient what the test will feel like and why it is being done.
4. Perform the study in a technically competent fashion, usually starting withthe nerve conduction studies and then proceeding with the EMG.
5. Interpret the results in order to arrive at the correct diagnosis or to narrowyour list of differential diagnoses.
6. Communicate the test results to the referring physician in a timely andmeaningful manner.
Table 1.1 The electrodiagnostic process
Recordingelectrodes
Stimulatingelectrodes
Sensorynerveactionpotential Take-off latency
Peak latency
Amplitude
Mediannerve
Figure 1.2 This isthe basic set-upfor a sensory nerveconduction study.The machine givesa tracing of thesensory nerveaction potential(SNAP). Theamplitude andlatency can easilybe measured.(Adapted fromMisulis K.Essentials ofClinicalNeurophysiology.London:Butterworth-Heinemann; 1997).
The terms you need to memorize in NCS are listed in Table 1.2. EMG terms arelisted and explained in Chapter 5 (Electromyography).
Electromyography
EMG is the process by which an examiner puts a needle into a particular muscle andstudies the electrical activity of that muscle. This electrical activity comes from themuscle itself – no shocks are used to stimulate the muscle. The EMG also differs fromthe NCS because it does not involve actually testing nerves. However, you do getinformation indirectly about the nerves by testing the muscles (remember that allmuscles are supplied by nerves, so if you can identify which muscles are affected by adisease process then you simultaneously obtain information about the nerves that supplythose muscles).
So, the EMG is different from NCS in the following ways:
1. You use a needle and put it into the muscle rather than electrodes that are placed onthe skin.
2. You don’t use any electrical shocks in EMG; rather you are looking at the intrinsicelectrical activity of the muscle.
3. You get direct information about the muscles in EMG and indirect informationabout the nerves that supply the muscles you test.
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Action potential – this is the waveform you see on the screen (in order to givemore details about what you are describing, more specific terms may includecompound nerve action potential, compound motor action potential, sensorynerve action potential, etc.)
Latency – time interval between the onset of a stimulus and the onset of aresponse (can also be referred to as a motor latency or a sensory latency).
Amplitude – the maximal height of the action potential.
Conduction velocity – how fast the fastest part of the impulse travels (can also bereferred to as a motor conduction velocity or a sensory conduction velocity).
F-wave – a compound muscle action potential evoked by antidromicallystimulating a motor nerve from a muscle using maximal electrical stimulus. Itrepresents the time required for a stimulus to travel antidromically toward thespinal cord and return orthodromically to the muscle along a very smallpercentage of the fibers.
H-reflex – a compound muscle action potential evoked by orthodromicallystimulating sensory fibers, synapsing at the spinal level and returningorthodromically via motor fibers. The response is thought to be due to amonosynaptic spinal reflex (Hoffmann reflex) found in normal adults in thegastrocnemius-soleus and flexor carpi radialis muscles.
Orthodromic – when the electrical impulse travels in the same direction as normalphysiologic conduction (e.g., when a motor nerve electrical impulse is transmittedtoward the muscle and away from the spine or a sensory impulse travels towardthe spine).
Antidromic – when the electrical impulse travels in the opposite direction ofnormal physiologic conduction (e.g., conduction of a motor nerve electricalimpulse away from the muscle and toward the spine).
Table 1.2 Nerve conduction study terms
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2Why do ElectrodiagnosticStudies?
Julie Silver
Electrodiagnostic testing is an important method for physicians to distinguish betweenmany nerve and muscle disorders. One of the ways to think of EMG and NCS is toconsider them pieces of a puzzle. The puzzle may be complicated with many pieces orfairly straightforward with few pieces needed to solve it. In order to understand whatyou are seeing, whether it is a real puzzle or a figurative medical puzzle, the more piecesyou can put into place, the clearer the picture becomes. In medicine, the other puzzlepieces are the history, physical examination, laboratory tests, imaging studies, etc.
One of the things that is important to remember is that electrodiagnostic studiesrepresent a physiologic piece of the diagnostic puzzle. For example, unlike an MRI or anx-ray, which are simply sophisticated photographs, the EMG and NCS provide informationin real time about what is occurring physiologically with respect to the nerve and themuscle. This is not to say that imaging studies are not useful, but rather to explain thatthese tests complement each other and each has a role in helping to establish the correctdiagnosis in neuromuscular disorders.
The take-home message is this: Electrodiagnostic studies are sometimes essential inestablishing a particular diagnosis and are sometimes not useful at all. As a clinician, it isimportant to understand when to recommend these studies just as it is important to knowwhen to order an imaging study. The more you learn about EMG and NCS, the morefamiliar you will become with their diagnostic usefulness.
In a practical sense, you can consider electrodiagnostic testing in any of the followingcircumstances:
1. A patient is complaining of numbness.2. A patient is complaining of tingling (paresthesias).3. A patient has pain.4. A patient has weakness.5. A patient has a limp.6. A patient has muscle atrophy.7. A patient has depressed deep tendon reflexes.8. A patient has fatigue.
Of course, it would be ridiculous to rely solely on any one of these signs or symptoms whenrecommending NCS/EMG. For example, a young woman comes in complaining of armpain. The differential diagnosis should immediately include trauma as a source of the pain.Upon questioning you learn that in fact she fell and on physical examination you note alarge abrasion that explains her pain. To even consider electrodiagnostic studies in this
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situation is absurd. The point here is that a list of signs and symptoms does not lead youto automatically order electrodiagnostic studies. Rather, these tests can be thought of asan extension of the history and physical examination when someone presents with anyone or more of the signs or symptoms listed that cannot be explained by the history andphysical examination alone.
Clearly electrodiagnostic studies are useful to establish the correct diagnosis, butthey are also useful to determine whether someone should have surgery and are oftenpreferred over imaging studies when certain types of surgery are a consideration. Theyare also done for prognostic reasons to follow the course of recovery (or deterioration)from an injury.
In summary, electrodiagnostic studies are used to:
1. Establish the correct diagnosis.2. Localize the lesion.3. Determine treatment even if the diagnosis is already known.4. Provide information about the prognosis.
Consider the following examples:
Example 1
A man comes in with hand pain, paresthesias and numbness that are most prominent inthe index and long fingers. Upon questioning he also reveals he has neck pain. Thephysical examination is inconclusive. The differential diagnosis includes carpal tunnelsyndrome (median nerve compression at the wrist) and cervical radiculopathy. An EMGand NCS are the studies of choice to establish the correct diagnosis.
Example 2
Another man comes in with the same symptoms but he doesn’t have neck pain. In thepast he was diagnosed with carpal tunnel syndrome and underwent an injection withlocal corticosteroid into the carpal tunnel that completely alleviated his symptoms for afew months (a good response to a corticosteroid injection in the carpal tunnel is boththerapeutic and diagnostic for carpal tunnel syndrome). Now, however, his symptomsare back with a vengeance. In this case of carpal tunnel syndrome, electrodiagnosticstudies can be recommended in order to determine the severity of his condition and tohelp decide whether conservative management or surgery is the most appropriate courseof treatment.
Example 3
A third man comes in who had carpal tunnel surgery 3 months ago. His symptoms aremuch better, but he is still quite weak. Prior to his surgery he had an EMG and NCS thatdemonstrated a very severe injury to the median nerve. Now, he is a candidate for repeatelectrodiagnostic studies to provide information about the prognosis. The new study canbe compared to the old study, and information extrapolated about the current status ofthe median nerve and predicted future improvement.
The Skilled and Compassionate Electrodiagnostician
Many patients are afraid to have electrodiagnostic studies. They may have heard that thesetests are extremely painful or they may have a genuine needle phobia. In order to get the
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information you need from these tests, it is important for you to be both technically skilledand able to put the patient at ease. The following suggestions will help to lessen thepatient’s anxiety:
1. Avoid keeping the patient waiting, as that will only increase his or her anxiety.2. Before you start, explain to the patient what you are going to do. Be sure the
patient understands that the electrical stimulation occurs only with the NCS andnot with EMG.
3. Explain that these tests will be useful in determining the diagnosis.4. Reassure the patient that you will stop the test at any point if they request you to do
so. Be sure to honor the request should it occur.5. Start with the area of greatest interest – especially if you suspect that the patient
won’t tolerate the entire study.6. Although not typically used, analgesic or sedating medication can be given. 7. During the test, distract the patient with conversation. It is usually easy to distract
someone by asking them questions about what they like to do, where they like to go,etc. Some electromyographers play music of the patient’s choosing during the test.
8. In most instances, it is best not to show patients the needle as many people associatemore pain with a long needle rather than with a larger diameter (the EMG needle islong and thin, so it really doesn’t hurt as much as a larger diameter needle). Inaddition, most patients feel more comfortable with the term ‘electrical stimulation’rather than ‘electrical shock’, which conjures up images of torture.
9. Assure the patient that you will minimize the length of the exam, doing only what isabsolutely necessary to obtain the required information.
10. Keep the room warm. This serves two purposes. First of all, the patient is generallydressed in a gown and therefore is prone to being cold. Keeping the room warm willmake him or her more comfortable. In addition, the results of your electrodiagnostictest may be affected if the patient’s extremity is cool (see Chapter 8, Pitfalls).
Special Precautions
There are a number of clinical situations that deserve special mention. These are caseswhere electrodiagnostic studies can be safely done, as long as the physician takes measuresto ensure the safety of the patient (and himself/herself) and the accuracy of the test.
Morbid Obesity
In patients who are very overweight, it may be difficult (or impossible) to localizespecific muscles. Care must be taken to ensure that the needle is indeed placed in theappropriate muscle. Extra-long needles may be used.
Thin Individuals
In very thin patients, it is important not to insert the needle too far as it can injure othertissues (e.g., a needle placed in the thoracic paraspinals may penetrate the lungs andcause a pneumothorax).
Bleeding Disorders
Individuals with known bleeding disorders or who are on anticoagulation therapy shouldbe assessed on an individual basis and the risks/benefits of the test evaluated. It may behelpful to have recent laboratory testing for coagulation parameters. Therapeutic levelsof anticoagulation are not a contraindication to EMG.
2 Why do Electrodiagnostic Studies? 7
Blood Precautions
It is imperative to always practice safe needle-stick procedures to protect yourself andthe patient from injury. These include always wearing gloves for the needle portion ofthe test, using a sterile disposable needle for the EMG, using a one-handed technique ifneeded for needle recapping and immediately disposing of all sharps in an appropriatecontainer.
Contraindications
Strict contraindications to electrodiagnostic testing are relatively few. Obviously anyonewho has a severe bleeding disorder or whose anticoagulation therapy is out of controlshould not undergo an EMG. NES are contraindicated in those with automaticimplanted cardiac defibrillators. A patient with a cardiac pacemaker should not receivedirect electrical stimulation over the pacemaker. Someone with an active skin/soft tissueinfection (e.g., cellulitis) should not have an EMG anywhere near the infection. There iscontroversy over whether someone who has had an axillary node dissection after amastectomy should undergo any needle punctures in the affected extremity. Theclinician should consider this a relative contraindication and weigh the risks/benefits ofthe study.
Complications
Complications from electrodiagnostic studies are extremely rare when performed by askilled clinician. Complications may include infection, bleeding and accidentalpenetration of the needle into something other than the intended muscle (e.g., lung,nerves, etc.).
Controversy
As with nearly every test in medicine, there is controversy about when to do electro-diagnostic studies. There is no doubt that EMG and NCS provide valuable informationand in many instances are worthwhile tests to pursue. However, they must be judiciouslyperformed – as is the case with all medical testing. Of course, there would not be anycontroversy if these studies were painless and free. But this is not the case. They docause some patient discomfort (although this can be minimized with a skilled and com-passionate approach) and they are relatively expensive tests to perform. So, it isimportant every time you consider performing electrodiagnostic studies to assess whetherthe test is necessary, whether it will help you to determine the diagnosis, treatment orprognosis of a patient’s condition, and whether there is another test that might be less intru-sive and/or more cost effective that will provide the same information. It is important toalways remember to first do no harm.
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3About the Machine
Julie Silver
The Basic Machine
Modern electrodiagnostic equipment consists of a computer and the associated hardwareand software (Fig. 3.1). The hardware is fairly standard and typically includes a visualmonitor, keyboard and hard and floppy disk drives. Some systems have additionalhardware for storage and other purposes. The software varies in the same manner thatall software varies – ease of use, ability to perform specific functions, etc. However, allbasic electrodiagnostic software allows the clinician to:
● perform both EMG and NCS ● collect data ● help to analyze the results (through automatic calculations that are usually pre-
programmed)● store the information.
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Figure 3.1 Pictureof EMG machine(courtesy ofCadwellLaboratories).
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Data entry is done using a keyboard and/or a mouse. When you are performing NCS,the information you need is displayed on a screen. During EMG studies, you will havethe same visual screen information but also there will be audio (noises) that you willhear. Both the visual and the audio data are critical to properly interpreting EMGfindings.
Recording Electrodes
It is important to understand electrode terms used in electrodiagnostic studies. Table 3.1lists the common terms and in which studies they are used.
Surface Electrodes
Surface electrodes are used for routine NCS. The electrodes are typically either ring ordisk electrodes (Fig. 3.2). They are also either disposable or non-disposable. The non-disposable electrodes are made of stainless steel, silver or – rarely – gold that is solderedto multistrand conducting wires. These electrodes stick to the skin by using adhesivetape and can be reused. They should be cleaned between patients. It is necessary to useconducting gel with non-disposable electrodes in order to reduce impedance and preventartifact (due to irregularities in the skin and the presence of hair follicles). Disposableelectrodes have a sticky underside that allows them to adhere to the skin without the needfor tape or gel.
Three surface electrodes are used in NCS: active and reference recording electrodesand a ground electrode. In EMG studies, surface electrodes are used for the ground andsometimes as a reference-recording electrode.
Needle Electrodes
Needle electrodes are generally reserved for EMG, but are occasionally used in NCS.Today nearly all needle electrodes are disposable and are used only on one patient.Needle electrodes are classified as monopolar, bipolar or concentric. Monopolar needlesare typically less expensive, less painful (due to a narrower diameter, and a teflon coatingon the shaft of the needle) and less electrically stable than bipolar or concentric needleelectrodes. With a monopolar needle, you need a separate surface reference electrodewhereas with a concentric needle, the reference is the barrel of the needle and you do notneed a separate surface reference electrode. See Chapter 5 (Electromyography) for furtherdescription of the needles.
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NCSActive (surface electrode – this is also referred to as the pickup electrode)Reference (surface electrode)Ground (surface electrode)
EMGActive (needle electrode)Reference (surface electrode)*Ground (surface electrode)
*A separate reference is used in EMG studies only if you are using a monopolar needle.Concentric needles have a reference built into the needle, so there is no need for aseparate reference.
Table 3.1 Electrodes used in NCS and EMG
3 About the Machine 11
A
B
C
Figure 3.2 A, Diskelectrade; B, ringelectrode; C,ground electrode.(courtesy ofCadwellLaboratories).
Amplifiers
Amplifiers are a very complicated part of the electrodiagnostic machinery, but theconcept is fairly simple. Amplifiers magnify the signal so that it can be displayed(Fig. 3.3). Integrated circuits or chips perform most amplification. Preamplifiers attenuatethe biological signal before it ever gets to the amplifier in order to: 1. make sure that thefilters have sufficient signal voltage to deal with, and 2. insure that the level of signalvoltage is much higher than that of system noise.1 The signal travels first to the pre-amplifier, then to the filters, and then to the amplifier. The differential amplifier is usedextensively in electrodiagnostic studies, because it has the advantage of common moderejection. What this means is that unwanted signals, rather than being amplified to thesame degree as the biological signals that you are trying to study, are rejected. The mostcommon unwanted signal in the clinic is 60-Hz activity, which is caused by line voltagepassing through electrical circuits.
The differential amplifier takes the electrical impulses from the active electrode andamplifies them. It then takes the impulses from the reference electrode, inverts them, andamplifies them. It then combines these two potentials. In this way, any common noise toboth electrodes (extraneous electrical activity, distant myogenic noise, and EKG artifacts)would be eliminated. Differences between the two electrodes, however, would be amplified.This is the desired signal. Any common factors such as extraneous noise would berejected leading to the term common mode rejection. The common mode rejection ratiois a measure of how well an amplifier eliminates this type of common noise.
Filters
Filters are used to faithfully reproduce the signal you want while trying to exclude bothhigh and low frequency electrical noise.2 Every signal in both NCS and EMG passesthrough both a low frequency and a high frequency filter before being displayed. Lowfrequency filters are called high pass because they let high frequency signals pass
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Figure 3.3Preamplifier(courtesy ofCadwellLaboratories).
through. The range at which there is a cut-off of low frequency signals depends on howyou set the filter. Similarly, high frequency filters are called low pass because they letlow frequency signals through. It is important to understand that there is always a trade-off when you use filters. The signal you want will be altered to some degree. For example,as the low frequency filter is reduced, more low frequency signals pass through and theduration of the recorded potential will be slightly longer. Likewise, if the high frequencyfilter is decreased, more high frequency signals are excluded and the latency of therecorded potential may be delayed. Table 3.2 summarizes the role of filters and gives theusual settings in NCS and EMG.
Display System
Display systems for electrodiagnostic studies are either via a video screen (computerscreen) or paper. New display systems (e.g., liquid crystal, digital, etc.) are beingdeveloped, but the standard display is the cathode ray tube (CRT). The CRT uses acontrolled electron beam (called the cathode ray) to excite phosphors on the screen thatpresents as a visual display. There are two settings on the display system with which youmust be acquainted – the sweep speed and sensitivity (also sometimes called the gain).The primary purpose of adjusting the sweep speed and sensitivity is so that you canoptimally see the signal displayed on the screen. The horizontal axis is the sweep speedand is shown in milliseconds (ms) (Fig. 3.4). The vertical axis is the sensitivity and thisrepresents response amplitude (millivolts in motor studies and microvolts in sensorystudies) (Fig. 3.5). Suggested motor NCS settings are listed in Table 3.3. The initialsettings for sensory NCS are listed in Table 3.4.
3 About the Machine 13
Low frequency High pass Filters out low frequency signals that if present, cause a wandering baseline
High frequency Low pass Filters out high frequency signals that if present, can obscure signals such as SNAPs or fibrillation potentials and can cause a ‘noisy’ baseline especially on sensory studies
Table 3.2 Filters
3.0 msecs
3.4 msecs
3.5 msecs
5 mV (Gain)
2 msec / division (Sweep)
1 msec / division (Sweep)
0.8 msec / division (Sweep)
5 mV (Gain)
5 mV (Gain)
Figure 3.4 Effectsof latency withchanges in sweepspeed (adaptedfrom Preston DC,Shapiro BE.ElectromyographyandNeuromuscularDisorders. London:Butterworth-Heinemann, 1998).
!
Artifacts and Technical Factors
Physiologic Factors (patient-related)
Stimulus Artifact
Stimulus artifact is an electrically recorded response that is elicited directly from thestimulator. It occurs in all NCS, however, it only becomes a problem when the trailing
Easy EMG14
Sweep in milliseconds
2.9
3.1
3.4
3 msec
1 mv(gain)
5 mv(gain)
3 msec
100 μv(gain)
3 msec
Figure 3.5 Effectof increasing thesensitivity (gain)of a CMAP(adapted fromPreston DC,Shapiro BE.ElectromyographyandNeuromuscularDisorders. London:Butterworth-Heinemann,1998).
Sweep speed 2–3 ms/div
Sensitivity (gain) 5000 microvolts/division (this means the same as 5 millivolts, 5mV or 5K microvolts)
Low frequency filter 10 Hz
High frequency filter 10 kHz
*Adapted from Misulis K. Essentials of Clinical Neurophysiology. London: Butterworth-Heinemann; 1997)
Table 3.3 Initial motor NCS settings*
Sweep speed 1–2 ms/div – generally 10 divisions are present in a horizontal screen
Sensitivity (gain) 20 microvolts/division
Low frequency filter 2–10 Hz
High frequency filter 2 kHz
*Adapted from Misulis K. Essentials of Clinical Neurophysiology. London: Butterworth-Heinemann; 1997)
Table 3.4 Initial sensory NCS settings*
edge of the recorded artifact overlaps with the potential being recorded (Fig. 3.6). Makingsure the ground is between the recording and stimulating electrodes can minimizestimulus artifact.
Filters
Filters were discussed earlier in this chapter, but they are mentioned here because theycan significantly contribute to the quality of your study. It is important to remember thatthe role of filters is to faithfully reproduce the signal you want while trying to excludeboth high and low frequency electrical noise.
Electrode Placement
There are many issues that occur when electrodes are improperly placed. This discussionwill be detailed throughout the rest of the book. Suffice it to say here that properelectrode placement is a critical part of performing accurate electrodiagnostic studies.
Stimulation
An important concept in NCS is to understand supramaximal stimulation. The bottomline is this: all measurements made in NCS are done with the assumption that the strengthof the stimulus is high enough to depolarize every axon in the nerve. This is achieved bygradually increasing the stimulus strength until you reach the point where the amplitude ofthe waveform is no longer increasing. That is the point of supramaximal stimulation. Ifsupramaximal stimulation is not achieved at a distal site, then you might mistakenlyinterpret this recording as signifying axonal loss due to the low amplitude. At a proximalsite, this might appear to be conduction block (failure of an action potential to be conductedpast a particular point whereas conduction is possible below the point of the block). Inboth instances, anomalous innervation or nerve injury may be wrongly suspected.
Of course, the old adage, too much of a good thing is not good, applies to manythings in life. When it comes to stimulation in NCS, too much stimulation may cause co-stimulation of adjacent nerves or may stimulate nerves farther from the site. So, the goal
3 About the Machine 15
Stimulusartifact
Stimulus artifact
AmplitudeLatency
29 μV2.1 msec
AmplitudeLatency
38 μV2.0 msec
AmplitudeLatency
45 μV1.9 msec
20 μV
2 msec
Figure 3.6 Largestimulus artifactmay falselydecrease theamplitude andincrease thelatency (adaptedfrom Preston DC,Shapiro BE.ElectromyographyandNeuromuscularDisorders. London:Butterworth-Heinemann, 1998).
is to reach supramaximal stimulation without applying so much stimulation that adjacentnerves are also stimulated.
Measurements
The machine will do most of your calculations for you. But you still need to measure thedistance between stimulations and between the stimulation and the recording electrode ofa patient’s limb when you are determining the conduction velocity. It is imperative that themeasurement is done accurately. Other than a simple oversight of not correctly recordingthe distance with your tape measure, the main problem that can occur is if the patient’slimb is moved in different positions, which changes the distance you are measuring. Thiscommonly occurs in ulnar nerve studies when the elbow is straight and then becomesflexed. Therefore, during an ulnar nerve study, it is best to keep the elbow flexed and inthe same position for the duration of that particular study. Skin measurements are amajor source of error in electrodiagnostic studies. This can be minimized by increasingthe distance of the nerve segment being studied (i.e., the shorter the distance, the greaterthe effect of a measurement error). In general, when measuring distance, follow the courseof the nerve, rather than measuring the shortest distance between the stimulating andrecording electrodes.
Sweep Speed and Sensitivity
Both the sweep speed and sensitivity can affect your NCS results. As the sensitivity isincreased, the onset latency will decrease. So, it is important to record all of your latencymeasurements using the same sensitivity and sweep speed.
REFERENCES
1. Misulis KE. Essentials of Clinical Neurophysiology. Newton, Massachusetts:Butterworth-Heinemann, 1997.
2. Preston DC, Shapiro, BE. Electromyography and Neuromuscular Disorders. Newton,Massachusetts: Butterworth-Heinemann, 1998.
Easy EMG16
4Nerve Conduction Studies
Lyn Weiss, Jay Weiss, Thomas Pobre, Arthur Kalman
Nerve conduction studies (NCS) can be defined as the recording of a peripheral neuralimpulse at some location distant from the site where a propagating action potential isinduced in a peripheral nerve. In other words, a nerve is stimulated at one or more sitesalong its course and the electrical response of the nerve is recorded.
Whether or not a nerve is injured can be evaluated by testing the ability of the nerve toconduct an electrical impulse. Nerve conduction studies allow us to accurately localizefocal lesions or detect generalized disease processes along accessible portions of theperipheral nervous system. The reliability of a study is increased when the technicalaspects of the study are standardized. This chapter will review why it can be helpful toutilize nerve conduction studies and how to perform them.
The nerve conduction studies most commonly performed are compound muscleaction potentials (CMAPs) for motor nerves, sensory nerve action potentials (SNAPs)for sensory nerves, compound nerve action potentials (CNAPs) for mixed (sensory andmotor) nerves and late responses (primarily F-waves and H-reflexes). For a discussionof F-waves and H-reflexes, see Chapter 12, Radiculopathy.
Physiology
When doing nerve conduction studies it is important to understand nerve physiology.After all, nerve studies are a physiological, not anatomic, test such as x-rays. In order totest nerve function we must understand how nerves conduct signals.
Nerves conduct impulses through a traveling wave of depolarization along their axon.The axon is the peripheral extension of the proximally located nerve cell body. The cellbody is located in the spinal cord for motor nerves (anterior horn cell) and peripherally inthe dorsal root ganglion for sensory nerves (Fig. 4.1). The surface membrane surroundingthe axon is called axolemma, and contained within the axon is the axoplasm. At rest, theaxon has an intracellular potential that is negative in relation to the extracellular potential.When an axon is conducting an impulse, voltage-dependent channels open and allow aninflux of sodium (Na+) ions. This influx of positive ions depolarizes the axon, changesthe resting potential further down the axon, causing those channels to open and thuscreates a wave of depolarization (Fig. 4.2).
While nerves have a physiological direction (from the spine in the case of motornerves and to the spine in the case of sensory nerves), if a nerve is electrically stimulatedanywhere along its course, waves of depolarization will travel in both directions fromthat point. Nerve conduction can be measured orthodromically (physiological direction ofnerve conduction) or antidromically (opposite to the physiological direction). Motor andsensory nerve action potentials can be measured through skin electrodes if the nerve is 17
!
sufficiently superficial. It is more common (and technically easier) to measure motornerves by picking up electrical activity from the muscle it innervates.
As a rule, nerve conduction study is done only on myelinated nerve fibers becauseunmyelinated fibers conduct extremely slowly, and do not contribute significantly to theCMAPs and SNAPs. A myelinated nerve fiber is composed of an axon and its surroundingmyelin sheath (Fig. 4.3). Myelin is a connective covering surrounding motor nerve axonsand many sensory nerve axons. Myelin is produced by Schwann cells and functions togreatly increase the speed of nerve conduction. Myelin acts as an excellent insulator andpermits saltatory conduction. This occurs when depolarization takes place only at theinternodal regions. For this reason, myelinated axons have their voltage-dependent sodiumchannels concentrated around the nodes, with few in the internodal regions. This type of‘jumping’ conduction, where time is not required to depolarize axons between the nodes,permits a greater than 10-fold increase in velocity.
Velocities in myelinated nerves range from 40 to 70 m/sec. Unmyelinated axons, incontrast, are much slower – in the range of 1–5 m/sec. Unmyelinated axons do not conductthrough saltatory conduction but have voltage-dependent channels uniformly throughoutthe nerve. The speed of nerve conduction is largely contingent upon the amount of time ittakes for voltage-dependent channels to open. As unmyelinated nerves have a far greater
Easy EMG18
Sensory root
Anterior horn cell
Motor root
Dorsal root ganglion
Motor nerve
Neuromuscularjunction
MuscleSensory receptor
Sensorynerve
Figure 4.1 Cellbody of sensoryand motornerves.
Figure 4.2 Waveof depolarization.
Na+/K+
pump
Cl- Na+Na+
Na+
K+
K+
K+Anions-
number of channels per length of nerve, they conduct at less than one-tenth the speed ofa myelinated nerve.
The most important points to remember about myelin are:
● Myelin helps nerves propagate an action potential faster.● The myelin sheath functions as insulator of the axon.● In myelinated nerves, depolarization occurs only at areas devoid of myelin (nodes of
Ranvier) resulting in saltatory conduction.● Conduction velocity is directly related to internodal length and efficiency of myelin
insulation.
A demyelinated axon is a myelinated nerve that has lost its myelin covering. This does notbecome an unmyelinated nerve. While an unmyelinated axon can conduct an impulse alongits entire length, a demyelinated axon may not be able to conduct across a demyelinatedarea. This loss of conduction across a lesion is referred to as conduction block. The termneurapraxia is used to describe a lesion where conduction block is present.
It is important to note that while axons have an ‘all or none’ response, an actionpotential represents the summation of many axons. Thus, a neurapraxic lesion can resultin an amplitude decrement from less than 1% to nearly 100%. In reality, neurapraxiclesions of less than 20% are rarely diagnosed due to the amplitude differences normallyseen from different sites of stimulation.
After a demyelinating lesion, as part of the recovery phase, there is typically regen-eration of immature myelin. This immature myelin will not insulate as well as maturemyelin and therefore during a NCS you may see a return of conduction but at a slower thannormal velocity. Therefore, conduction slowing and conduction block are indicative ofdemyelinating, but not axonal lesions.
The Action Potential
The action potential is a summation of many potentials. In a CMAP it is the summationof motor units (muscle fibers) that are firing, while a SNAP is a summation of individualnerve fibers, each with its own amplitude and slightly different conduction velocities.This summation yields a characteristic (usually bell-shaped) curve. The part of the curvethat begins to rise first represents the components from the fastest fibers. The typicalaction potential is shown on a time versus amplitude chart (Fig. 4.4). The amplitude canbe measured from onset to peak (A–B) or from peak to trough (B–C). The duration is thetime from the onset to recovery (A–D). The area is the area under the negative phase of thepotential. (In electrodiagnostic terminology, negative refers to an upward deflection frombaseline and positive refers to a downward deflection from baseline.)
4 Nerve Conduction Studies 19
Nodeof
Ranvier
Myelin
Saltatory conduction Figure 4.3Myelinated nerve.
!
Components of the Action Potential
Latency
The latency represents the time it takes from stimulation of the nerve to the measurementof the beginning of the sensory nerve action potential (SNAP) or the compound muscleaction potential (CMAP). In a CMAP, the onset latency represents the arrival time (at thepickup electrode over the muscle) of the fastest-conducting nerve fibers. There is normalvariation in the conduction velocity of the individual nerve fibers producing a temporallydispersed curve. This is usually a gaussian or bell-shaped curve representing the numberof fibers (amplitude) and how fast they are traveling (latency). The nerve fibers thatcontribute to the trough of the curve are amongst the slowest fibers.
In sensory nerves, the latency is solely dependent on the speed of conduction of thefastest fibers and the distance the wave of depolarization travels. In motor nerves, inaddition to the speed of the nerve and the distance traveled, the latency is also dependenton the amount of time it takes to synapse at the neuromuscular junction and the speed ofintramuscular conduction. While this is typically brief (estimated to be approximatelyone millisecond) the exact duration can vary. Usually the latency is measured to thenegative (upward) departure from baseline. If an initial positive departure is seen, theelectrodes usually require repositioning, because it is likely that the recording electrode isover a muscle not innervated by the nerve being stimulated.
It must be stressed that a latency measurement without a standardized or recordeddistance is meaningless. For example, if a patient has a large hand, the standard distanceof 8 cm for median motor latency may not allow you to stimulate above the wrist. If youstimulate at 10 cm, but don’t record that you stimulated at a distance of 10 cm, it willappear that the patient has slowing of the median nerve across the wrist, because it willtake longer to travel a further distance. Normal latencies are listed in Chapter 22.
Conduction Velocity
Conduction velocity is how fast the nerve is propagating an action potential. It can becalculated by the formula:
velocity = distance/time
Easy EMG20
Time (millisecond)
Am
plit
ud
e (m
illiv
olt
)
LatencyRecovery
Trough
Duration
Amplitude
Figure 4.4Compoundmuscle actionpotential.
As stated above, sensory nerves do not have a myoneural junction. Therefore, conductionvelocity can be calculated directly by measuring the time it takes (in milliseconds) for thepropagated action potential to travel the measured distance (in centimeters). Since motornerves do conduct across a myoneural junction, the conduction velocity cannot bemeasured directly. Therefore, we use the formula:
velocity = change in distance/change in time
At least two sites must be stimulated (the same nerve is stimulated both proximally anddistally while recording over the same muscle). The difference in distance from the twostimulation sites is then divided by the difference in latencies of the two action potentialsobtained. Normal conduction velocities average above 50 meters/second in the upperextremities and above 40 meters/second in the lower extremities.
Amplitude
The amplitude of a CMAP represents the sum of the amplitudes of individual potentials.These individual potentials are generated by muscle fibers that are depolarized by nervefiber axons of similar conduction velocity. The amplitude is therefore dependent on theintegrity of the axons, the muscle fibers it depolarizes, and on the extent of variability ofthe conduction velocity of individual fibers. If some fibers are slow and others are fast thenthe action potential will be of longer duration (temporal dispersion) and lower amplitude(Fig. 4.5). When there is a CMAP with low amplitude, it is important to distinguishwhether this is occurring because of temporal dispersion or is due to decreased number ofaxons (Fig. 4.6).
The way you figure this out is that the duration of the action potential is prolonged intemporal dispersion and not prolonged if the amplitude is truly reduced. The area underthe curve is an alternative way to estimate the number of axons/muscle fibers that aredepolarized. In most cases, area measurements and amplitude measurements yield similarresults and either is used in common practice. Motor nerve amplitudes are measured inmillivolts. Sensory nerve amplitudes are much smaller and are measured in microvolts.CMAP amplitude is most often measured from baseline to negative peak or can bemeasured peak-to-peak. SNAP amplitude is measured from negative peak to positive peakor baseline to negative peak.
4 Nerve Conduction Studies 21
Time (millisecond)
Am
plit
ud
e (m
illiv
olt
)Figure 4.5Temporaldispersion
Duration
The duration is the time from the onset latency to termination latency. In other words, thetime from departure from baseline to final return to baseline. In some demyelinatingdiseases with nerve fibers affected differently, the duration may be increased (temporaldispersion). Generally, temporal dispersion is seen in acquired as opposed to congenitalneuropathies.
Technical Aspects
Stimulators
Stimulators are normally two metal or felt pad electrodes placed between 1.5 to 3 cmapart. When stimulating, in most cases the cathode (black or negative pole) is placedtoward the direction in which the nerve is to be stimulated. The potential sites forstimulation are reviewed later in this chapter. Conduction gel should be used to ensureelectrical contact. This may need to be reapplied periodically.
Sites of Stimulation
In order to accurately stimulate a nerve, it is necessary to recall the nerve’s anatomy.Given a strong enough impulse, any nerve can be stimulated. The more superficial thenerve, the easier (and more accurate) stimulation becomes. In reality, nerves are usuallystimulated when they are relatively superficial. This permits an electrical impulse thatthe patient can tolerate. Superficial stimulation also allows a more precise localization ofthe site on the nerve where it is stimulated. The farther away the nerve is from thecathode the stronger the stimulus required. Supramaximal stimulation occurs when furtherincreases in the intensity of the stimulus will not change the amplitude of the recordedpotential. Increases beyond this point however, can change the latency or stimulate adjacentnerves. Care should be taken not to ‘over stimulate’.
Some nerves may only be accessible to stimulation for a limited distance alongthe course of the nerve, whereas others can be stimulated at many sites along thenerve. In simple motor nerve studies usually two stimulus sites are used. In cases ofsuspected entrapment, it is important to be able to stimulate proximal and distal tothe suspected area.
Easy EMG22
Time (millisecond)
Am
plit
ud
e (m
illiv
olt
)
Figure 4.6 Axonalloss. Dotted lineindicates normalamplitude.
Recording Electrodes
Three electrodes are used to record a potential in nerve conduction studies and electro-myography. They are the active, reference and ground electrodes.
Active electrode: The active electrode, also referred to as E1 or G1, should be placedover the muscle belly (preferably over the motor point, where the nerve enters themuscle) during motor studies. During sensory studies, the active electrode should beplaced directly over the nerve (where the nerve is as superficial as possible).
Reference electrode: The reference electrode (sometimes called the E2 or G2) shouldbe placed on a nearby tendon or bone away from the muscle when attempting to record aCMAP. When performing sensory nerve action potentials (SNAPS), it has been shown that3–4 cm is the optimal inter-electrode separation. If SNAP electrodes are placed too closeto each other, decreased amplitude resembling an axonal lesion can occur. Compoundmuscle action potentials (CMAP) are less affected than SNAPS when electrodes areplaced less than 3–4 cm apart.
Ground electrode: The third type of electrode is called the ground electrode.Grounding is important for obtaining a response that is free of too much artifact. Usuallythe ground is larger than the recording electrodes and provides a large surface area incontact with the patient. The ground electrode should be placed between the stimulatingelectrode and the recording electrode.
Late Responses
The H-reflex is a monosynaptic or oligosynaptic spinal reflex involving both motor andsensory fibers. It electrically tests some of the same fibers as are tested in the ankle jerkreflexes. In fact it is rare to be unable to obtain an H-reflex in the presence of an anklejerk reflex. If this occurs, technical factors should be considered. In theory it is asensitive measure in assessing radiculopathy because 1. it helps to assess proximallesions, 2. it becomes abnormal relatively early in the development of radiculopathy, and3. it incorporates sensory fiber function proximal to the dorsal root ganglion. The H-reflex primarily assesses afferent and efferent S1 fibers. Clinically, L5 and S1radiculopathies may appear similar on EMG due to the overlap of myotomes. H-reflexesare probably of greatest value in distinguishing S1 from L5 radiculopathies.
When assessing for S1 radiculopathy, the H-reflex latency is recorded from thegastrocnemius-soleus muscle group upon stimulating the tibial nerve in the popliteal fossa(Fig. 4.7). The H-reflex is elicited with a submaximal stimulation with the cathodeproximal to the anode. As the intensity of the stimulation is gradually increased from peakH-amplitude, we generally see a diminishment of the H-amplitude with a concurrentincrease in the M wave amplitude. With supra maximal stimulation, the H-reflex is usuallyabsent.
The H-reflex can also be used in C6/C7 radiculopathy by recording over the flexorcarpi radialis muscle and stimulating the median nerve at the elbow. The median H-reflexis less commonly performed and clinically is less likely to be helpful for radiculopathythan a lower extremity H-reflex. Generally, gastrocnemius-soleus H-reflex latency side-to-side differences of greater than 1.5 ms are suggestive of S1 radiculopathy.
Although the H-reflex is sensitive, it has certain limitations: 1. patients with S1
radiculopathy can have a normal H-reflex; 2. an abnormal H-reflex is only suggestive,but not definitive for radiculopathy because the abnormality may originate in othercomponents of the long pathway involved, such as the peripheral nerves, plexuses, orspinal cord; 3. once the H-reflex becomes abnormal, it usually does not return to normal,
4 Nerve Conduction Studies 23
even over time; and finally the H-reflex is often absent in otherwise normal individualsover the age of 60 years. The reflexes therefore can be considered a sensitive, but notspecific indicator of pathology. Latency of the H-reflex is dependent on the age and leglength of the patient (Table 4.1). A side-to-side amplitude difference of 60% or moremay also indicate pathology.
F-waves are low amplitude late responses thought to be due to antidromic activation ofmotor neurons (anterior horn cells) following peripheral nerve stimulation, which thencause orthodromic impulses to pass back along the involved motor axons. Someelectromyographers have called this a ‘backfiring’ of axons. It is called the F-wave becauseit was first noted in intrinsic foot muscles. The F-wave has small amplitude, a variableconfiguration, and a variable latency. Generally F-wave amplitudes are up to 5% ofthe orthodromically generated motor response (M-response). The most widely used
Easy EMG24
Ground
Poplitealstimulation
Active
H-reflex
Reference
Figure 4.7 Setupfor H-reflex
4 Nerve Conduction Studies 25
Hei
gh
tA
ge
(yea
rs o
ld)
(cm
)15
2025
3035
4045
5055
6065
7075
8085
90
100
18.8
919
.14
19.3
919
.64
19.8
920
.14
20.3
920
.64
20.8
921
.14
21.3
921
.64
21.8
922
.14
22.3
922
.64
110
20.2
920
.54
20.7
921
.04
21.2
921
.54
21.7
922
.04
22.2
922
.54
22.7
923
.04
23.2
923
.54
23.7
924
.04
120
21.6
921
.94
22.1
922
.44
22.6
922
.94
23.1
923
.44
23.6
923
.94
24.1
924
.44
24.6
924
.94
25.1
925
.44
130
23.0
923
.34
23.5
923
.84
24.0
924
.34
24.5
924
.84
25.0
925
.34
25.5
925
.84
26.0
926
.34
26.5
926
.84
135
23.7
924
.04
24.2
924
.54
24.7
925
.04
25.2
925
.54
25.7
926
.04
26.2
926
.54
26.7
927
.04
27.2
927
.54
140
24.4
924
.74
24.9
925
.24
25.4
925
.74
25.9
926
.24
26.4
926
.74
26.9
927
.24
27.4
927
.74
27.9
928
.24
141
24.6
324
.88
25.1
325
.38
25.6
325
.88
26.1
326
.38
26.6
326
.88
27.1
327
.38
27.6
327
.88
28.1
328
.38
142
24.7
725
.02
25.2
725
.52
25.7
726
.02
26.2
726
.52
26.7
727
.02
27.2
727
.52
27.7
728
.02
28.2
728
.52
143
24.9
125
.16
25.4
125
.66
25.9
126
.16
26.4
126
.66
26.9
127
.16
27.4
127
.66
27.9
128
.16
28.4
128
.66
144
25.0
525
.325
.55
25.8
26.0
526
.326
.55
26.8
27.0
527
.327
.55
27.8
28.0
528
.328
.55
28.8
145
25.1
925
.44
25.6
925
.94
26.1
926
.44
26.6
926
.94
27.1
927
.44
27.6
927
.94
28.1
928
.44
28.6
928
.94
146
25.3
325
.58
25.8
326
.08
26.3
326
.58
26.8
327
.08
27.3
327
.58
27.8
328
.08
28.3
328
.58
28.8
329
.08
147
25.4
725
.72
25.9
726
.22
26.4
726
.72
26.9
727
.22
27.4
727
.72
27.9
728
.22
28.4
728
.72
28.9
729
.22
148
25.6
125
.86
26.1
126
.36
26.6
126
.86
27.1
127
.36
27.6
127
.86
28.1
128
.36
28.6
128
.86
29.1
129
.36
149
25.7
526
26.2
526
.526
.75
2727
.25
27.5
27.7
528
28.2
528
.528
.75
2929
.25
29.5
150
25.8
926
.14
26.3
926
.64
26.8
927
.14
27.3
927
.64
27.8
928
.14
28.3
928
.64
28.8
929
.14
29.3
929
.64
151
26.0
326
.28
26.5
326
.78
27.0
327
.28
27.5
327
.78
28.0
328
.28
28.5
328
.78
29.0
329
.28
29.5
329
.78
152
26.1
726
.42
26.6
726
.92
27.1
727
.42
27.6
727
.92
28.1
728
.42
28.6
728
.92
29.1
729
.42
29.6
729
.92
153
26.3
126
.56
26.8
127
.06
27.3
127
.56
27.8
128
.06
28.3
128
.56
28.8
129
.06
29.3
129
.56
29.8
130
.06
154
26.4
526
.726
.95
27.2
27.4
527
.727
.95
28.2
28.4
528
.728
.95
29.2
29.4
529
.729
.95
30.2
155
26.5
926
.84
27.0
927
.34
27.5
927
.84
28.0
928
.34
28.5
928
.84
29.0
929
.34
29.5
929
.84
30.0
930
.34
156
26.7
326
.98
27.2
327
.48
27.7
327
.98
28.2
328
.48
28.7
328
.98
29.2
329
.48
29.7
329
.98
30.2
330
.48
Tab
le 4
.1H
-ref
lex
valu
e b
ased
on
th
e ag
e an
d h
eig
ht:
(H
= 2
.74
+ 0
.05
x ag
e +
0.1
4 x
hei
gh
t +
1.4
)
Easy EMG26
Hei
gh
tA
ge
(yea
rs o
ld)
(cm
)15
2025
3035
4045
5055
6065
7075
8085
90
157
26.8
727
.12
27.3
727
.62
27.8
728
.12
28.3
728
.62
28.8
729
.12
29.3
729
.62
29.8
730
.12
30.3
730
.62
158
27.0
127
.26
27.5
127
.76
28.0
128
.26
28.5
128
.76
29.0
129
.26
29.5
129
.76
30.0
130
.26
30.5
130
.76
159
27.1
527
.427
.65
27.9
28.1
528
.428
.65
28.9
29.1
529
.429
.65
29.9
30.1
530
.430
.65
30.9
160
27.2
927
.54
27.7
928
.04
28.2
928
.54
28.7
929
.04
29.2
929
.54
29.7
930
.04
30.2
930
.54
30.7
931
.04
161
27.4
327
.68
27.9
328
.18
28.4
328
.68
28.9
329
.18
29.4
329
.68
29.9
330
.18
30.4
330
.68
30.9
331
.18
162
27.5
727
.82
28.0
728
.32
28.5
728
.82
29.0
729
.32
29.5
729
.82
30.0
730
.32
30.5
730
.82
31.0
731
.32
163
27.7
127
.96
28.2
128
.46
28.7
128
.96
29.2
129
.46
29.7
129
.96
30.2
130
.46
30.7
130
.96
31.2
131
.46
164
27.8
528
.128
.35
28.6
28.8
529
.129
.35
29.6
29.8
530
.130
.35
30.6
30.8
531
.131
.35
31.6
165
27.9
928
.24
28.4
928
.74
28.9
929
.24
29.4
929
.74
29.9
930
.24
30.4
930
.74
30.9
931
.24
31.4
931
.74
166
28.1
328
.38
28.6
328
.88
29.1
329
.38
29.6
329
.88
30.1
330
.38
30.6
330
.88
31.1
331
.38
31.6
331
.88
167
28.2
728
.52
28.7
729
.02
29.2
729
.52
29.7
730
.02
30.2
730
.52
30.7
731
.02
31.2
731
.52
31.7
732
.02
168
28.4
128
.66
28.9
129
.16
29.4
129
.66
29.9
130
.16
30.4
130
.66
30.9
131
.16
31.4
131
.66
31.9
132
.16
169
28.5
528
.829
.05
29.3
29.5
529
.830
.05
30.3
30.5
530
.831
.05
31.3
31.5
531
.832
.05
32.3
170
28.6
928
.94
29.1
929
.44
29.6
929
.94
30.1
930
.44
30.6
930
.94
31.1
931
.44
31.6
931
.94
32.1
932
.44
171
28.8
329
.08
29.3
329
.58
29.8
330
.08
30.3
330
.58
30.8
331
.08
31.3
331
.58
31.8
332
.08
32.3
332
.58
172
28.9
729
.22
29.4
729
.72
29.9
730
.22
30.4
730
.72
30.9
731
.22
31.4
731
.72
31.9
732
.22
32.4
732
.72
173
29.1
129
.36
29.6
129
.86
30.1
130
.36
30.6
130
.86
31.1
131
.36
31.6
131
.86
32.1
132
.36
32.6
132
.86
174
29.2
529
.529
.75
3030
.25
30.5
30.7
531
31.2
531
.531
.75
3232
.25
32.5
32.7
533
175
29.3
929
.64
29.8
930
.14
30.3
930
.64
30.8
931
.14
31.3
931
.64
31.8
932
.14
32.3
932
.64
32.8
933
.14
176
29.5
329
.78
30.0
330
.28
30.5
330
.78
31.0
331
.28
31.5
331
.78
32.0
332
.28
32.5
332
.78
33.0
333
.28
177
29.6
729
.92
30.1
730
.42
30.6
730
.92
31.1
731
.42
31.6
731
.92
32.1
732
.42
32.6
732
.92
33.1
733
.42
178
29.8
130
.06
30.3
130
.56
30.8
131
.06
31.3
131
.56
31.8
132
.06
32.3
132
.56
32.8
133
.06
33.3
133
.56
Tab
le 4
.1H
-ref
lex
valu
e b
ased
on
th
e ag
e an
d h
eig
ht:
(H
= 2
.74
+ 0
.05
x ag
e +
0.1
4 x
hei
gh
t +
1.4
) (c
on
t’d
)
4 Nerve Conduction Studies 27
Hei
gh
tA
ge
(yea
rs o
ld)
(cm
)15
2025
3035
4045
5055
6065
7075
8085
90
179
29.9
530
.230
.45
30.7
30.9
531
.231
.45
31.7
31.9
532
.232
.45
32.7
32.9
533
.233
.45
33.7
180
30.0
930
.34
30.5
930
.84
31.0
931
.34
31.5
931
.84
32.0
932
.34
32.5
932
.84
33.0
933
.34
33.5
933
.84
181
30.2
330
.48
30.7
330
.98
31.2
331
.48
31.7
331
.98
32.2
332
.48
32.7
332
.98
33.2
333
.48
33.7
333
.98
182
30.3
730
.62
30.8
731
.12
31.3
731
.62
31.8
732
.12
32.3
732
.62
32.8
733
.12
33.3
733
.62
33.8
734
.12
183
30.5
130
.76
31.0
131
.26
31.5
131
.76
32.0
132
.26
32.5
132
.76
33.0
133
.26
33.5
133
.76
34.0
134
.26
184
30.6
530
.931
.15
31.4
31.6
531
.932
.15
32.4
32.6
532
.933
.15
33.4
33.6
533
.934
.15
34.4
185
30.7
931
.04
31.2
931
.54
31.7
932
.04
32.2
932
.54
32.7
933
.04
33.2
933
.54
33.7
934
.04
34.2
934
.54
186
30.9
331
.18
31.4
331
.68
31.9
332
.18
32.4
332
.68
32.9
333
.18
33.4
333
.68
33.9
334
.18
34.4
334
.68
187
31.0
731
.32
31.5
731
.82
32.0
732
.32
32.5
732
.82
33.0
733
.32
33.5
733
.82
34.0
734
.32
34.5
734
.82
188
31.2
131
.46
31.7
131
.96
32.2
132
.46
32.7
132
.96
33.2
133
.46
33.7
133
.96
34.2
134
.46
34.7
134
.96
189
31.3
531
.631
.85
32.1
32.3
532
.632
.85
33.1
33.3
533
.633
.85
34.1
34.3
534
.634
.85
35.1
190
31.4
931
.74
31.9
932
.24
32.4
932
.74
32.9
933
.24
33.4
933
.74
33.9
934
.24
34.4
934
.74
34.9
935
.24
191
31.6
331
.88
32.1
332
.38
32.6
332
.88
33.1
333
.38
33.6
333
.88
34.1
334
.38
34.6
334
.88
35.1
335
.38
192
31.7
732
.02
32.2
732
.52
32.7
733
.02
33.2
733
.52
33.7
734
.02
34.2
734
.52
34.7
735
.02
35.2
735
.52
193
31.9
132
.16
32.4
132
.66
32.9
133
.16
33.4
133
.66
33.9
134
.16
34.4
134
.66
34.9
135
.16
35.4
135
.66
194
32.0
532
.332
.55
32.8
33.0
533
.333
.55
33.8
34.0
534
.334
.55
34.8
35.0
535
.335
.55
35.8
195
32.1
932
.44
32.6
932
.94
33.1
933
.44
33.6
933
.94
34.1
934
.44
34.6
934
.94
35.1
935
.44
35.6
935
.94
196
32.3
332
.58
32.8
333
.08
33.3
333
.58
33.8
334
.08
34.3
334
.58
34.8
335
.08
35.3
335
.58
35.8
336
.08
197
32.4
732
.72
32.9
733
.22
33.4
733
.72
33.9
734
.22
34.4
734
.72
34.9
735
.22
35.4
735
.72
35.9
736
.22
198
32.6
132
.86
33.1
133
.36
33.6
133
.86
34.1
134
.36
34.6
134
.86
35.1
135
.36
35.6
135
.86
36.1
136
.36
199
32.7
533
33.2
533
.533
.75
3434
.25
34.5
34.7
535
35.2
535
.535
.75
3636
.25
36.5
200
32.8
933
.14
33.3
933
.64
33.8
934
.14
34.3
934
.64
34.8
935
.14
35.3
935
.64
35.8
936
.14
36.3
936
.64
Tab
le 4
.1H
-ref
lex
valu
e b
ased
on
th
e ag
e an
d h
eig
ht:
(H
= 2
.74
+ 0
.05
x ag
e +
0.1
4 x
hei
gh
t +
1.4
) (c
on
t’d
)
Easy EMG28
Hei
gh
tA
ge
(yea
rs o
ld)
(cm
)15
2025
3035
4045
5055
6065
7075
8085
90
201
33.0
333
.28
33.5
333
.78
34.0
334
.28
34.5
334
.78
35.0
335
.28
35.5
335
.78
36.0
336
.28
36.5
336
.78
202
33.1
733
.42
33.6
733
.92
34.1
734
.42
34.6
734
.92
35.1
735
.42
35.6
735
.92
36.1
736
.42
36.6
736
.92
203
33.3
133
.56
33.8
134
.06
34.3
134
.56
34.8
135
.06
35.3
135
.56
35.8
136
.06
36.3
136
.56
36.8
137
.06
204
33.4
533
.733
.95
34.2
34.4
534
.734
.95
35.2
35.4
535
.735
.95
36.2
36.4
536
.736
.95
37.2
205
33.5
933
.84
34.0
934
.34
34.5
934
.84
35.0
935
.34
35.5
935
.84
36.0
936
.34
36.5
936
.84
37.0
937
.34
206
33.7
333
.98
34.2
334
.48
34.7
334
.98
35.2
335
.48
35.7
335
.98
36.2
336
.48
36.7
336
.98
37.2
337
.48
207
33.7
333
.98
34.2
334
.48
34.7
334
.98
35.2
335
.48
35.7
335
.98
36.2
336
.48
36.7
336
.98
37.2
337
.48
208
34.0
134
.26
34.5
134
.76
35.0
135
.26
35.5
135
.76
36.0
136
.26
36.5
136
.76
37.0
137
.26
37.5
137
.76
209
34.1
534
.434
.65
34.9
35.1
535
.435
.65
35.9
36.1
536
.436
.65
36.9
37.1
537
.437
.65
37.9
210
34.2
934
.54
34.7
935
.04
35.2
935
.54
35.7
936
.04
36.2
936
.54
36.7
937
.04
37.2
937
.54
37.7
938
.04
215
34.9
935
.24
35.4
935
.74
35.9
936
.24
36.4
936
.74
36.9
937
.24
37.4
937
.74
37.9
938
.24
38.4
938
.74
220
35.6
935
.94
36.1
936
.44
36.6
936
.94
37.1
937
.44
37.6
937
.94
38.1
938
.44
38.6
938
.94
39.1
939
.44
230
37.0
937
.34
37.5
937
.84
38.0
938
.34
38.5
938
.84
39.0
939
.34
39.5
939
.84
40.0
940
.34
40.5
940
.84
Tab
le 4
.1H
-ref
lex
valu
e b
ased
on
th
e ag
e an
d h
eig
ht:
(H
= 2
.74
+ 0
.05
x ag
e +
0.1
4 x
hei
gh
t +
1.4
) (c
on
t’d
)
parameter is the latency of the shortest reproducible response. The F-wave can be found inmany muscles of the upper and lower extremities. Unfortunately F-waves have not turnedout to be as sensitive a test as initially hoped. The reasons for this are:
1. the pathways involve only the motor fibers, 2. as with the H-reflex, it involves a long neuronal pathway so that if there is a focal
lesion it might be obscured, 3. if an abnormality is present, the F-wave will not pinpoint the exact location because
any lesion, from the anterior horn cell to the muscle being tested, can affect the F-wave similarly,
4. since muscles have multiple root innervations, the shortest latency may reflect thehealthy fibers in the non-affected root, and
5. the latency and amplitude of an F-wave is variable so that multiple stimulationsmust be performed to find the shortest latency. If not enough stimulations are done(usually more than 10), the shortest latency may not be apparent. Thus, use of F-waves in evaluating for radiculopathy are extremely limited and should not be thesole basis upon which the diagnosis is made. See Table 4.2 for a comparison of H-reflex and F-waves.
F-wave Ratio
Because errors can occur when measuring distances for F-wave conduction velocities, analternative F-wave technique was developed which did not require distance measurements.The ratio is as follows:
(F-wave latency – CMAP latency) – 1 ms––––––––––––––––––––––––––––––––––––––––CMAP latency × 2
(M = CMAP latency; this ratio may be rewritten as (F – M – 1)/2 M). The ratio assumesthat the distance from the elbow (or knee) to the hand (or foot) is approximately equal tothe distance from the elbow (or knee) to the spinal cord (Fig. 4.8). Therefore, stimulationmust be performed at the elbow or knee.
The normal F-wave ratio in the upper limb is approximately 1 ± 0.3 and in thelower limb the normal F-ratio is 1.1 ± 0.3. A ratio higher than 1.3 indicates a proximallesion, since the numerator of the equation includes the proximal stimulation from theF-wave. A ratio below 0.7 indicates a distal lesion, since a larger CMAP latency willdecrease the numerator and increase the denominator. Therefore, an F-ratio is notnecessarily more sensitive than F-latency, but it does allow one to assess whether theslowing is in the proximal or distal segment of the nerve. It should be noted that F-wavesare non-specific. Therefore, interpreting NCS results using F-waves must be done inconjunction with other information.
Important Points to Remember
● When stimulating proximal and distal sites, the waveforms should be similar inmorphology and duration. For motor studies, amplitude should not decrease bymore than 20% on proximal stimulation (when compared to the distal amplitude).
● Non-identical waveforms may be secondary to accidental stimulation of anothernerve. For example, the peroneal and tibial nerves are very close in the poplitealfossa. If the pulse width (duration of the stimulus) is increased, the wrong nerve maybe stimulated. Usually, the CMAP that results will have an initial positive (downward)
4 Nerve Conduction Studies 29
!
Easy EMG30
Parameter H-reflex F-wave
Derivation of name Originally described Originally obtained in by Hoffman foot muscles
Type of synapse Monosynaptic or Polysynapticoligosynaptic
Pathway Sensory orthodromic Motor antidromic Motor antidromic Motor orthodromic
Stimulus required Submaximal (stronger Supramaximalstimulation produces inhibition secondary to collision of orthodromic impulses by antidromic conduction in motor axons)
Where they can be Soleus Most muscles (distal preferred)elicited? (Normals) Flexor carpi radialis
Stimulation site Posterior tibial nerve Along peripheral nerve in popliteal fossa
Stimulus cathode Proximal Proximal
Size of response Amplification of motor Small (motor neurons are (compared to M) response centrally activated infrequently with
(due to reflex antidromic stimulation)activation of motor neurons)
Facilitation Enhanced by N/Amaneuvers that increase motor-neuron pool excitability (contraction or CNS lesion)
Uses S1
Radiculopathy Demyelinating polyneuropathies(sensitive but not Guillain–Barréspecific) Proximal nerve or root injury Guillain–Barré (not test of choice – non-specific) syndrome
Latency, amplitude Reproducible latency Variable in amplitude, latency and configuration and configuration and configuration
(amplitude dependent on stimulation)
Side-to-side > 1.5 msec >2 msec from handdifference >3 msec from calf
>4 msec from foot
Ratio N/A F – M – 1–––––––––2 M
Table 4.2 Comparison of H-reflex and F-wave
deflection, since the active electrode is not over the muscle being stimulated. (If youare not sure which nerve is being stimulated, check for the physiological response. Forexample, if the ankle plantar flexes, the tibial nerve is usually being stimulated.)
● An increased duration (and smaller amplitude) on proximal stimulation could indicatea segmental demyelination in the segment being stimulated. In this situation (referredto as temporal dispersion), the area under the curve of the CMAP should not change.All of the axons are still contributing to the CMAP, but some are conducting muchslower than others (see Fig. 4.8).
● A decrease of more than 20% amplitude with the proximal stimulation (compared tothe distal amplitude) could indicate a conduction block across the segment. Aconduction block occurs when an area of demyelination is so severe that saltatoryconduction cannot occur. The impulse is ‘blocked’ from propagating and thereforethose axons cannot help to contribute to the amplitude of the CMAP. Remember,however, that this is a focal myelin problem, not an axonal problem, even though theamplitude is affected.
● With motor nerves, a distance of at least 10 cm between stimulation points shouldbe used in order to decrease the likelihood of a measurement error significantlyaffecting the calculated conduction velocity. Since velocity = distance/time, a 1 cmerror in measuring over a 5-cm distance will result in a 20% error in distance and willsignificantly affect the calculated conduction velocity. If the distance is 10 cm, a1 cm error only results in a 10% error in distance. Generally, due to skin elasticityand other factors, a measurement will be accurate to within about 1 cm. Obesity inthe patient may decrease the ability to accurately measure the length of the nervesegment.
● You can estimate the amount of axonal loss in an acute peripheral nerve lesion if youcompare the amplitude of the CMAP on the unaffected side. For example, if the
4 Nerve Conduction Studies 31
Distance
hand to elbow ≅ elbow to spine
Distan
ce
foo
t to kn
ee ≅ knee to
spin
e
Figure 4.8 F-waveratios arecalculated basedon theassumption thatthe distance fromthe elbow (orknee) to the hand(or foot) isapproximatelyequal to thedistance from theelbow (or knee)to the spinal cord
Easy EMG32
Nerve Active electrode Reference Ground Stimulationelectrode
MEDIAN – Place on the Place on the Placed on 1. Midwrist:Motor anatomic center proximal the dorsum Distal (see Fig. A1.1) of the abductor phalanx of the of the stimulation is
pollicis brevis. thumb. Place hand on the (Usually about 1/2 3–4 cm distal between palmar the distance from to the the active surface of the distal wrist recording electrode the hand crease to the electrode and the between the metacarpal stimulator tendons of phalangeal joint.) the flexor
carpi radialis and the palmaris longus. Stimulation should be 8 cm proximal to the active electrode. 2. Elbow:Stimulate proximal and medial to the antecubital space, just lateral to the brachial artery. 3. Axilla:Stimulation is performed in the axilla at least 10 cm proximal to the elbow stimulation
MEDIAN – Place 14 cm Place 3–4 cm Place on Since this is Sensory proximal from proximal to the dorsum in the (Orthodromic) the ring cathode the recording of the hand physiological (see Fig. A1.2) at the midwrist. electrode between direction,
(This should be the stimulate about the same stimulating distally from spot where the ring the 2nd digit motor portion electrodes using ring was stimulated.) and the electrodes.
recording Ring electrode cathode: The
cathode is placed near the PIP joint. Ring anode: Place around the second DIP
Table 4.3 Nerve conduction studies setup
4 Nerve Conduction Studies 33
Nerve Active electrode Reference Ground Stimulationelectrode
MEDIAN – Place over the Place the Ground is The Sensory proximal reference placed on stimulation (Antidromic) interphalangeal electrode over the dorsum points occur: (see Fig. A1.3) joint on the the distal of the hand 7 cm proximal
2nd finger interphalangeal between to the active joint the active electrode at
electrode the mid and palm, and stimulator 7 cm proximal
to the mid palm at the wrist (between the tendons of the flexor carpi radialis and the palmaris longus). (For large hands, 8 cm can be used. For small hands, 6 cm can be used.)
ULNAR – motor Place on the Place distally Place on 1. Wrist:(see Fig. A1.4) center of the over the the dorsum stimulate
abductor digiti 5th digit of the 8 cm minimi. It may hand proximally help to palpate between from the that muscle by the active active abducting the and electrode. 5th digit stimulating This is usually
electrode just medial to the flexor carpi ulnaris tendon. 2. Below the elbow: when stimulating at the elbow region, you must flex the elbow so there is an angle of about 90 degrees. Feel for the ulnar groove (the funny bone) and stimulate just below this area.
Table 4.3 Nerve conduction studies setup (cont’d)
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Nerve Active electrode Reference Ground Stimulationelectrode
3. Above the elbow:Stimulation site is located at least 10 cm proximal to the below elbow stimulation in line with the path of the ulnar nerve. 4. Axilla: This stimulation site is located at least 10 cm proximal to the above elbow site at about the midpoint of the arm in the axilla
Remember that the arm should be maintained with the same elbow flexion whenstimulating and measuring the nerve.The responses from all four sites should be similar in waveform, amplitude andduration.
Dorsal ulnar On the dorsum Base of the Place on 14 cm cutaneous of the hand, 5th digit the dorsum proximal to nerve (see between the of the the active Fig. A1.5) fourth and fifth hand electrode,
metacarpal bones between between the the active ulna and the and flexor carpi stimulating ulnaris electrode muscle
ULNAR Place 14 cm Position 3–4 cm Place on Ring sensory proximally from proximal to the dorsum cathode:(orthodromic) the stimulating the active of the Place over (see Fig A1.6) ring cathode on electrode hand the PIP joint
the ulnar side between of the 5th of the wrist the finger.
stimulating Ring anode:and Place over recording the 5th DIP electrodes joint
Table 4.3 Nerve conduction studies setup (cont’d)
4 Nerve Conduction Studies 35
Nerve Active electrode Reference Ground Stimulationelectrode
ULNAR sensory Place on the Place over the Place on Stimulate at (antidromic) 5th digit 5th DIP joint, so the dorsum the wrist a (see Fig. A1.7) over the PIP joint that a distance of the distance of
of not less hand 14 cm than 3 cm is between proximal maintained the active from the
and active stimulating electrode electrodes near the
proximal crease of the wrist
RADIAL sensory Place over the Place on Place Stimulate (antidromic) sensory branch the lateral between 10–14 cm (see Fig. A1.8) as it crosses side of the the active proximal to
the extensor head of the electrode the active pollicis longus 2nd metacarpal and the electrode tendon. Can about 3–4 cm stimulating over the be palpated on distal to the site radial side of ulnar side of the active the forearm anatomic snuffbox electrodewhen the thumb is extended
Alternative Ring electrode Ring electrode Place on Stimulate Radial over the over the the dorsum 11 cm Sensory metacarpal interphalangeal of the proximal to (antidromic) phalangeal joint joint of the hand the active (see Fig. A1.8) of the thumb thumb electrode, in
the anatomical snuffbox
RADIAL motor Place over the Place over the Place Forearm: (see Fig. A1.9) extensor indicis ulnar styloid between 8 cm proximal
proprius on the the active to the ulnar dorsum of the electrode styloid just hand. Locate by and the radial to theextending the stimulation extensor 2nd digit. (A site carpi ulnaris needle is muscle. sometimes used Elbow:instead of a Stimulate surface electrode.) 6 cm distalNote that the to the lateral amplitude of the epicondyle CMAP cannot be of the compared if using humerus a needle for the (which is active electrode between the
biceps tendon and the brachio-radialis muscle.)
Table 4.3 Nerve conduction studies setup (cont’d)
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Nerve Active electrode Reference Ground Stimulationelectrode
Axilla: stimulate at the medial edge of the triceps with the arm externally rotated and the forearm supinated
LATERAL Draw a line from Place the Place The cathode ANTEBRACHIAL the stimulation reference between is placed at CUTANEOUS point to the radial electrode 4 cm the active the elbow antidromic styloid. Place the distal to the electrode crease lateral sensory reference electrode active and the to the biceps (see Fig. A1.10) 12 cm distal to the electrode stimulation tendon
cathode along sitethis line
MUSCULO- Place just distal Place just Place over The cathode CUTANEOUS to the midportion proximal to the deltoid is placed Motor (see of the biceps the antecubital muscle above the Fig. A1.11) muscle fossa, where upper clavicle
the biceps and lateral to tendon meets the the muscle sternoclei-fibers domastoid
muscle. The anode is placed superiorly to the cathode (Erb’s point)
AXILLARY Place on the Place over the Place The cathode Motor (see middle of the insertion of between is placed Fig. A1.12) deltoid muscle the deltoid on the active lateral to
the lateral electrode where the surface of and the sternoclei-the humerus stimulation domastoid
site muscle meets the clavicle, just above the clavicle. The anode is placed superiorly and angled medially (Erb’s point)
Table 4.3 Nerve conduction studies setup (cont’d)
4 Nerve Conduction Studies 37
Nerve Active electrode Reference Ground Stimulationelectrode
PERONEAL* Place on the Place on the Place Ankle:(see Fig. A1.13) anatomic center 5th toe between Measure 8 cm
of the extensor the active proximal to digitorum brevis electrode the EDB on (EDB). Ask the and the the lateral patient to extend stimulation anterior their toes and site surface of palpate for the the foot.muscle on the anterior lateral Fibula:surface on the Stimulate dorsum of the foot below the (usually located head of the about 6 cm from fibula the lateral anterior to malleolus.) the neck of
the fibula.
Popliteal:Measure at least 10 cm proximal from the fibula and stimulate in the lateral border of the popliteal fossa. Look for ankle dorsiflexion
Sural – sensory Line up the active Place distal Place Measure (see Fig. A1.14) electrode inferior (at least 3 cm) between 14 cm
to the lateral to the active the active proximal malleolus (about electrode and electrode from the 2 cm) and make parallel to and the active sure it is parallel the sole of stimulation electrode to the sole of the foot site near the the foot midline of
the gastroc-nemius. Work your way laterally until an acceptable SNAP is achieved
* Note: In many normal individuals, the EDB muscle may be atrophied. If low amplitudeis obtained, it may be useful to place the active electrode over the tibialis anteriormuscle and stimulate at the fibular head.
Table 4.3 Nerve conduction studies setup (cont’d)
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Nerve Active electrode Reference Ground Stimulationelectrode
Posterior Tibial Place on the Place on the Place 1. Go slightly 1 – motor (see abductor hallucis great toe’s between posterior to Fig. A1.15) muscle. Feel for medial surface the active the medial
the navicular electrode malleolus and bone of the foot and the stimulate and go stimulation 10 cm 1 fingerbreadth site proximal to toward the the active plantar surface of electrode.the foot and 2. Stimulate 1 fingerbreadth in the toward the popliteal great toe fossa, slightly
lateral to its midline. (Look for ankle plantar flexion with stimulation.)
SUPERFICIAL Place about one Place at least Place on Stimulate PERONEAL fingerbreadth 3 cm distal to the anterior 14 cm SENSORY medial to the the active tibia proximal to (see Fig. A1.16) lateral malleolus electrode between the active
the active electrode electrode along the and the anterior and stimulation lateral site surface of
the leg
SCIATIC Place on the EDB Place on the Place Stimulate (see Fig. A1.17) muscle (peroneal small toe ground on using a
component) or (peroneal the dorsum needle in the abductor hallucis comp.) or great of the foot middle of muscle (tibial toe (tibial the gluteal component) comp.) fold
LATERAL Draw a line from Place the Place Stimulate FEMORAL the ASIS to the reference between 1 cm medial CUTANEOUS – lateral border of electrode the active to the ASIS. Antidromic the patella. Place about 3 cm electrode If using a (see Fig. A1.18) the active distal to the and the cathode
electrode reference stimulation needle for 16–18 cm distally electrode along site stimulation, along this line the same line place a
connecting the monopolar ASIS and the needle 1 cm lateral patella medial to the
ASIS, and place the anode several centimeters proximal
Table 4.3 Nerve conduction studies setup (cont’d)
amplitude of a median CMAP is 10 millivolts on the non-affected side, and 5millivolts on the affected side, you can estimate that approximately 50% of theaxons have been lost.
● When stimulating the ulnar nerve, the elbow should be bent to 70–90 degrees. If theelbow is held straight, the calculated conduction velocity will be falsely decreased.However the most important thing to remember is that if both elbows are not in thesame position, there will be a false side-to-side velocity difference.
Table 4.3 includes, in chart form with illustrations, the proper placement of electrodesfor the most commonly used motor and sensory studies. For the normal values of mostperipheral nerve studies, see Chapter 22.
4 Nerve Conduction Studies 39
Nerve Active electrode Reference Ground Stimulationelectrode
H-REFLEX Measure the Place on the Place Stimulate in (see Fig. A1.19) distance between Achilles tendon between the popliteal
the popliteal the active fossa, slightly crease and the electrode lateral to the medial malleolus. and the midline. Place the active stimulation Remember electrode halfway site to turn the between the stimulator above measured around with distances. (Over the cathode the medial proximal to gastrocnemius the anode. A muscle.) stimulus just
greater than that to evoke a minimal M response is applied to the posterior tibial nerve in the center of the popliteal crease
F-WAVE Same setup used for motor nerve conduction of Position the individual nerves cathode
proximal and use a supra-maximal stimulus to the nerve using standard electrode placements
Table 4.3 Nerve conduction studies setup (cont’d)
5ElectromyographyLyn Weiss, Jay Weiss, Walter Gaudino, Victor Isaac, Kristin Gustafson
Electromyographic (EMG) testing involves evaluation of the electrical activity of a muscleand is one of the fundamental parts of the electrodiagnostic medical consultation. It is bothan art and a science. It requires a thorough knowledge of the anatomy of the muscles beingtested, machine settings and the neurophysiology behind the testing.
The electromyographer must be cognizant that the test is inherently uncomfortable. Itis important to obtain the confidence and cooperation of the patient. Most patients aremore comfortable when time is taken to explain the reasons for the testing and whatinformation can be gained from the testing. It is a fallacy that the test is not uncomfortableand any attempt to convince a patient to the contrary is certain to fail. Some things thatcan be done to allay the patient’s fear are to perform the study in a quiet room, speakingin a confident and calming manner, playing music of the patient’s choice and keeping theroom temperature comfortable.
Muscle Physiology
EMG assesses skeletal or voluntary muscle (rather than smooth or cardiac muscle). Themuscle fibers that account for the strength of a contraction are extrafusal fibers (as opposedto intrafusal fibers of the muscle spindle). The extrafusal fibers are relaxed at rest with anintracellular resting potential of approximately –80 mV (similar to nerve fibers). Thesarcolemma is a plasma membrane surrounding a muscle fiber. The action potentialfrom a motor nerve fiber will synapse at the neuromuscular junction and then propagatealong the sarcolemma. The sarcolemma has extensions into the muscle fibers called t-tubules. The depolarization of the t-tubules causes release of calcium from thesarcoplasmic reticulum. The calcium release results in changes in the actin and myosin.This shortens the actin-myosin functional unit, resulting in muscle contraction. EMG isactually measuring the electrical excitation of the muscle fibers.
Motor Units
Muscles contract and produce movement through the orderly recruitment of motor units.A motor unit is defined as one anterior horn cell, its axon, and all the muscle fibersinnervated by that motor neuron. A motor unit is the fundamental structure that is assessedin electromyography. The motor unit architecture refers to its size, distribution, andendplate area. When a person starts to contract a muscle, the first motor units to fire areusually the smallest. These are the Type I motor units. As the contraction increases, there isan orderly recruitment of larger motor units (which have a higher threshold). They begin tofire and add to the force of the contraction. 41
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Before You Begin
Most students of electrodiagnostic medicine are a little intimidated by the EMG part ofthe test. Sometimes, practicing with an orange can help you get the feel of the needle andhow to position it. The ‘feel’ of transitioning the needle between the rind and the pulp of anorange is similar to piercing the muscle after inserting the needle through the skin. Inkeeping with the first tenet of medicine, ‘first do no harm’, it is important to know whereto place the needle and why you are testing a certain muscle so as not to subject the patientto unnecessary testing. A good working knowledge of muscle anatomy is an essential toolfor placing the needle in the appropriate muscle.
Electrodes
Just as with nerve conduction studies, you need a ground, a reference and an activeelectrode. The needle is the ‘active electrode’; the reference may be separate or part of theneedle itself. If the reference is separate it should be placed over the same muscle that isbeing tested by the needle. The ground can be placed anywhere on the extremity beingtested.
Universal precautions must always be practiced during the needle portion of the test.This is to protect you as well as the patient. Universal precautions include using gloves,proper needle disposal, and using a one-handed technique for needle recapping. This canbe done by securing the needle cap to the preamplifier and using one hand to place theneedle back in the cap between muscle testing (Fig. 5.1).
Types of Needle Electrodes
Monopolar Needle
Monopolar needles are made of stainless steel and have a fine point insulated except atthe distal 0.2 to 0.4 mm segment (Fig. 5.2). They require a surface electrode or a secondneedle in the subcutaneous tissue as a reference lead. A separate surface electrodeplaced on the skin serves as a ground. A monopolar needle records the voltage changesbetween the tip of the electrode and the reference. It registers a larger potential than aconcentric needle using the same source. The reasons for this include the concentricneedle’s shape, picking up from a 180-degree field, whereas the monopolar picks upfrom a full 360-degree field around the needle. These differences in configuration helpexplain the larger amplitudes and increased polyphasicity recorded when a monopolarneedle is used. A monopolar needle also has a smaller diameter and a teflon or similarcoating. This makes the monopolar less uncomfortable than a concentric needle. This,combined with its cost advantage over the concentric, has led to its preferentialclinical use.
Standard or Concentric Needle
A concentric needle is a stainless steel cannula similar to a hypodermic needle with awire in the center of the shaft (Fig. 5.3). The pointed tip of the needle has an oval shape.While the wire is bare at the tip, the shaft can conduct electrical activity along its entirelength. The needle, when near a source of electrical activity, registers the potentialdifference between the wire and the shaft. It is important to remember that the exposedactive electrode is on the beveled portion of the cannula and thus is picking up from onedirection (180 degrees rather than 360 degrees as in a monopolar needle). A separatesurface electrode serves as the ground. The concentric electrode is less ‘noisy’ than themonopolar electrode, providing a clearer signal.
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5 Electromyography 43
Figure 5.1 Needlerecapping.
Figure 5.2Monopolarneedle.
A
B
Recording electrode
Reference electrode
Groundelectrode
Bipolar Needle
The cannula of the bipolar needle contains two fine stainless steel or platinum wires(Fig. 5.4). This electrode is larger in diameter than the standard coaxial concentric needle.It registers the potential electrical difference between the two inside wires while thecannula serves as the ground. The bipolar needle detects potentials from a much smallerarea than the standard coaxial concentric needle. This needle is also slightly moreuncomfortable than a monopolar needle because of its increased diameter. This electrodeis used primarily for research, not in routine clinical studies.
Single-fiber Needle
Single-fiber needles may wire exposed along the shaft serving as the leading edge torecord from individual muscle fibers rather than motor units. These electrodes are usedto assess neuromuscular junction transmission and fiber density, topics that are beyondthe scope of this text.
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Recording electrode
Reference (cannula) electrode
Separate groundelectrode
Figure 5.3Concentricneedle.
Figure 5.4Bipolar concentricneedle.
Recording electrode
Reference (cannula) electrode
Cannula groundelectrode
Planning the Examination
It is important to plan out which muscles you will test before you begin. This plan maychange, as you proceed, depending on the results of the muscles being tested. If you thinkthe patient will only be able to tolerate a limited number of muscles, start with the ones thatwill contribute the most to your diagnosis. The test is uncomfortable, and many people areafraid of needles. Therefore, try to test as few muscles as possible without sacrificing thequality of the examination.
Starting the Test
The EMG examination can be divided into four components:
● insertional activity● examination of muscle at rest● analyzing the motor unit● recruitment.
Prior to evaluating insertional activity and examination of the muscle at rest it is importantto make sure that the low frequency filter is set at 10–30 Hz and the high frequency filter isset at 10,000–20,000 Hz (10–20 kHz), the amplifier sensitivity is set at 50–100 microvoltsper division and the sweep speed is usually set at 10 msec per division. The needleshould be inserted into the muscle quickly and deliberately. Tensing the skin will allowquicker needle insertion and less discomfort to the patient.
For the first two components of the examination, insertional activity and examinationof the resting muscle, the needle electrode is directed through the muscle in four quadrants.Each of these quadrants can be examined at three or four different depths, allowing 12 to 16discrete areas of muscle to be examined electrically. The EMG has been likened to an‘electrical biopsy’and as with any biopsy the more areas examined the lower the chance offalse negatives.
Insertional Activity
Healthy muscle at rest is electrically silent as soon as needle movement stops, as long asthe endplate region is avoided. During this portion of the examination, the muscle beingtested should be at rest. The best way to electrically silence the muscle (if the patientcannot relax the muscle) is to tell the patient to contract the antagonist muscle. Forexample, if you put a needle in the biceps muscle, and the patient’s elbow is bent, motorunits in the biceps muscle are probably firing. Telling the patient to straighten the elbowwill activate motor units in the triceps muscle (and inactivate motor units in the bicepsmuscle). Since it is difficult to activate both the agonist and antagonist muscles at thesame time, the agonist muscle usually will relax. (Remember that the biceps muscle isalso a supinator. Therefore, pronating the arm is also important in order to put the bicepsmuscle at rest. Here again, a working knowledge of where muscles are, what they do,and what nerves innervate them is essential.)
If the needle is properly placed in the muscle you are testing you will hear and seebrief electrical activity associated with the needle movement. This is called insertionalactivity. The sound associated with this needle movement has been described as ‘crisp’and is temporally related to the high-frequency positive and negative spikes that areeasily visualized on the monitor. This should be done in four different quadrants and at
5 Electromyography 45
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four different depths. To reposition the needle pull it back carefully to the plane wherethe muscle and fascia transition (with practice you will soon be able to ‘feel’ when youleave the muscle) and then insert at a new angle. Try not to pull back too far or you willpull the needle all the way out and have to restick the needle into the patient.
Normal insertional activity typically only lasts a few hundred milliseconds, justbarely longer than the needle movement itself. It is thought to be generated by the needletip physically depolarizing the muscle fibers as it pierces and/or displaces them.
Decreased insertional activity occurs when the needle is inserted into an atrophiedmuscle. The sensation of inserting the needle has been described as putting a needle intosand. Remember that the initial sound and electromyographic recording of needleinsertion into muscle is actually the muscle fiber being injured by needle movement.With muscle atrophy, there will be decreased response to needle insertion, as there isless muscle tissue. Caution should be used in interpretation, especially without clinicallyvisible muscle wasting, to make sure that the needle was indeed in muscle and not othertissue such as adipose or connective tissue.
Increased insertional activity may occur when there is muscle pathology and isevidenced by the presence of positive sharp waves and sometimes fibrillation potentialsthat are apparent only on insertion and do not persist. Increased insertional activity mayprecede actual denervation. On insertion, any electrical activity that lasts longer than300 milliseconds is considered increased. These determinations require a subjectiveassessment based on the experience of the electromyographer (Fig. 5.5).
Examination of the Muscle at Rest
Once the needle is inserted into the muscle, pause several seconds to assess forspontaneous activity. Normal muscles should be electrically silent after needle insertion.For this portion of the test, the muscle should still be at rest.
Spontaneous Activity
Spontaneous activity is typically abnormal and occurs in the presence of pathology.Normal muscle has a resting membrane potential of –80 mv relative to the extracellular
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Increased insertional activity
Normal muscle
Figure 5.5 (Top)Normalinsertionalactivity. (Bottom)Increasedinsertionalactivity.
fluids. After injury or denervation, the membrane potential becomes more positive dueto an influx of Na+ into the damaged cell membrane. The muscle cell tends to becomeless negative and therefore closer to the potential needed for the generation ofspontaneous action potentials. This occurs when the cell resting membrane potentialreaches –60 mv.
The term ‘denervation potentials’ is a misnomer and should not be used to describespontaneous activity. Spontaneous activity is a more appropriate term. Irritation can bebrought about by many factors other than nerve injury, such as metabolic andinflammatory muscle disease, and local muscle trauma. Either the muscle or the nervemay generate spontaneous activity (Table 5.1).
Positive sharp waves (PSW), fibrillations, complex repetitive discharges and myotonicdischarges are examples of abnormal spontaneous potentials that are generated at the levelof the muscle fiber. Abnormal findings, due to a dysfunction of the neural input to themuscle, can lead to the development of myokymic discharges as well as cramps,neuromyotonic discharges, tremors, multiples and fasciculations. The more commontypes of spontaneous activity will be described below. Because of their small amplitude,the gain on the EMG machine must be set to 50–100 microvolts for the potentials to bevisualized.
Positive sharp waves (PSWs) are muscle fiber action potentials that can be recordedfrom a muscle with impaired muscle innervation or from an injured portion of a muscle.PSWs consist of a primary positive (downward) deflection from the baseline (positivewave), followed by a return to the baseline. These waves are either monophasic orbiphasic in morphology (Fig. 5.6). They tend to fire regularly at a rate of 0.5 to 15 Hz,however, they also may have irregular firing patterns. Amplitudes tend to vary between20 to 1000 microvolts with durations of 10–30 ms. PSWs sound like dull thuds, and tendto appear earlier than fibrillation potentials after muscle is deprived of its nerve supply.
Fibrillation potentials (fibs) are the spontaneous action potentials of single musclefibers that are firing autonomously. This can occur in the presence of impairedinnervation. This process repeats on a time interval dependent upon the repolarization-to-threshold turnaround time. These potentials usually fire in a regular pattern at rates of0.5–15 Hz, although they may fire irregularly early after denervation. The fibrillationpotentials are usually triphasic in morphology and range from 20 to 1000 microvolts insize (Fig. 5.7). They sound like raindrops hitting a tin roof. Fibrillation potentials and
5 Electromyography 47
Spontaneous activity generated by the muscle– fibrillation potentials (fibs)– positive sharp wave (PSW)– myotonic discharges– complex repetitive discharges
Spontaneous activity generated by the nerve– myokymic discharges– cramps– neuromyotonic discharges– tremors– multiples (multiple motor unit potentials, i.e. doublets or triplets)– *fasciculations
*Fasciculations can be considered muscle or nerve generated.
Table 5.1 Spontaneous activity generated by muscle or nerve
PSWs may be recorded from both neurogenic and myopathic disease states and whenseen on EMG essentially signifies the same thing – spontaneous discharge of the musclefibers most often due to impaired innervation of the muscle being tested (Table 5.2).
Spontaneous fibs and PSWs are usually reported on a scale of zero to four. Zeromeans that no fibs or PSWs are present. The rest of the grading is subjective. As ageneral rule, if one PSW or fib is seen per screen (using a sweep of 10 milliseconds perdivision) the score is +1. In this situation, the fibs or PSWs may not be present in everyarea of the muscle. If spontaneous potentials are present in more areas of the muscle orare more numerous, the score is +2. If fibs and PSWs essentially fill the screen, they aregraded as +4.
Fibs and PSWs usually indicate a process of acute or ongoing impaired innervation.These spontaneous potentials however, may not be seen on EMG testing until three weeksor more after an injury. See Chapter 6 for further details on timing of EMG findings afternerve injury.
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Train of positive sharp waves
Positive sharp wave
Figure 5.6Positive sharpwave.
Figure 5.7Fibrillation.
Fibrillation potentialwaveform
Fibrillation potentials
Chronic muscle disorders– inflammatory myopathies– muscular dystrophies– inclusion body myositis– congenital myopathies– rhabdomyolysis– muscle trauma– trichinosis
Neurogenic disorders– radiculopathy– axonal peripheral neuropathy– plexopathies– entrapment neuropathies– motor neuron disease– mononeuropathies
Table 5.2 Conditions associated with positive sharp waves and fibrillation potential
Complex repetitive discharges (CRD) are groups of spontaneously firing actionpotentials. The etiology of the CRD is a local muscular ‘arrhythmia’ with an affected areaof muscle electrically stimulating adjacent muscle fibers and therefore perpetuating therhythm. They appear as runs of simple or complex spike patterns that repeat in a regularpattern. They have a frequency of 10–100 Hz. The amplitudes of the responses are between50 and 500 microvolts. These potentials start and stop abruptly (Fig. 5.8). They have auniform frequency, and sound like a motorboat that misfires occasionally. Thesepotentials are seen in both neurogenic and myopathic disorders (Table 5.3). They tend tobe seen in more longstanding disorders and are suggestive that the injury is greater thansix months old.
Myotonic discharges are the action potentials of muscle fibers firing in a prolongedfashion after activation. Clinically this is seen as delayed relaxation of a muscle after aforceful contraction. This may also be seen after striking a muscle belly with a reflexhammer, as in percussion myotonia. Myotonic discharges have two potential forms. Thewave may either have PSW morphology or a pattern of biphasic or triphasic potentials.These potentials tend to fire at a variable rate with a waxing and waning appearance.The frequency varies between 20 to 100Hz (Fig. 5.9). This variation in frequencygives the discharge its characteristic ‘dive bomber’ sound. Myotonic discharges arefound in the following conditions: myotonic dystrophy, myotonia congenita, paramyotonia,hyperkalemic periodic paralysis, polymyositis, acid maltase deficiency and chronicradiculopathy and neuropathies.
Myokymic discharges are groups of spontaneous motor unit potentials that have aregular firing pattern and rhythm. They are seen in two forms. In the continuous formthey are seen as single or paired discharges of motor unit potentials that fire at rates of5–10 Hz. In the discontinuous form they are seen as bursts of motor potentials, whichrepeat at 0.1–10 Hz. This form of the myokymic response sounds like soldiers marching(Fig. 5.10). Myokymic responses may be seen in facial muscles in Bell’s palsy, multiplesclerosis, and polyradiculopathy. They are also seen in limb muscles in chronic nerve
5 Electromyography 49
Figure 5.8Complexrepetitivedischarge.
Chronic muscle disorders– myopathies– inflammatory– limb-girdle dystrophy– myxedema– Schwartz–Jampel syndrome
Neurogenic disorders– chronic neuropathies or radiculopathies– poliomyelitis– spinal muscular atrophy– motor neuron disease– hereditary neuropathies
Table 5.3 Conditions associated with complex repetitive discharges
lesions and in radiation plexopathy. The term myokymia is used clinically to describe a‘worm-like’ quivering of the muscle. However, this clinical finding is usually associatedwith neuromyotonic, rather than myokymic discharges, on EMG.
Endplate Region
Healthy muscle should have no spontaneous activity, unless the needle is in the endplateregion of a muscle fiber (where the nerve enters the muscle). If the needle is in theendplate region, it should be repositioned, as you are not likely to ascertain anythingabout a muscle from this location and it can be quite painful for the patient. There arethree things to look for that may tell you the needle is in the endplate region:
1. MEPPs (miniature endplate potentials)2. Endplate spikes3. Pain (the patient may feel a dull ache or increased pain relative to other positions).
MEPPs are believed to represent the spontaneous release of acetylcholine (Ach) at thepresynaptic terminal. When Ach attaches to the receptors there is subsequent activationof the sodium and potassium channels of the muscle, which in turn creates a smallcurrent.
Endplate spikes are believed to be single muscle fiber depolarizations. A needle maycause sufficient irritation to the presynaptic nerve terminal to release a large amount ofAch. This may subsequently produce a threshold adequate for depolarization.
Endplate spikes and MEPPs do not necessarily have to be found together. MEPPsare of short duration (1–2 milliseconds), fire with irregular activity every few seconds orso, are small in size (10–20 microvolts), and have monophasic negative (upward) waveforms(Fig. 5.11). Endplate spikes are typically biphasic with an initial negative deflection, ofintermediate amplitude (about 100–200 microvolts), and have longer duration than MEPPs(3–5 milliseconds). Like MEPPs, they fire irregularly. The endplates should be avoidedbecause of patient discomfort and possible interpretation errors. (Positive waves in theendplate do not indicate denervation, and can be a normal finding.) To move away fromthe endplate, advance the needle slightly and firmly. Now the muscle should beelectrically quiet and the patient more comfortable.
Analyzing the Motor Unit
Once the muscle has been assessed for insertional activity and activity at rest, the motorunit itself should be analyzed. During this portion of the needle test, the patient is asked
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Note waxing and waning in frequency and amplitude
Figure 5.9Myotonicdischarges.
Figure 5.10Myokymicdischarges.
to minimally contract the muscle. Too often, electromyographers tell the patient tomaximally contract the muscle. If the muscle is fully contracted, it is almost impossibleto isolate and therefore analyze individual motor units.
When analyzing motor units, the sweep speed should be set at 10 msec/division andthe gain should be 200–500 microvolts per division. Most assessments of motor unitmorphology can be made more accurately by freezing the screen or by using a triggerand delay line. Trigger and delay lines are available on most EMG machines by pressinga button. This is necessary for a detailed analysis of motor units. The trigger is set torecord a tracing when a certain amplitude threshold is reached. When a potential exceedsthe trigger threshold, that potential is displayed on the screen. That potential remains onthe screen until the next potential reaches threshold. Then the new potential replaces theprevious potential. This allows the electromyographer to ‘freeze’ a MUAP above certainamplitude and analyze it.
At low levels of contraction (when few motor units are firing), slight movements ofthe needle can ‘tune in’ the desired potential. At this point, the same potential will beconstantly replaced in the same location on the screen. The delay line determines theposition of the potential on the screen. Thus, the placement of the delay line determineshow much time before and after the potential being examined is being displayed. The‘strobe’ effect of potentials being locked into the same position allows detailed analysis
5 Electromyography 51
Normal(with muscle at rest)
100 μV
100 μV
10 msecs
10 msecs
Needle in endplate region(miniature endplate potentials noted)
Figure 5.11Miniatureendplatepotential (MEPP).
Figure 5.12MUAPcomponents.
Rise time
Amplitude
Duration
Baseline
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of all components of motor unit morphology including amplitude, duration and numberof phases as well as stability. Subtle changes can become apparent.
In addition, satellite potentials, separated from the main motor unit action potential byan isoelectric interval, fire in a time-locked relationship to the main action potential. Thesepotentials usually follow, but may precede, the main action potential in the same locationand therefore will become apparent. These will likely only be evident in this manner, aswithout a trigger and delay function they may appear as different motor units. The triggerand delay function is an extremely valuable tool in performing motor unit analysis.
Components of the Motor Unit
Analysis of the motor unit morphology should include the following parameters: 1. amplitude, 2. rise time, 3. duration and 4. phases. Figure 5.12 depicts the variouscomponents of the MUAP morphology.
Amplitude
In a healthy motor unit, all of the muscle fibers discharge in near synchrony. Muscle fiberslocated near the tip of the electrode make the greatest contribution to the amplitude of themotor unit potential. Their contribution to the amplitude decreases significantly as thedistance from the needle tip increases. Therefore the same motor unit can give rise topotentials of different amplitude and appearance at different recording sites.
MUAP amplitude is measured from the most positive to the most negative peak, andreflects fiber density. Amplitude of the motor units may be normal, increased ordecreased. With a concentric needle, amplitude ranges from several hundred microvolts toa few millivolts. Amplitudes are larger with a monopolar needle because the monopolarneedle picks up electrical activity from a full 360-degree field around the needle. Increasedamplitude of motor units can be seen with reinnervation, as is seen with neuropathicinjuries after a period of months. Decreased amplitude may be seen in myopathies.
Rise Time
Rise time is the time lag from the peak of the initial positive deflection to the subsequentnegative upward peak. This helps estimate the distance between the recording tip anddischarging motor unit. The more vertical the waveform, the shorter (quicker) the risetime. A distant motor unit has longer rise time because the resistance and capacitance ofthe intervening tissue act as a high frequency filter. A unit accepted for qualitativemeasurement should produce a sharp sound, while a distant unit will produce a dullsound indicating the need to reposition the needle electrode closer to the source. Anacceptable rise time is 0.5 milliseconds or less.
Duration
Duration is measured from the initial departure from baseline to the final return to thebaseline. Normal duration is about 5–15 milliseconds. It indicates the degree ofsynchrony of firing among all individual muscle fibers with variable length, conductionvelocity and membrane excitability. A slight shift in the needle position influences theduration much less than the amplitude.
When all the fibers of a motor unit fire in relative synchrony, the duration will beshort. If there is asynchrony of firing (e.g., with reinnervation) the duration will belonger. Increased duration is seen in neuropathic processes, while decreased duration isseen in myopathic disorders. Duration is decreased in myopathies because fewer musclefibers contribute to the motor unit.
5 Electromyography 53
Phases
A phase is the portion of the waveform between the successive crossings of the baseline.The number of phases, determined by counting negative and positive peaks, equals thenumber of baseline crossing plus one. Normally, motor unit potentials have four or fewerphases. Polyphasic motor units (more than four phases) suggest desynchronized dischargeor drop-off of individual fibers. Normal muscles may have about 10% polyphasic MUAPsusing a concentric needle and 25% polyphasic MUAPs when using a monopolar needle.If more than approximately 20% of the motor units analyzed with a concentric needle or40% with a monopolar needle consist of five or more phases, the motor units of thatmuscle are considered polyphasic. Motor unit duration is a better measure of pathologythan polyphasicity.
Remember that the spatial relationship between the needle and the muscle fibersplays an important role in the shape of the waveform, so any slight repositioning of theelectrode can change the morphology of the motor unit.
Recruitment
Recruitment is an often misunderstood and misused term. Recruitment refers to theorderly addition of motor units so as to increase the force of a contraction. A contractionbecomes stronger in two ways: the firing motor units increase their rate of firing andadditional motor units commence firing.
The settings on the machine for evaluating recruitment should be a sweep of 10 milliseconds per division and a gain of 200–500 microvolts per division. Recruitmentanalysis should begin with the patient being told to think about contracting the musclebeing analyzed. Observe for the firing of a single MUAP. It usually begins to fire at 2–3 Hzin an irregular pattern.
Normally the motor unit will fire in a regular pattern at about 5Hz. At around 10 Hzanother MUAP will be recruited to fire. The new motor unit (MU) will initially fire atabout 5 Hz. The normal firing rate of most motor units, before additional units arerecruited, is 10 Hz. To calculate the firing rate of the MU, note how many times a MUwith an identical morphology repeats across a screen set at 100 msec/screen (sweepspeed of 10 msec/division). Multiply that number by ten to get the motor unit firing per1000 msec or one second. Remember that Hz indicates cycles per second. In neuropathicprocesses, some motor units will be unavailable to fire (see Fig. 5.13). A MU that is able tofire will try to ‘make up’ for the inability of other units to fire by firing at a higher frequency.Therefore, the motor unit will have an increased firing frequency before another motor unitis recruited, which is referred to as decreased recruitment. In decreased recruitment, thereare fewer motor units firing at higher frequency. Recruitment ratio is another term used todescribe the firing rate of a motor unit. This ratio is the rate of firing of the most rapidlyfiring motor unit (in Hz) divided by the number of units firing. A recruitment ratio of over 8is considered abnormal and suggests a neurogenic process.
Neuropathic recruitment, also called neurogenic recruitment, can be seen in neu-ropathies, radiculopathies, motor neuron disease and nerve trauma. Few motor units fire atan increased rate, or firing frequency (Fig. 5.13). The firing rates of these MUAPs aregreater than 20 Hz (20 cycles per second) and may increase to over 30 Hz or more.Pathologic states can tell us much about physiology. In severe neuropathic lesions, whenthere are few functional motor units, we can see motor units firing at 30 Hz before asecond motor unit in that area is recruited. This indicates that weakness is not due topain or poor effort, but due to physiologic factors. Functional motor units are simply not
available. If only a few motor units are firing but they are firing at a normal rate, recruitmentis normal. The decreased activation of the muscle may be due to either decreased effort or acentral nervous system lesion.
The term ‘increased recruitment’ or ‘early recruitment’ is sometimes used to describe amyopathic process. In myopathic recruitment, a large number of motor units are ‘recruited’for a minimal contraction. In myopathies, the individual muscle fiber contribution to eachmotor unit is reduced (see Fig. 5.13). Since myopathic motor units cannot increase theirforce output, they quickly recruit additional motor units to increase the force of acontraction. If referring to the recruitment ratio, there will be a decreased rate of firing(numerator) per number of motor units recruited (denominator). Recruitment ratios below 3suggest a myopathic process.
Myopathic MUAPs tend to have an early recruitment of short duration low amplitudeMUAPs firing at increased rates (Fig. 5.14). In a myopathy it is difficult to obtain only oneor two motor units per screen at minimal contraction. Polyphasicity and spontaneouspotentials can be seen in both neuropathies and myopathies. Because these motor unitshave low amplitude, analysis cannot be done as easily with a trigger and delay or capturefunction but must be done with a constant sweep.
In EMG evaluation of MUAP recruitment, it is important to realize that we areprimarily evaluating Type I motor units because they recruit first. By the time the Type IIfibers recruit, the baseline will be obscured by Type I potentials. This is problematic inthose myopathies that involve predominately Type II fibers, such as steroid myopathies,since only the Type I fibers are evaluated. In steroid myopathies, even though the patienthas a myopathy clinically and on biopsy, the EMG may be normal.
Summary
EMG evaluation requires patience and effort on the part of both the electromyographerand the patient. The amount of information obtained from the test is dependent uponappropriate planning and selection of the muscles as well as experience in waveformrecognition. Table 5.4 reviews the common muscles tested during the needle portion of the
Easy EMG54
Myopathic
Neuropathic
Normal
Figure 5.13Schematic ofnormal,neuropathic andmyopathicprocesses.
!
examination, as well as the muscle’s innervation, location and needle placement. This willhelp you plan out which muscles to test as well as ensure proper needle placement. This isa relatively comprehensive list and it is rare that most or even many of these muscles willbe necessary in an individual study. The choice of muscles examined should be dictatedby the clinical circumstances.
Many muscles are very close together (in the forearm for example), and due toindividual differences in size (and less often to differences in anatomy), as well as depth ofneedle insertion, the needle may not always be in the desired muscle. A test maneuver maybe necessary to confirm needle placement. Activating the muscle tests placement. If theneedle is in the muscle being activated, large crisp motor units will be seen and heard.Videotapes that can be a valuable tool in waveform recognition are available from theAmerican Association of Electrodiagnostic Medicine (AAEM).
5 Electromyography 55
1 mV
Normal
Myopathic10 msec
200 μV
200 μV
Neuropathic
Figure 5.14Normal,neuropathic andmyopathicrecruitment.
Easy EMG56
Muscle Nerve Cord Division Trunk C4 C5
Sternoclei- Spinal Accessory domastoid Nerve(see Fig. A2.1)
Trapezius (see Spinal Accessory CN XI, C3Fig. A2.2) Nerve
Rhomboid Major Dorsal Scapular N/A N/A N/A C5(see Fig. A2.3) Nerve
Rhomboid Minor Dorsal Scapular N/A N/A N/A C5 (see Fig. A2.3) Nerve
Levator Scapulae Dorsal Scapular N/A N/A N/A C3, C5 (see Fig. A2.4) Nerve C4
Supraspinatus Suprascapular N/A N/A Upper C5 (see Fig. A2.5) Nerve Trunk
Table 5.4 Common muscles – innervation, location and needle placement
5 Electromyography 57
C6 C7 C8 T1 Needle Insertion Origin Insertion Action
At the midpoint The sternal The lateral Rotates the between the head arises surface of headmastoid process from the the and the sternal upper part of mastoid origin; enter the the process muscle obliquely, manubrium and direct the sterni. The needle parallel clavicular to the muscle head arises fibers from the
medial third of the clavicle
At the angle of External Spine of Adducts, the neck and occipital scapula, rotates, shoulder or protuberance, acromion, elevates, midway between superior lateral and the spine of the nuchal line, third of depresses scapula and the ligamentum clavicle scapulaspinous processes nuchae, at the same level spines of
C7–T12
At the midpoint Spines of Medial Adducts of the medial T2–T5 border of scapulascapular border, scapula midway between the scapular spine and the inferior angle beneath the trapezius
At the point just Spines of Root of Adducts medially to C7–T1 spine of scapulamedial border of scapula the scapular spine beneath the trapezius
At the The The Elevates posteromedial transverse postero- the scapulaborder of the processes of medial scapula, between the upper border of the superior four cervical the scapula, angle and the vertebrae between spine of the the scapula beneath superior the trapezius angle and
the spine of the scapula
C6 At the Supraspinous Superior Abducts supraspinous fossa fossa of facet of armjust above the scapula greater spine of the tubercle of scapula beneath humerus the trapezius
Easy EMG58
Muscle Nerve Cord Division Trunk C4 C5
Infraspinatus Suprascapular N/A N/A Upper C5 (see Fig. A2.6) Nerve Trunk
Subscapularis Upper and Lower Posterior Posterior Upper C5Subscapular Cord Division Trunk Nerve
Teres Major (see Lower Posterior Posterior Upper C5Fig. A2.7) Subscapular Cord Division Trunk
Nerve andMiddleTrunk
Deltoid (see Axillary Nerve Posterior Posterior Upper C5Fig. A2.8) Cord Division Trunk
Teres Minor Axillary Nerve Posterior Posterior Upper C5(see Fig. A2.9) Cord Division Trunk
Coracobrachialis Musculocutaneous Lateral Anterior Upper C5(see Fig. A2.10) Nerve Cord Division and
Middle Trunk
Biceps Brachii Musculocutaneous Lateral Anterior Upper C5(see Fig. A2.11) Nerve Cord Division Trunk
Brachialis Musculocutaneous Lateral Anterior Upper C5(see Fig. A2.12) Nerve Cord Division Trunk
Latissimus Dorsi Thoracodorsal Posterior Posterior Upper, (see Fig. A2.13) Nerve Cord Division Middle
and Lower Trunk
Table 5.4 Common muscles – innervation, location and needle placement (cont’d)
5 Electromyography 59
C6 C7 C8 T1 Needle Insertion Origin Insertion Action
C6 At the midpoint Infraspinous Middle Externally of infraspinous fossa facet of rotates arm fossa beneath greater the trapezius tubercle of
humerus
C6 Subscapular Lesser Internally fossa tubercle of rotates arm
humerus
C6 C7 Along the lateral Dorsal surface Medial lip Internally lower border of of inferior of inter- adducts the scapula angle of tubercular and rotates (lateral and scapula groove of arm rostral to the humerus inferior angle) beneath the trapezius
C6 5 cm beneath the Lateral third Deltoid Abducts, lateral border of of clavicle, tuberosity flexes, the acromion acromion, and of extends,
spine of humerus and scapula internally
and externally rotates arm
C6 Immediately Upper portion Lower Externally lateral to the of lateral facet of rotates arm middle third of border of greater the lateral border scapula tubercle of of the scapula humerus
C6 C7 5–9 cm distal to Coracoid Middle Flexes and the coracoid process third of adducts process along the medial arm volar aspect of surface of the arm humerus
C6 At the midarm Long head, Radial Flexes and anteriorly, into supraglenoid tuberosity supinates bulk of the tubercle; of radius forearm; muscle short head, assists in
coracoid flexion of process arm at
shoulder
C6 5 cm proximal to Lower Coronoid Flexes the elbow crease anterior process of forearm at just lateral to and surface of ulna and elbowunder the biceps humerus ulnar
tuberosity
C6 C7 C8 Along the Spines of Floor of Adducts, posterior T7–T12 bicipital extends, axillary fold thoracolumbar groove of and directly lateral fascia, iliac humerus internally to the inferior crest, ribs rotates angle of the 9–12 armscapula
Easy EMG60
Muscle Nerve Cord Division Trunk C4 C5
Serratus Anterior Long Thoracic Anterior Rami C5 (see Fig. A2.14) Nerve
Triceps (see Radial Nerve Posterior Posterior Upper, Fig. A2.15) Cord Division Middle
and Lower Trunk
Anconeus (see Radial Nerve Posterior Posterior Upper, Fig. A2.16) Cord Division Middle
and Lower Trunk
Brachioradialis Radial Nerve Posterior Posterior Upper C5 (see Fig. A2.17) Cord Division Trunk
Extensor Radial Nerve Posterior Posterior Upper carpi radialis Cord Division and (see Fig. A2.18) Middle
Trunk
Supinator (see Posterior Posterior Posterior Upper C5Fig. A2.19) Interosseous Cord Division Trunk
Nerve (Radial Nerve)
Extensor Carpi Posterior Posterior Posterior Middle Ulnaris (see Interosseous Cord Division and Fig. A2.20) Nerve (Radial Lower
Nerve) Trunk
Table 5.4 Common muscles – innervation, location and needle placement (cont’d)
5 Electromyography 61
C6 C7 C8 T1 Needle Insertion Origin Insertion Action
C6 C7 Along the At the outer The medial Protracts midaxillary line surfaces and border of scapula; directly over the superior the assists rib, anterior to borders of scapula, upward the bulk of the the upper from the rotation of latissimus dorsi eight or nine superior scapulabut, in a woman, ribs angle to posterior to the costal breast tissue surface of
the inferior angle
C6 C7 C8 At the midarm Long head, Posterior Extends the level posterior to infraglenoid surface of elbow the lateral aspect tubercle; olecranon of the shaft of lateral head, process of the humerus superior to ulna
radial groove of humerus;medial head, inferior to radial groove
C6 C7 C8 2.5–3.75 cm distal Lateral Olecranon Extends to the olecranon epicondyle and upper forearmalong the radial of humerus posterior border of the surface of ulna ulna
C6 2–3 cm lateral to Lateral Base of Flexes the biceps supracondylar radial forearm tendon ridge of styloid
humerus process
C6 C7 At the upper Lower third Radial Extends forearm 5–7.5 cm of the lateral surface of (dorsi-distal to the lateral supracondylar the base of flexion) epicondyle along ridge of the the second and radially a line connecting humerus and third abducts the epicondyle metacarpal hand at and second bone wristmetacarpal bone
C6 With the forearm Lateral Lateral Supinates pronated, insert epicondyle, side of forearmthe needle 3–5 cm radial upper part distal to the collateral of radius lateral epicondyle, and annular toward the shaft ligaments of the radius
C7 C8 With the The common At the Extends forearm extensor ulnar side (dorsi-pronated, at the tendon from of the flexion) mid to upper the lateral base of and forearm just epicondyle of the fifth ulnarly radial to the the humerus metacarpal deviates lateral margin bone hand at of the shaft of wristthe ulna
Easy EMG62
Muscle Nerve Cord Division Trunk C4 C5
Extensor Posterior Posterior Posterior Middle Digitorum Interosseous Cord Division and (see Fig. A2.21) Nerve (Radial Lower
Nerve) Trunk
Extensor Digiti Posterior Posterior Posterior Middle Minimi (see Interosseous Cord Division and Fig. A2.22) Nerve (Radial Lower
Nerve) Trunk
Abductor Pollicis Posterior Posterior Posterior Middle Longus (see Interosseous Cord Division and Fig. A2.23) Nerve (Radial Lower
Nerve) Trunk
Extensor Pollicis Posterior Posterior Posterior Middle Longus (see Interosseous Cord Division and Fig. A2.24) Nerve (Radial Lower
Nerve) Trunk
Extensor Pollicis Posterior Posterior Posterior Middle Brevis (see Interosseous Cord Division and Fig. A2.25) Nerve (Radial Lower
Nerve) Trunk
Extensor Indicis Posterior Posterior Posterior Middle (see Fig. A2.26) Interosseous Cord Division and
Nerve (Radial Lower Nerve) Trunk
Pronator Teres Median Nerve Lateral Anterior Upper (see Fig. A2.27) Cord Division and
Middle Trunk
Flexor Carpi Median Nerve Lateral Anterior Upper Radialis (see Cord Division and Fig. A2.28) Middle
Trunk
Table 5.4 Common muscles – innervation, location and needle placement (cont’d)
5 Electromyography 63
C6 C7 C8 T1 Needle Insertion Origin Insertion Action
C7 C8 With the forearm Common The dorsal Extends pronated, at extensor surface of phalanges mid-forearm, tendon from all in digits 2 midway between the lateral phalanges through 4the ulna and epicondyle of of digits 2 radius the humerus through 4
C7 C8 With the forearm Common Extensor Extends pronated, at extensor expansion, little fingermid-forearm tendon and base of mid-way between interosseous middle the ulna and membrane and distal radius phalanges
C7 C8 With the forearm Interosseous Lateral Abducts pronated, at the membrane, surface of thumb mid-forearm middle third base of radiallyalong the shaft of posterior first of the radius surfaces of metacarpal
radius and ulna
C7 C8 With the forearm Interosseous Base of Extends all pronated, at the membrane distal parts of mid-forearm and middle phalanx of thumb but along the radial third of thumb specifically border of the posterior extension ulna surface of of distal
ulna phalanx; assists adduction of thumb
C7 C8 4–6 cm proximal Interosseous Base of Extends to the wrist over membrane proximal proximal the ulnar aspect and posterior phalanx of phalanx of of the radius surface of thumb thumb
middle third radius
C7 C8 5–7 cm proximal Posterior Extensor Extends to the ulnar surface of expansion index styloid just radial ulna and of index fingerto the shaft of interosseous finger the ulna membrane
C6 C7 With the arm Medial Middle of Pronates supinated, at epicondyle lateral side forearm2–3 cm distal and and coronoid of radius 1 cm medial to process of the biceps tendon ulna
C6 C7 With the arm Medial Volar Flexes hand supinated, at the epicondyle surface of at wrist volar surface of the of the the base of (palmar forearm, 7–9 cm humerus the second flexion); distal to the medial metacarpal assists in epicondyle along radial a line directed abduction toward the muscle of handtendon at the wrist
Easy EMG64
Muscle Nerve Cord Division Trunk C4 C5
Palmaris Longus Median Nerve Lateral Anterior Middle (see Fig. A2.29) and Division Trunk
Medial and Cord Lower
Trunk
Flexor Digitorum Median Nerve Lateral Anterior Middle Superficialis and Division Trunk (see Fig. A2.30) Medial and
Cord LowerTrunk
Flexor Digitorum Anterior Lateral Anterior Middle Profundus (see Interosseous and Division Trunk Fig. A2.31) Nerve (Median Medial and
Nerve) and Cord LowerUlnar Nerve Trunk
Flexor Pollicis Anterior Lateral Anterior Middle Longus (see Interosseous and Division Trunk Fig. A2.32) Nerve (Median Medial and
Nerve) Cord LowerTrunk
Pronator Anterior Lateral Anterior Middle Quadratus (see Interosseous and Division Trunk Fig. A2.27) Nerve (Median Medial and
Nerve) Cord LowerTrunk
Abductor Pollicis Median Nerve Medial Anterior Lower Brevis (see Cord Division Trunk Fig. A2.33)
Table 5.4 Common muscles – innervation, location and needle placement (cont’d)
5 Electromyography 65
C6 C7 C8 T1 Needle Insertion Origin Insertion Action
C7 C8 T1 With the arm Medial Flexor Flexes hand supinated at the epicondyle of retinac- at wristvolar surface of humerus ulum, the forearm palmar 6–8 cm distal to aponeu-the medial rosis epicondyle along a line directed toward the muscle tendon at the wrist
C7 C8 T1 With the arm Medial The sides Flexes the supinated, at the epicondyle of the proximal volar surface of of the second inter-the forearm humerus by phalanges phalangeal approximately the common of digits 2 joints7–9 cm distal to tendon, through 5 the biceps tendon coronoid (mid forearm) and process of 2–3 cm medial to ulna, and the ventral oblique line midline of the radius
C7 C8 T1 With the arm Anteromedial Bases of Flexes distal supinated, at surface of distal phalanges 5–7.5 cm distal ulna, phalanges of fingers; to the olecranon interosseous of fingers assists in process and membrane flexion of 1–1.5 cm medial hand at to the shaft of wristthe ulna
C7 C8 T1 With the arm Anterior Base of Flexes supinated, surface of distal thumb, 5–7.5 cm proximal radius, phalanx of particularly to the radial interosseous thumb distal styloid and 0.1 cm membrane, phalanx; lateral to the and assists in radial artery coronoid ulnar
process adduction of thumb
C7 C8 T1 2.5 cm proximal The distal The distal Pronates to the ulnar fourth of the fourth of forearmstyloid, midpoint volar surface the lateral between radial of the ulna border and and ulna bone, the volar deep to 2.5 cm to surface of penetrate the the radius interosseous membrane
C8 T1 Obliquely near Flexor Lateral Abducts the muscle origin retinaculum, side of thumbalong the muscle, scaphoid, base of midway along and proximalthe shaft of the trapezium phalanx 1st metacarpal of thumb
Easy EMG66
Table 5.4 Common muscles – innervation, location and needle placement (cont’d)
Muscle Nerve Cord Division Trunk C4 C5
Opponens Pollicis Median Nerve Medial Anterior Lower (see Fig. A2.34) Cord Division Trunk
Flexor Pollicis Median Nerve: Medial Anterior Lower Brevis (see superficial head. Cord Division Trunk Fig. A2.35) Ulnar Nerve:
deep head.
Flexor Carpi Ulnar Nerve Medial Anterior Lower Ulnaris (see Cord Division Trunk Fig. A2.36)
Abductor digiti Ulnar Nerve Medial Anterior Lower minimi (see Cord Division Trunk Fig. A2.37)
Opponens digiti Ulnar Nerve Medial Anterior Lower minimi (see Cord Division Trunk Fig. A2.38)
5 Electromyography 67
C6 C7 C8 T1 Needle Insertion Origin Insertion Action
C8 T1 Lateral to the Flexor Lateral side Moves first APB, the most retinaculum of first metacarpal lateral part of and metacarpal across palm the thenar trapezium and rotates eminence it into
opposition
C8 T1 Superficial head: The The Flexes a depth of superficial superficial proximal 0.5–1 cm at the head head is phalanx of midpoint of a originates in inserted at thumb; line drawn the flexor the radial assists in between the retinaculum aspect of opposition, metacarpo and the base of ulnar -phalangeal trapezium. the adduction joint and the The deep proximal (entire pisiform. head phalanx of muscle), Deep head: the originates in the and palmar same as that for the ulnar thumb. abduction the superficial aspect of the The deep (superficial head, but insert first head is head) of the needle to a metacarpal inserted at thumb depth of 1–2 cm bone the ulnar
aspect of the base of the proximal phalanx of the thumb
C8 T1 5–8 cm distal to Lateral Base of Flexes and the medial epicondyle fifth ulnarly epicondyle along and posterior metacarpal deviates a line connecting surface of hand at the medial ulna wristepicondyle and pisiform bone
C8 T1 Insert the needle Pisiform and Pisiform Abducts obliquely at the tendon of and little finger midpoint of the flexor carpi tendon of 5th metacarpal ulnaris flexor along the ulnar carpi(medial) border ulnaris of the hand
C8 T1 The midpoint Flexor Medial Opposes between the 5th retinaculum side of little finger metacar- and hook of fifth pophalangeal hamate metacarpal joint (metacar-pophalangeal crease) and the pisiform (distal wrist crease), just radial to the abductor digiti minimi
Easy EMG68
Muscle Nerve Cord Division Trunk C4 C5
Flexor digiti Ulnar Nerve Medial Anterior Lower minimi (see Cord Division Trunk Fig. A2.39)
Palmar Ulnar Nerve Medial Anterior Lower Interosseous Cord Division Trunk (see Fig. A2.40)
First Dorsal Ulnar Nerve Medial Anterior Lower Interosseous Cord Division Trunk (see Fig. A2.41)
Adductor Pollicis Ulnar Nerve Medial Anterior Lower (see Fig. A2.42) Cord Division Trunk
Lumbricals (4) Median Nerve Medial Anterior Lower (see Fig. A2.43) (two lateral) and Cord Division Trunk
Ulnar Nerve (two medial)
Table 5.4 Common muscles – innervation, location and needle placement (cont’d)
5 Electromyography 69
C6 C7 C8 T1 Needle Insertion Origin Insertion Action
C8 T1 The midpoint The hook of The ulnar Flexes between the fifth the hamate side of the proximal metacarpo- and the flexor base of the phalanx of phalangeal joint retinaculum proximal the fifth (metacarpo- phalanx of digitphalangeal crease) the little and the ulnar finger aspect of the pisiform (distal wrist crease), just radial to the opponens digiti minimi
C8 T1 Just ulnar to the Medial side Bases of Adducts 2nd metacarpal of second proximal fingers; bone or just radial metacarpal; phalanges flexes to the 4th and lateral sides in same metacarpo-5th metacarpal of fourth sides as phalangeal bones, and fifth their joints; respectively on metacarpals origins; extends the palmer extensor interpha-surface of the expansion langeal hand joints.
C8 T1 Obliquely just The ulnar The radial Abducts proximal to the border of the aspect of the index 2nd metacarpo- first the base finger phalangeal metacarpal of the (radial joint, and direct bone (outer proximal deviation)it rostrally along head) and phalanx of the muscle belly the radial the index on the dorsum of border of the finger the hand second
metacarpal bone (inner head)
C8 T1 The first web Capitate and Medial side Adducts space just anterior bases of of base of thumb(volar) to the second and proximal edge of the first third phalanx of dorsal metacarpals the thumb interosseous and (oblique proximal to the head); palmar first metacarpo- surface of phalangeal third joint on the metacarpal palmar surface of (transverse the hand head)
C8 T1 Proximal to the Lateral side Lateral side Flexes metacarpopha- of tendons of of extensor metacarpo-langeal joint and flexor expansion phalangeal radial to the flexor digitorum joints and tendon on the profundus extends Palmar surface of inter-the hand phalangeal
joints
Easy EMG70
Muscle Nerve Cord Division Trunk C4 C5
Pectoralis major Lateral and Lateral Anterior Upper, C5 (see Fig. A2.44) Medial Pectoral Cord and Division Middle,
Nerves Medial and LowerTrunk
Pectoralis minor Medial Pectoral Lateral Anterior Upper, C5 (see Fig. A2.44) Nerve and Cord Division Middle,
Lateral/and and Medial Lower
Trunk
Table 5.4 Common muscles – innervation, location and needle placement (cont’d)
5 Electromyography 71
C6 C7 C8 T1 Needle Insertion Origin Insertion Action
C6 C7 C8 T1 Medial to the The clavicular The lateral Adducts anterior axillary part lip of the and fold over the bulk originates at inter- internally of the muscle the sternal tubercular rotates
half of the sulcus on arm. clavicle. the shaft Clavicular The of the portion: sternocostal humerus assists in part flexion of originates armat the anterior surface of the sternum, the edge of the first six or seven ribs, and the aponeurosis of the external oblique muscle of the abdomen
C6 C7 C8 T1 The midclavicular The outer Coracoid Depresses line overlying surfaces of process of the the third rib the third to the shoulder
fifth ribs scapula (frequently second to fourth)
Easy EMG72
Muscle Nerve Division L2 L3 L4 L5 S1 S2 S3
Iliopsoas (see Femoral Nerve posterior L2 L3 Fig. A2.45)
Sartorius (see Femoral Nerve posterior L2 L3 Figs A2.46 & A2.47)
Rectus Femoris Femoral Nerve posterior L2 L3 L4 (see Figs A2.46 & A2.48)
Vastus Lateralis Femoral Nerve posterior L2 L3 L4 (see Figs A2.46 & A2.49 )
Vastus Femoral Nerve posterior L2 L3 L4 Intermedius (see Figs A2.46 & A2.50)
Vastus Medialis Femoral Nerve posterior L2 L3 L4 (see Figs A2.46 & A2.51)
Pectineus (see Femoral Nerve posterior L2 L3 Fig. A2.52)
Adductor Brevis Obturator anterior L2 L3 L4 (see Fig. A2.53) Nerve
Adductor Obturator anterior L2 L3 L4 Longus (see Nerve Fig. A2.54)
Gracilis (see Obturator anterior L2 L3 L4 Fig. A2.55) Nerve
Table 5.4 Common muscles – innervation, location and needle placement (cont’d)
5 Electromyography 73
Needle Insertion Origin Insertion Action
3–4 cm lateral to the Iliac fossa; ala of Lesser trochanter Flexes and femoral artery pulse just sacrum, and on the shaft of internally below the inguinal lumbar spine the femur, rotates thigh ligament anteromedially
5–7.5 cm distal to the Anterior-superi Upper medial Flexes and anterior superior iliac or iliac spine side of tibia externally spine along a line to the rotates thigh; medial epicondyle of the flexes and tibia rotates leg
medially
The anterior thigh Anterior-inferior Base of patella; Flexes thigh; midway between the iliac spine; tibial tuberosity extends leganterior superior iliac posterior-spine and the patella superior rim of
acetabulum
The anterolateral thigh Intertrochanteric Lateral side of Extends leg7.5–10 cm above the line; greater patella; tibial patella trochanter; tuberosity
linea aspera; gluteal tuberosity; lateral inter-muscular septum
The anterior thigh Upper shaft of Upper border of Extends leg midway between the femur; lower patella; tibial anterior superior iliac lateral tuberosity spine and the patella and intermuscular under the rectus femoris septum
The anteromedial thigh Intertrochanteric Medial side of Extends leg5–7.5 cm above the line; linea patella; tibial patella aspera; medial tuberosity
intermuscular septum
2.5 cm medial to the Superior ramus Along a line Adducts and femoral artery pulse just of the pubis from the lesser flexes thighbelow the inguinal trochanter to ligament the linea aspera
of the femur
In the proximal 1/6 of the Body and Pectineal line; Adducts, flexes, thigh, one-quarter the inferior pubic upper part of and externally distance from the medial ramus linea aspera rotates thigh border to the anterior border of the thigh
In the proximal 1/5 of the Body of pubis Middle third of Adducts, flexes, thigh, one-quarter the below its crest linea aspera and externally distance from the medial rotates thigh border to the anterior border of the thigh
The junction of the upper Body and Medial surface Adducts and and middle thirds of the inferior pubic of of upper quarter flexes thigh; thigh, along the medial ramus of tibia flexes and aspect of the thigh internally
rotates thigh
Easy EMG74
Muscle Nerve Division L2 L3 L4 L5 S1 S2 S3
Adductor Obturator and anterior L2 L3 L4Magnus (see Sciatic Nerve Fig. A2.56)
Gluteus Medius Superior posterior L4 L5 S1 (see Fig. A2.57) Gluteal Nerve
Gluteus Minimus Superior posterior L4 L5 S1 (see Fig. A2.58) Gluteal Nerve
Tensor Fasciae Superior posterior L4 L5 S1Latae (see Gluteal Nerve Fig. A2.59)
Gluteus Maximus Inferior posterior L5 S1 S2 (see Fig. A2.60) Gluteal Nerve
Semitendinosus Sciatic Nerve anterior L5 S1 S2(see Fig. A2.61) (tibial
portion)
Semi- Sciatic Nerve anterior L5 S1 S2 membranosus (tibial(see Fig. A2.62) portion)
Biceps Femoris Tibial Nerve anterior L5 S1 S2 (see Fig. A2.63) (long head) and
and Common posteriorPeroneal Nerve (short head) divisions of Sciatic Nerve
Extensor Deep Peroneal posterior L5 S1 Digitorum Nerve Longus (see Fig. A2.64)
Tibialis Anterior Deep Peroneal posterior L4 L5 (see Fig. A2.65) Nerve
Table 5.4 Common muscles – innervation, location and needle placement (cont’d)
5 Electromyography 75
Needle Insertion Origin Insertion Action
Upper one-third of thigh, Ischiopubic Linea aspera; Adducts, flexes, immediately posterior to ramus; ischial medial and extends the medial border of the tuberosity supracondylar thighthigh line; adductor
tubercle
2.5 cm distal to the Superolateral Greater Abducts and aids mid-point of the iliac surface of ilium trochanter internal rotation crest of thigh
Midway between the Ilium between Greater Abducts and iliac crest and the greater anterior and trochanter aids internal trochanter of the femur inferior gluteal rotation of
lines thigh
Midway between the Iliac crest; Iliotibial tract Flexes, abducts, anterior superior iliac anterior - and internally spine and the greater superior iliac rotates thigh trochanter of the femur spine
Midpoint of the line Posterosuperior Gluteal Extends, connecting the posterior ilium and tuberosity of abducts, and inferior iliac spine and sacrum femur and externally greater trochanter iliotibial tract rotates thigh
One-third to midway Ischial Medial surface Extends thigh; along a line connecting tuberosity of upper part flexes and the semitendinosus of tibia rotates leg tendon (easily palpable medially as it forms the proximal medial margin of the popliteal fossa) with the ischial tuberosity.
Mid-thigh, at or just Ischial Medial condyle Extends thigh; medial to the midline tuberosity of tibia flexes and and immediately rotates leg subcutaneous medially
Long head: one-third to Long head from Head of fibula Extends thigh; midway along a line ischial flexes and connecting the fibular tuberosity; short rotates leg head with the ischial head from mediallytuberosity. Short head: linea aspera Palpate the tendon of the and upper long head of the biceps supracondylar femoris in the popliteal line fossa. Insert the needle just medial to the tendon
5–7.5 cm distal to the Lateral condyle Bases of middle Extends toes; tibial tuberosity and of tibia, and distal dorsiflexes foot 4–5 cm lateral to the interosseous phalanges shaft of the tibia membrane, and
fibula
Just lateral to the Proximal half of Medial (first) Dorsiflexes and proximal half of the anterior tibial cuneiform bone inverts ankleshaft of the tibia interosseous and base of
membrane and first metatarsal Lateral tibial condyle
Easy EMG76
Muscle Nerve Division L2 L3 L4 L5 S1 S2 S3
Extensor Hallucis Deep Peroneal posterior L5 S1Longus (see Nerve Fig. A2.66)
Peroneus Tertius Deep Peroneal posterior L5 S1(see Fig. A2.67) Nerve
Extensor Deep Peroneal posterior L5 S1 Digitorum Brevis Nerve (see Fig. A2.68)
Peroneus Longus Superficial posterior L5 S1 (see Fig. A2.69) Peroneal (peroneal
Nerve division of Sciatic Nerve)
Peroneus Brevis Superficial posterior L5 S1 (see Fig. A2.70) Peroneal (peroneal)
Nerve division of Sciatic Nerve
Lateral Tibial Nerve anterior L5 S1 Gastrocnemius (see Fig. A2.71)
Medial Tibial Nerve anterior S1 S2 Gastrocnemius (see Fig. A2.71)
Popliteus (see Tibial Nerve anterior L4 L5 S1 Fig. A2.72)
Soleus (see Tibial Nerve anterior S1 S2 Fig. A2.73)
Tibialis Posterior Tibial Nerve anterior L4 L5 S1 (see Fig. A2.74)
Table 5.4 Common muscles – innervation, location and needle placement (cont’d)
5 Electromyography 77
Needle Insertion Origin Insertion Action
Approximately 8 cm Middle half of Base of distal Extends big toe; proximal to the anterior surface phalanx of big dorsiflexes and bimalleolar line of the of fibula; toe inverts footankle just lateral to the interosseous shaft of the tibia membrane
Approximately 7 cm Distal one-third Base of fifth Dorsiflexes and proximal to the of fibula; metatarsal everts footbimalleolar line of the interosseous ankle and 2–3 cm membrane lateral to the shaft of the tibia
The superficial muscle Calcaneus, Extensor hood Assists in tissue located on the lateral of second to extension of all proximal lateral aspect talocalcaneal fourth toes toes except of the dorsum of the ligament and little toefoot apex of interior
extensor retinaculum
5–7.5 cm below the Lateral tibial Medial Everts and fibular head along the condyle; head cuneiform bone plantar flexes lateral aspect of the and upper and base of first footfibula lateral side of metatarsal
fibula
9–10 cm above the lateral Lower lateral Base of fifth Everts and malleolus just posterior side of fibula; metatarsal plantar flexes to the lateral aspect of intermuscular footthe fibula septa
The midpoint of the Posterior surface Calcaneus Plantar flexes lateral mass of the calf of lateral foot
femoral condyle
Midpoint of the medial Posterior surface Calcaneus Plantar flexes mass of the calf of medial foot
femoral condyles
The floor of the popliteal Lateral femoral Medially on Medially rotates fossa in the proximal leg condyle proximal and flexes kneemidway between the posterior tibia insertions of the outer and inner hamstring tendons
Just distal to the belly of Proximal tibia, Calcaneus Plantar flexes the medial gastrocnemius, interosseous anklemedial to the Achilles membrane, and tendon fibula
1 cm medial to the Posterior shafts Navicular and Plantar flexes margin of the tibia at of tibia, fibula, medial and inverts foot the junction of the upper and interosseous cuneiform two-thirds with the membrane bones lower third of the shaft; direct the needle obliquely through the soleus and flexor digitorum muscles
Easy EMG78
Muscle Nerve Division L2 L3 L4 L5 S1 S2 S3
Flexor Hallucis Tibial Nerve Anterior L5 S1 S2 Longus (see Fig. A2.75)
Abductor Digiti Lateral Plantar Anterior S1 S2 S3 Minimi (see Fig. A2.76)
Flexor digiti Lateral Plantar Anterior S1 S2Minimi (see of Tibial Nerve Fig. A2.77)
Dorsal Interossei Lateral Plantar Anterior S2 S3 (see Fig. A2.78) Nerve (Tibial
Nerve)
Plantar Interossei Lateral Plantar Anterior S2 S3 (see Fig. A2.79) Nerve (Tibial
Nerve)
Adductor Lateral Plantar Anterior S1 S2 S3 Hallucis (see Nerve (Tibial Fig. A2.80) Nerve)
Abductor Medial Plantar Anterior S1 S2Hallucis (see Nerve (Tibial Fig. A2.81) Nerve)
Flexor Digitorum Medial Plantar Anterior S1 S2 Brevis (see Nerve (Tibial Fig. A2.82) Nerve)
Flexor Hallucis Medial Plantar Anterior S1 S2 Brevis (see Nerve (Tibial Fig. A2.83) Nerve)
Table 5.4 Common muscles – innervation, location and needle placement (cont’d)
5 Electromyography 79
Needle Insertion Origin Insertion Action
The posterolateral aspect Lower two- Base of distal Flexes distal of the leg, at the junction thirds of fibula; phalanx of big phalanx of big of the upper two-thirds interosseous toe toe with the lower third membrane;
intermuscular septa
Along the lateral border Calcaneus Lateral side of Abducts fifth of the foot midway first phalanx of toebetween the fifth fifth toe metatarsal head and the calcaneus
On plantar aspect of foot, Base of fifth Base of first Flexes proximal midway between the metatarsal phalanx of fifth phalanx of fifth cuboid and navicular toe toebones
On dorsum of foot, Adjacent shafts Proximal Abduct toes; between the metatarsals of metatarsals phalanges of flex proximal,
second toes and extend (medial and distal lateral sides), phalangesand third and fourth toes (lateral sides)
On plantar aspect of Medial sides of Medial sides of Adduct toes; foot, between the metatarsals 3–5 base of proximal flex proximal, metatarsals phalanges 3–5 and extend
distal phalanges
4–5 cm proximal to the Oblique head: Proximal Adducts big toesecond metatarsal head Bases of phalanx of big on the plantar surface of metatarsals 2–4 toe the foot to a depth of Transverse head: 2 cm or more (the muscle Capsule of lies deep); this will access lateral four the thick, fleshy oblique metatarso-head phalangeal
joints
The muscle belly directly Medial tubercle Base of proximal Abducts big toebeneath the navicular of calcaneus phalanx of big bone toe
Midway between the Medial tubercle Middle Flexes middle third metatarsal head of calcaneus phalanges of phalanx of and the calcaneus on the lateral four second through plantar surface of the toes fifth toesfoot
The plantar surface of Cuboid; third Proximal Flexes big toethe foot 2.5 cm proximal cuneiform phalanx of big to the first metatarsal toe head
Easy EMG80
Paraspinal MusclesMuscle Spinal Nerve Needle Insertion Action
Cervical paraspinal Posterior primary 2 cm lateral to the Extension of muscles (including rami of cervical spinal spinous process of the the head multifidus, nerves corresponding corresponding level. supraspinalis, to the respective Note that the C7 level is interspinales, level (intermediate the most prominent rectus capitis and muscles may be spinous process obliquus capitis innervated by (see Fig. A2.84) multiple levels)
Thoracic paraspinal Posterior primary 2 cm lateral to the Extension muscles (see rami of thoracic spinous process of the of the backFig. A2.85) spinal nerves corresponding level
corresponding to the respective level (intermediate muscle may be innervated by multiple levels)
Lumbosacral Posterior primary 2 cm lateral to the Extension of paraspinal rami of lumbar and spinous process of the the hipmuscles (see sacral spinal nerves corresponding level. Fig. A2.86) corresponding to the Note that the L3–L4
respective level intervertebral level is (intermediate about the level of the muscles may be posterior, superior iliac innervated by crestmultiple levels)
Reference:Chung, K.W, Ph.D., Gross Anatomy, 2nd edn Oxford University Press. Pages 1–107.Leis, A.A,. Atlas of Electromyography, Oxford, New York, Lippicott Williams of WilkensPages 1–195.
Table 5.4 Common muscles – innervation, location and needle placement (cont’d)
6Injury to Peripheral Nerves
Lyn Weiss
Injury to peripheral nerves can be broken down into those affecting the myelin and thoseaffecting the axons. It is important to remember however, that rarely is the myelin involvedwithout at least some involvement of the axon (and vice versa). It is the electromyographerwho diagnoses what type of injury exists, how severe the injury is, and where the injuryis located.
The Seddon Classification of Nerve Injuries divides nerve injuries into three categories– neurapraxia, axonotmesis and neurotmesis. Neurapraxia is defined as conduction block –only the myelin is affected. Axonotmesis refers to an injury only affecting the nerve’s axons.The stroma (supporting connective tissues) is intact. Neurotmesis refers to a completeinjury involving the myelin, axon and all the supporting structures.
Demyelinating Injuries
Demyelinating injuries can slow electrical conduction over the entire length of the nerve(uniform demyelination), slow segments of the nerve (segmental demyelination), slowfocal areas of the nerve (focal demyelination), or produce conduction block (when focaldemyelination is so severe that nerve action potential propagation across that segment doesnot occur). These changes are described below.
1. Uniform demyelination – the entire length of the nerve displays a slower conductionvelocity. This is typically seen in hereditary disorders such as Charcot–Marie–ToothDisease.
2. Segmental demyelination – uneven degree of demyelination of different nervefibers throughout the course of the nerve. This can produce variable slowing of differentnerve fibers, which presents as temporal dispersion (Fig. 6.1). For example, in the samenerve some fibers may be conducting at 50 meters/sec, some at 40 meters/sec and some at30 meters/sec. The sum will be a waveform that has lower amplitude but is moredispersed (wider). Remember that the sum of all the nerve fibers contributes to the shapeof the CMAP.
3. Focal nerve slowing – localized area of demyelination causing nerve slowing,which presents as a decrease in conduction velocity across the lesion (Fig. 6.2). Forexample, if someone applies a tourniquet over one part of an arm, the myelin will becompromised only in that one area. The nerve would conduct normally both above andbelow that area. Conduction velocity would be slowed across the area of demyelination.This occurs frequently in the ulnar nerve about the elbow.
4. Conduction block – an area of focal demyelination that is so severe that the actionpotential cannot propagate through the area of demyelination. This presents as decreasedamplitude with proximal stimulation since the affected nerve fibers cannot contribute to 81
!
the amplitude. The distal CMAP amplitude is maintained because the nerve fiber distalto the block is intact (Fig. 6.3). For example, if there is a tourniquet applied to the upperarm and the focal demyelination is so severe that the action potential can no longerpropagate, the CMAP obtained when stimulating proximal to this point will not includethose affected nerve fibers and will therefore have a lower amplitude. However, when thenerve is stimulated distal to this area of compromise, the CMAP will be normal. This isbecause the axon itself has not been significantly compromised. Clinically, conductionblocks present as weakness. Conduction velocity slowing alone, without conductionblock, does not produce clinical weakness.
Because the axon is essentially intact in a purely demyelinating injury, EMG testing willbe normal, unless conduction block is present. In conduction block, decreased recruitmentmay be noted.
Axonal Injuries
Injury to the axon will lead to Wallerian degeneration distal to the site of the lesion. Inmuscles distal to that lesion, you will see a decrease in CMAP amplitude with stimulation,both distal and proximal, to the lesion (Fig. 6.4; Fig. 6.5 shows a normal reading forcomparison). On needle examination, abnormal spontaneous potentials (fibrillations
Easy EMG82
Time (millisecond)
Am
plit
ud
e (m
illiv
olt
)
Figure 6.1Segmentaldemyelination.
Figure 6.2 Focalnerve slowing.
Am
plit
ud
e (m
illiv
olt
)
Time (milllisecond)
!
6 Injury to Peripheral Nerves 83
Time (milllisecond)
Am
plit
ud
e (m
illiv
olt
)Figure 6.3Conduction block.
Figure 6.4 Axonalneuropathy.
Figure 6.5Normal.
Time (millisecond)(dotted line indicates normal amplitude)
Am
plit
ud
e (m
illiv
olt
)
Time (milllisecond)
Am
plit
ud
e (m
illiv
olt
)
and positive sharp waves) will be noted. The motor units may be polyphasic with highamplitude and long duration, depending on the chronicity of the injury. Recruitment ofmotor units will be decreased and firing frequency of single motor units will beincreased (normal firing frequency for a MUAP is about 10 Hz or 10 cycles per second).
NCS/EMG Findings
(See Table 6.1)
Nerve Conduction Studies
Demyelinating Injuries
Uniform Demyelinating
In uniform demyelinating lesions nerve conduction studies will be slowed throughoutthe nerve since the entire nerve is affected. Distal latencies will be prolonged; againbecause of the uniform slowing (distal latencies representing the most distal conductionvelocity). Amplitudes should not be significantly affected, since the axons are intact andthe slowing is consistent through all fibers of the nerve.
Segmental Demyelination
Since there is variable slowing of different nerve fibers within the nerve, conductionvelocity will be slowed and distal latencies will be prolonged in segmentally demyelinatinginjuries. CMAP amplitudes will be decreased because of temporal dispersion, not becauseof axonal damage. Therefore, the CMAP will be longer in duration and the area under theCMAP will be normal.
Focal Demyelination
In focal demyelination, only one segment of the nerve is affected. Therefore, conductionvelocity will be normal unless stimulation is across the area of focal demyelination. In thissegment, you will see slowing of conduction velocity. Slowing is usually evident if there isa more than 10 meter/second drop in conduction velocity across the segment, compared todistally. Latencies and amplitudes should be normal.
Conduction Block
As stated above, conduction block is a focal demyelination that is so severe that the actionpotential cannot propagate past that point. Therefore, distal latencies and conductionvelocities remain normal. Distal amplitudes will be normal. However, when the nerve isstimulated across the area of conduction block, a drop in amplitude is noted. To beconsidered significant, this drop in proximal amplitude should be more than 20% of thedistal amplitude. For example if the distal amplitude is 10 microvolts and the proximalamplitude is 7 microvolts, conduction block should be considered.
Axonal Injuries
Nerve conduction studies in axonal injuries will show decreased amplitude with bothproximal and distal stimulation. If the contralateral extremity is not affected, you cancompare side-to-side amplitudes to estimate the amount of axonal loss. Usually, a 50%side-to-side difference is considered significant. Latencies and conduction velocitiesshould not be significantly affected. Sometimes, since the fastest fibers may be affected, aless than 20% increase in latency or decrease in conduction velocity may be noted. If
Easy EMG84
!
6 Injury to Peripheral Nerves 85
Co
nd
itio
nC
MA
P am
plit
ud
e C
MA
P am
plit
ud
e C
on
du
ctio
n v
elo
city
Dis
tal l
aten
cyFi
bs/
PSW
Rec
ruit
men
tw
ith
dis
tal
wit
h p
roxi
mal
st
imu
lati
on
stim
ula
tio
n
(sti
mu
lati
ng
acr
oss
th
e le
sio
n)
Un
ifo
rm d
emye
linat
ing
No
rmal
No
rmal
Dec
reas
edIn
crea
sed
–N
orm
al
Seg
men
tal d
emye
linat
ing
No
rmal
or
dec
reas
ed
Dec
reas
ed s
eco
nd
ary
Dec
reas
edM
ay b
e –
No
rmal
seco
nd
ary
to
to d
isp
ersi
on
incr
ease
d (
if
dis
per
sio
nfa
stes
t fi
ber
s ar
e af
fect
ed)
Foca
l dem
yelin
atin
g
No
rmal
No
rmal
Slo
wed
acr
oss
are
a N
orm
al–
No
rmal
wit
ho
ut
con
du
ctio
n
of
foca
l b
lock
*d
emye
linat
ion
Foca
l dem
yelin
atio
n
No
rmal
(Dec
reas
ed b
y m
ore
N
orm
al o
r fo
cal
No
rmal
–D
ecre
ased
cau
sin
g c
on
du
ctio
n
than
20%
)sl
ow
ing
blo
ck*
Axo
no
tmes
isD
ecre
ased
Dec
reas
edN
orm
al t
o 2
0%
No
rmal
to
+
Dec
reas
edd
ecre
ase
20%
incr
ease
Neu
rotm
esis
Un
ob
tain
able
Un
ob
tain
able
Un
ob
tain
able
Un
ob
tain
able
++
Un
ob
tain
able
*Fo
r th
e p
urp
ose
s o
f th
is t
able
, ass
um
e a
pro
xim
al a
rea
of
foca
l dem
yelin
atio
n o
r co
nd
uct
ion
blo
ck.
Tab
le 6
.1N
CS/
EMG
fin
din
gs
in p
erip
her
al n
erve
inju
ries
neurotmesis is present, the CMAP or SNAP amplitude will be unobtainable bothproximal and distal to the lesion.
EMG Findings
Abnormal spontaneous potentials (fibrillations and positive sharp waves) are usuallyonly found if there has been axonal injury. Therefore, no abnormal spontaneous activityshould be noted in any of the demyelinating lesions. MUAP morphology and recruitmentshould be normal. The only exception would be in conduction block, where decreasedrecruitment would be seen.
With Wallerian degeneration, the degeneration occurs distal to the site of the lesion.Therefore, all distal muscles innervated by the injured nerve should show spontaneousactivity if the test is performed before reinnervation occurs (see below). Polyphasicity,prolonged duration and increased amplitude of the MUAP may be noted, again dependingupon the timing of the test. Recruitment will be decreased. In a neurotmetic lesion, therewill be profound denervation and no motor units will be recruited.
Timing of Electrodiagnostic Testing – When to Schedule an EMG/NCS
In order to get the most information with the least amount of discomfort to the patient, itis important to time the test appropriately. Keep in mind the following timetableregarding how nerves respond electrophysiologically to injury:
1. Abnormal spontaneous activity includes fibrillation potentials (fibs) and positivesharp waves (PSWs). Such findings may take days to weeks before being detectable onEMG testing. The more distal the muscle, the longer the axon length, and the longer ittakes for membrane instability to occur. Proximal muscles may show changes within oneweek, but collateral sprouting will also provide reinnervation to these muscles first. Moredistal muscles may require three weeks before fibs or PSWs are seen. Therefore, if the testis done too early (e.g., in the first few weeks after injury) it may be falsely negative. If a testis performed long after the injury, reinnervation may have already occurred. In this case,there may not be fibs and PSWs present. Motor units may show evidence of reinnervation– long duration, polyphasic and increased amplitude.
2. Sensory nerve action potentials (SNAPs) and compound muscle action potentials(CMAPs) amplitudes begin to decrease within several days after nerve injury. It maytake over one week before SNAPs and CMAPs are unobtainable. Therefore, if NCS aredone in the first few days after injury, they may appear normal when in fact, if they weredone at least 11 days following the injury, they would reveal reduced amplitudesconsistent with the suspected injury.
3. Axons regrow at a rate of about 1 mm/day (about an inch per month). Therefore,if you are doing a study or serial studies where you want to determine the prognosis, it isimportant to keep in mind how long the anticipated recovery period would be based onaxonal regeneration.
Easy EMG86
7How to Plan Out theExamination
Lyn Weiss, Carlo Esteves, Limeng Wang
To perform electrodiagnostic testing accurately and efficiently, a well-planned approachis necessary. Such measures will decrease potential discomfort and increase the yield ofinformation. The clinician should start by taking a thorough history, performing a physicalexamination and, if available, reviewing laboratory and radiological studies. Electro-diagnostic testing serves as an adjunct to the history and physical examination in theevaluation of neuromuscular disease/pathology. Although the nature of neurologicdysfunction in a specific disease process may be suggested by symptoms or signs obtainedduring physical examination, only electrodiagnostic studies can provide an objectivephysiologic measure of neurologic function.
Once the history and physical are performed, you should develop a differentialdiagnosis that will help guide which nerves and muscles are tested. There are severalquestions that can help you narrow your selections (Fig. 7.1).
● Are the symptoms compatible with a central disorder (hyperreflexia, increased tone,central distribution) or a peripheral disorder (hyporeflexia, decreased tone, peripheraldistribution)? If the history and physical are compatible with a central disorder, othertesting may be more appropriate (i.e., MRI of the brain or spinal cord). If a peripheraldistribution is suggested, proceed with EMG/NCS testing.
● Does the history and physical suggest a disorder of nerves (neuropathic) or muscles(myopathic)? A neuropathic disorder may present with sensory findings and/orweakness in a peripheral nerve distribution. A myopathic disorder should beconsidered if there is predominantly proximal weakness and no sensory symptoms(see Chapter 17).
● If a neuropathic disorder is more likely, try to determine if the motor and sensoryloss reflects a peripheral neuropathy (predominantly distal affecting more than oneextremity) or a peripheral nerve distribution.
● If a peripheral nerve lesion is probable, use Table 7.1 to try to localize the lesion.Table 7.1 will help you identify the patient’s symptoms, depending on whether theproblem is at the root, trunk, cord division or peripheral nerve level. It will also helpyou determine which nerves and muscles should be tested.
● If a peripheral neuropathy is suspected, electrodiagnostic testing will help determinethe type of neuropathy (motor and/or sensory; axonal and/or demyelinating).
General Points to Remember
● If you get an abnormal result, it is important to continue testing until you get anormal result. For example, if you suspect carpal tunnel syndrome and the needle 87
testing of the abductor pollicis brevis (APB) is abnormal (fibrillations or positivesharp waves are present), other muscles should be tested. A more proximal medianneuropathy may be present, or a generalized disorder may be present.
● To assess for peripheral neuropathy, motor and sensory nerves in two or threeextremities must be tested.
● When performing needle testing to rule out local nerve injury or entrapment, startwith the most distally innervated muscles and proceed proximally.
● If the patient is reluctant to proceed with the electrodiagnostic test, go directly to thatportion of the test that is most likely to yield pertinent information. For example, someelectromyographers have a prescribed list and schedule of nerves to test. While thismay suffice for 90% of patients, flexibility is necessary if you know the patient canonly tolerate limited testing.
Table 7.1 shows commonly tested nerves in the upper and lower extremities, the rootlevels, the muscles they innervate, and some of the physical findings that can be expectedif the nerve is compromised. This table can be used to help plan out the electrodiagnostictest. Table 7.2 describes common muscles tested on needle study, along with nerve androot levels. This will assist with planning out the examination. For example, if a C6nerve root is suspected, try to examine several muscles that include C6. If a radial nerveinjury is suspected, these tables will help decide which muscles to test based on theirinnervation.
Easy EMG88
EMG not indicated
Myopathic vs. Neuropathic
Myopathic(proximal weakness,no sensory findings)
Neuropathic
Mononeuropathy(sensory or motor findings in aperipheral nerve distribution)
root lesion plexuslesion
peripheralnerve
motor sensory
axonal demyelinating axonal demyelinating
Polyneuropathy(distal predominance)
Numbness/weakness in the extremities
Peripheral nervoussystem findings
(hyporeflexia, decreased tone,fasciculations)
Central nervoussystem findings
(hyperreflexia, increased tone,hemiparesis)
Figure 7.1Algorithm forplanning theelectrodiagnosticexamination.
7 How to Plan Out the Examination 89
Ro
ot
lesi
on
Ro
ots
Ner
ves
Mu
scle
sSi
gn
s an
d s
ymp
tom
s
C5
Do
rsal
sca
pu
lar
Rh
om
bo
id m
ajo
rW
eakn
ess
or
abse
nt
scap
ula
ad
du
ctio
n.
Do
rsal
sca
pu
lar
Rh
om
bo
id m
ino
rW
eakn
ess
in s
ho
uld
er r
ang
e o
f m
oti
on
.D
ors
al s
cap
ula
r Le
vato
r sc
apu
lae
Wea
knes
s in
arm
ab
du
ctio
n, a
dd
uct
ion
, fle
xio
n a
nd
med
ial/l
ater
al r
ota
tio
n.
Sup
rasc
apu
lar
Sup
rasp
inat
us
Wea
knes
s in
fle
xio
n o
f fo
rear
m a
t el
bo
w a
nd
su
pin
atio
n o
f fo
rear
m.
Sup
rasc
apu
lar
Infr
asp
inat
us
Dim
inis
hed
sen
sati
on
ove
r th
e la
tera
l arm
Sub
scap
ula
r Su
bsc
apu
lari
sSu
bsc
apu
lar
Tere
s m
ajo
rA
xilla
ry
Del
toid
Axi
llary
Te
res
min
or
Mu
scu
locu
tan
eou
s C
ora
cob
rach
ialis
Mu
scu
locu
tan
eou
s B
icep
sM
usc
ulo
cuta
neo
us
Bra
chia
lisLo
ng
th
ora
cic
Serr
atu
s an
teri
or
Rad
ial
Bra
chio
rad
ialis
Rad
ial
Sup
inat
or
Pect
ora
l Pe
cto
ralis
maj
or
Pect
ora
l Pe
cto
ralis
min
or
C6
Sup
rasc
apu
lar
Sup
rasp
inat
us
Wea
knes
s in
arm
ab
du
ctio
n, a
dd
uct
ion
, fle
xio
n a
nd
med
ial/l
ater
al r
ota
tio
n.
Sup
rasc
apu
lar
Infr
asp
inat
us
Wea
knes
s in
ext
ensi
on
/fle
xio
n o
f fo
rear
m a
t el
bo
w a
nd
pro
nat
ion
of
fore
arm
.Su
bsc
apu
lar
Sub
scap
ula
ris
Wea
knes
s in
ext
ensi
on
(d
ors
ifle
xio
n)
wri
st a
nd
rad
ial a
bd
uct
ion
of
han
d a
t w
rist
. Su
bsc
apu
lar
Tere
s m
ajo
rD
imin
ish
ed s
ensa
tio
n o
ver
the
late
ral f
ore
arm
, th
um
b, i
nd
ex, a
nd
on
e-h
alf
of
Axi
llary
D
elto
idm
idd
le fi
ng
er (
rad
ial s
ide)
Axi
llary
Te
res
min
or
Mu
scu
locu
tan
eou
s B
icep
sM
usc
ulo
cuta
neo
us
Bra
chia
lisM
usc
ulo
cuta
neo
us
Co
raco
bra
chia
lisTh
ora
cod
ors
al
Lati
ssim
us
do
rsi
Lon
g t
ho
raci
c Se
rrat
us
ante
rio
r
Tab
le 7
.1U
pp
er e
xtre
mit
ies
Easy EMG90
Ro
ot
lesi
on
Ro
ots
Ner
ves
Mu
scle
sSi
gn
s an
d s
ymp
tom
s
Rad
ial
Tric
eps
Rad
ial
An
con
eus
Rad
ial
Bra
chio
rad
ialis
Rad
ial
Exte
nso
r ca
rpi r
adia
lisR
adia
l Su
pin
ato
rM
edia
n
Pro
nat
or
tere
sM
edia
n
Flex
or
carp
i rad
ialis
Pect
ora
l Pe
cto
ralis
maj
or
Pect
ora
l Pe
cto
ralis
min
or
C7
Sub
scap
ula
r Te
res
maj
or
Wea
k o
r ab
sen
t ex
ten
sio
n o
f fo
rear
m a
t el
bo
w a
nd
pro
nat
ion
of
fore
arm
. M
usc
ulo
cuta
neo
us
Co
raco
bra
chia
lisU
nab
le t
o f
lex
(pal
mar
fle
xio
n)
han
d a
t w
rist
an
d e
xten
d fi
ng
ers
at M
CP.
Tho
raco
do
rsal
La
tiss
imu
s d
ors
iIn
abili
ty t
o d
ors
ifle
x th
e w
rist
an
d u
lnar
dev
iati
on
.Lo
ng
th
ora
cic
Serr
atu
s an
teri
or
Wea
knes
s in
ext
ensi
on
(d
ors
ifle
xio
n)
wri
st a
nd
rad
ial a
bd
uct
ion
of
han
d a
t w
rist
. R
adia
l Tr
icep
sW
eakn
ess
in e
xten
sio
n o
f p
roxi
mal
an
d d
ista
l ph
alan
x o
f th
um
b.
Rad
ial
An
con
eus
Dim
inis
hed
sen
sati
on
ove
r m
idd
le fi
ng
erR
adia
l Ex
ten
sor
carp
i rad
ialis
Rad
ial
Exte
nso
r ca
rpi u
lnar
isR
adia
l Ex
ten
sor
dig
ito
rum
Rad
ial
Exte
nso
r d
igit
i min
imi
Rad
ial
Ab
du
cto
r p
olli
cis
lon
gu
sR
adia
l Ex
ten
sor
po
llici
s lo
ng
us
Rad
ial
Exte
nso
r p
olli
cis
bre
vis
Rad
ial
Exte
nso
r in
dic
isM
edia
n
Pro
nat
or
tere
sM
edia
n
Flex
or
carp
i rad
ialis
Med
ian
Pa
lmar
is lo
ng
us
Med
ian
Fl
exo
r d
igit
oru
m
sup
erfi
cial
isM
edia
n a
nd
uln
ar
Flex
or
dig
ito
rum
pro
fun
du
s
Tab
le 7
.1U
pp
er e
xtre
mit
ies
(co
nt’
d)
7 How to Plan Out the Examination 91
Ro
ot
lesi
on
Ro
ots
Ner
ves
Mu
scle
sSi
gn
s an
d s
ymp
tom
s
Med
ian
Fl
exo
r p
olli
cis
lon
gu
sM
edia
n
Pro
nat
or
qu
adra
tus
Pect
ora
l Pe
cto
ralis
maj
or
Pect
ora
l Pe
cto
ralis
min
or
C8
Rad
ial
Exte
nso
r ca
rpi u
lnar
isW
eakn
ess
in f
lexi
on
of
dis
tal p
hal
ang
es o
f fi
ng
ers.
R
adia
l Ex
ten
sor
dig
ito
rum
Inab
ility
to
ad
du
ct in
dex
, rin
g a
nd
litt
le fi
ng
ers
tow
ard
s m
idd
le fi
ng
er.
Rad
ial
Exte
nso
r d
igit
i min
imi
Dif
ficu
lty
of
abd
uct
ion
of
ind
ex, m
idd
le a
nd
rin
g fi
ng
er f
rom
mid
dle
lin
e o
f m
idd
le
Rad
ial
Ab
du
cto
r p
olli
cis
lon
gu
sfi
ng
er b
oth
rad
ial a
nd
uln
ar a
bd
uct
ion
.R
adia
l Ex
ten
sor
po
llici
s lo
ng
us
Wea
knes
s in
fle
xio
n a
nd
uln
ar d
evia
tio
n o
f h
and
at
wri
st.
Rad
ial
Exte
nso
r p
olli
cis
bre
vis
Wea
knes
s in
ab
du
ctio
n, f
lexi
on
an
d o
pp
osi
tio
n o
f lit
tle
fin
ger
to
war
ds
thu
mb
.R
adia
l Ex
ten
sor
ind
icis
Un
able
to
ad
du
ct t
he
thu
mb
in b
oth
uln
ar a
nd
pal
mar
dir
ecti
on
s.M
edia
n
Palm
aris
lon
gu
sD
imin
ish
ed s
ensa
tio
n o
ver
the
dis
tal h
alf
of
the
fore
arm
’s u
lnar
sid
e, t
he
5th
an
d
Med
ian
Fl
exo
r d
igit
oru
m
hal
f o
f th
e 4t
h fi
ng
er o
n t
he
uln
ar s
ide
sup
erfi
cial
isM
edia
n a
nd
uln
ar
Flex
or
dig
ito
rum
p
rofu
nd
us
Med
ian
Fl
exo
r p
olli
cis
lon
gu
sM
edia
n
Pro
nat
or
qu
adra
tus
Med
ian
A
bd
uct
or
po
llici
s b
revi
sM
edia
n
Op
po
nen
s p
olli
cis
Med
ian
Fl
exo
r p
olli
cis
bre
vis
Uln
ar
Flex
or
carp
i uln
aris
Uln
ar
Palm
aris
bre
vis
Uln
ar
Ab
du
cto
r d
igit
i min
imi
Uln
ar
Op
po
nen
s d
igit
i min
imi
Uln
ar
Flex
or
dig
iti m
inim
iU
lnar
Pa
lmar
inte
ross
eou
sU
lnar
D
ors
al in
tero
sseo
us
Tab
le 7
.1U
pp
er e
xtre
mit
ies
(co
nt’
d)
Easy EMG92
Ro
ot
lesi
on
Ro
ots
Ner
ves
Mu
scle
sSi
gn
s an
d s
ymp
tom
s
Uln
ar
Ad
du
cto
r p
olli
cis
Med
ian
an
d u
lnar
Lu
mb
rica
ls (
4)Pe
cto
ral
Pect
ora
lis m
ajo
rPe
cto
ral
Pect
ora
lis m
ino
r
T1M
edia
n
Palm
aris
lon
gu
sW
eakn
ess
in fi
ng
er a
bd
uct
ion
. Dif
ficu
lty
of
abd
uct
ion
of
ind
ex, m
idd
le a
nd
rin
g
Med
ian
Fl
exo
r d
igit
oru
m
fin
ger
fro
m m
idd
le li
ne
of
mid
dle
fin
ger
bo
th r
adia
l an
d u
lnar
ab
du
ctio
n.
sup
erfi
cial
isIn
abili
ty t
o a
dd
uct
ind
ex, r
ing
an
d li
ttle
fin
ger
s to
war
ds
mid
dle
fin
ger
.M
edia
n a
nd
uln
ar
Flex
or
dig
ito
rum
W
eakn
ess
in li
ttle
fin
ger
ab
du
ctio
n, f
lexi
on
an
d o
pp
osi
tio
n o
f lit
tle
fin
ger
to
war
ds
pro
fun
du
sth
um
b.
Med
ian
Fl
exo
r p
olli
cis
lon
gu
sW
eakn
ess
in a
dd
uct
ion
of
the
thu
mb
in b
oth
uln
ar a
nd
pal
mar
dir
ecti
on
s an
d
Med
ian
Pr
on
ato
r q
uad
ratu
sab
du
ctio
n o
f th
um
b.
Med
ian
A
bd
uct
or
po
llici
s b
revi
sD
imin
ish
ed s
ensa
tio
n o
ver
the
med
ial s
ide
of
the
up
per
hal
f o
f th
e fo
rear
m a
nd
th
e M
edia
n
Op
po
nen
s p
olli
cis
low
er h
alf
of
the
arm
. M
edia
n
Flex
or
po
llici
s b
revi
sU
lnar
Fl
exo
r ca
rpi u
lnar
isU
lnar
Pa
lmar
is b
revi
sU
lnar
A
bd
uct
or
dig
iti m
inim
iU
lnar
O
pp
on
ens
dig
iti m
inim
iU
lnar
Fl
exo
r d
igit
i min
imi
Uln
ar
Palm
ar in
tero
sseo
us
Uln
ar
Do
rsal
inte
ross
eou
s U
lnar
A
dd
uct
or
po
llici
sM
edia
n a
nd
uln
ar
Lum
bri
cals
(4)
Pect
ora
lPe
cto
ralis
maj
or
Pect
ora
lPe
cto
ralis
min
or
Tab
le 7
.1U
pp
er e
xtre
mit
ies
(co
nt’
d)
7 How to Plan Out the Examination 93
Tru
nk
lesi
on
Tru
nks
Ner
ves
Mu
scle
sSi
gn
s an
d s
ymp
tom
s
Up
per
D
ors
al s
cap
ula
R
ho
mb
oid
maj
or
Wea
knes
s o
f sh
ou
lder
an
d u
pp
er a
rm a
bd
uct
ion
, fle
xio
n, a
nd
ext
ern
al r
ota
tio
n.
tru
nk
Do
rsal
sca
pu
la
Rh
om
bo
id m
ino
rW
eakn
ess
in e
lbo
w f
lexi
on
an
d r
adia
l wri
st e
xten
sio
n.
C5,
C6
Do
rsal
sca
pu
la
Leva
tor
scap
ula
eSe
nso
ry lo
ss a
t th
e C
5 an
d C
6 d
erm
ato
mes
– t
he
late
ral a
rm, f
ore
arm
, an
d fi
rst
two
Su
pra
scap
ula
r Su
pra
spin
atu
s d
igit
sSu
pra
scap
ula
r In
fras
pin
atu
sSu
pra
scap
ula
r Su
bsc
apu
lari
sSu
pra
scap
ula
r Te
res
maj
or
Axi
llary
D
elto
idA
xilla
ry
Tere
s m
ino
rM
usc
ulo
cuta
neo
us
Co
raco
bra
chia
lisM
usc
ulo
cuta
neo
us
Bic
eps
Mu
scu
locu
tan
eou
s B
rach
ialis
Tho
raco
do
rsal
La
tiss
imu
s d
ors
iR
adia
l Tr
icep
sR
adia
l A
nco
neu
sR
adia
l B
rach
iora
dia
lisR
adia
l Ex
ten
sor
carp
i rad
ialis
R
adia
l Su
pin
ato
rM
edia
n
Pro
nat
or
tere
sM
edia
n
Flex
or
carp
i rad
ialis
Pect
ora
l Pe
cto
ralis
maj
or
Pect
ora
l Pe
cto
ralis
min
or
Mid
dle
M
usc
ulo
cuta
neo
us
Co
raco
bra
chia
lisW
eak
or
abse
nt
exte
nsi
on
of
fore
arm
at
elb
ow
. tr
un
kTh
ora
cod
ors
al
Lati
ssim
us
do
rsi
Wea
k/ab
sen
t ex
ten
sio
n (
do
rsif
lexi
on
) an
d r
adia
l ab
du
ctio
n o
f h
and
at
wri
st. U
nab
le
C7
Rad
ial
Tric
eps
to f
lex
(pal
mar
fle
xio
n)
han
d a
t w
rist
an
d e
xten
d fi
ng
ers
at M
CP.
Rad
ial
An
con
eus
Inab
ility
to
do
rsif
lex
the
wri
st a
nd
uln
ar d
evia
tio
n.
Rad
ial
Exte
nso
r ca
rpi r
adia
lisW
eak
or
abse
nt
exte
nsi
on
of
pro
xim
al a
nd
dis
tal p
hal
anx
of
thu
mb
.R
adia
l Ex
ten
sor
carp
i uln
aris
D
imin
ish
ed s
ensa
tio
n o
ver
mid
dle
fin
ger
an
d s
om
etim
es t
he
ind
ex fi
ng
er
Tab
le 7
.1U
pp
er e
xtre
mit
ies
(co
nt’
d)
Easy EMG94
Tru
nk
lesi
on
Tru
nks
Ner
ves
Mu
scle
sSi
gn
s an
d s
ymp
tom
s
Rad
ial
Exte
nso
r d
igit
oru
mR
adia
l Ex
ten
sor
dig
iti m
inim
iR
adia
l A
bd
uct
or
po
llici
s lo
ng
us
Rad
ial
Exte
nso
r p
olli
cis
lon
gu
s R
adia
l Ex
ten
sor
po
llici
s b
revi
sR
adia
l Ex
ten
sor
ind
icis
Med
ian
Pr
on
ato
r te
res
Med
ian
Fl
exo
r ca
rpi r
adia
lisM
edia
n
Palm
aris
lon
gu
sM
edia
n
Flex
or
dig
ito
rum
su
per
fici
alis
Med
ian
an
d u
lnar
Fl
exo
r d
igit
oru
m p
rofu
nd
us
Med
ian
Fl
exo
r p
olli
cis
lon
gu
sM
edia
n
Pro
nat
or
qu
adra
tus
Pect
ora
l Pe
cto
ralis
maj
or
Pect
ora
l Pe
cto
ralis
min
or
Low
er t
run
kTh
ora
cod
ors
al
Lati
ssim
us
do
rsi
Wea
k o
r ab
sen
t ab
du
ctio
n, f
lexi
on
an
d o
pp
osi
tio
n o
f lit
tle
fin
ger
to
war
ds
thu
mb
.C
8, T
1R
adia
l Tr
icep
sIn
abili
ty t
o a
dd
uct
ind
ex, r
ing
an
d li
ttle
fin
ger
s to
war
ds
mid
dle
fin
ger
.R
adia
l A
nco
neu
sD
iffi
cult
y o
f ab
du
ctio
n o
f in
dex
, mid
dle
an
d r
ing
fin
ger
fro
m m
idd
le li
ne
of
mid
dle
R
adia
l Ex
ten
sor
carp
i uln
aris
fin
ger
bo
th r
adia
l an
d u
lnar
ab
du
ctio
n.
Rad
ial
Exte
nso
r d
igit
oru
mU
nab
le t
o a
dd
uct
th
e th
um
b in
bo
th u
lnar
an
d p
alm
ar d
irec
tio
ns.
Rad
ial
Exte
nso
r d
igit
i min
imi
Wea
knes
s in
ext
ensi
on
of
fore
arm
an
d f
lexi
on
of
dis
tal p
hal
ang
es.
Rad
ial
Ab
du
cto
r p
olli
cis
lon
gu
sD
imin
ish
ed s
ensa
tio
n o
ver
dis
tal h
alf
of
the
fore
arm
uln
ar s
ide,
th
e 5t
h a
nd
hal
f o
f R
adia
l Ex
ten
sor
po
llici
s lo
ng
us
the
4th
fin
ger
on
th
e u
lnar
sid
eR
adia
l Ex
ten
sor
po
llici
s b
revi
sR
adia
l Ex
ten
sor
ind
icis
Med
ian
Pa
lmar
is lo
ng
us
Med
ian
Fl
exo
r d
igit
oru
m s
up
erfi
cial
isM
edia
n a
nd
uln
ar
Flex
or
dig
ito
rum
pro
fun
du
s
Tab
le 7
.1U
pp
er e
xtre
mit
ies
(co
nt’
d)
7 How to Plan Out the Examination 95
Tru
nk
lesi
on
Tru
nks
Ner
ves
Mu
scle
sSi
gn
s an
d s
ymp
tom
s
Med
ian
Fl
exo
r p
olli
cis
lon
gu
sM
edia
n
Pro
nat
or
qu
adra
tus
Uln
ar
Ab
du
cto
r d
igit
i min
imi
Uln
ar
Op
po
nen
s d
igit
i min
imi
Uln
ar
Flex
or
dig
iti m
inim
iU
lnar
Pa
lmar
inte
ross
eou
sU
lnar
D
ors
al in
tero
sseo
us
Uln
ar
Ad
du
cto
r p
olli
cis
Med
ian
an
d u
lnar
Lu
mb
rica
ls (
4)Pe
cto
ral
Pect
ora
lis m
ajo
rPe
cto
ral
Pect
ora
lis m
ino
r
Co
rd le
sio
nC
ord
sN
erve
sM
usc
les
Sig
ns
and
sym
pto
ms
Post
erio
r Su
bsc
apu
lar
Sub
scap
ula
ris
Wea
knes
s in
sh
ou
lder
RO
M a
nd
arm
ab
du
ctio
n, a
dd
uct
ion
, fle
xio
n, e
xten
sio
n,
cord
Sub
scap
ula
r Te
res
maj
or
late
ral r
ota
tio
n.
C5
to T
1A
xilla
ry
Del
toid
Wea
k o
r ab
sen
t ex
ten
sio
n o
f fo
rear
m a
t el
bo
w.
Axi
llary
Te
res
min
or
Wea
k o
r ab
sen
t ex
ten
sio
n (
do
rsif
lexi
on
) an
d r
adia
l ab
du
ctio
n o
f h
and
at
wri
st.
Tho
raco
do
rsal
La
tiss
imu
s d
ors
alU
nab
le t
o s
up
inat
e an
d e
xten
d fi
ng
ers
at M
CP.
Rad
ial
Tric
eps
Inab
ility
to
do
rsif
lex
the
wri
st a
nd
uln
ar d
evia
tio
n.
Rad
ial
An
con
eus
Wea
k o
r ab
sen
t ex
ten
sio
n o
f p
roxi
mal
an
d d
ista
l ph
alan
x o
f th
um
b.
Rad
ial
Bra
chio
rad
ialis
Dim
inis
hed
sen
sati
on
ove
r th
e la
tera
l arm
– d
elto
id p
atch
on
up
per
arm
, lat
eral
R
adia
l Ex
ten
sor
carp
i rad
ialis
fore
arm
an
d fi
rst
3 d
igit
sR
adia
l Su
pin
ato
rR
adia
l Ex
ten
sor
carp
i uln
aris
Rad
ial
Exte
nso
r d
igit
oru
mR
adia
l Ex
ten
sor
dig
iti m
inim
iR
adia
l A
bd
uct
or
po
llici
s lo
ng
us
Rad
ial
Exte
nso
r p
olli
cis
lon
gu
s
Tab
le 7
.1U
pp
er e
xtre
mit
ies
(co
nt’
d)
Easy EMG96
Co
rd le
sio
nC
ord
sN
erve
sM
usc
les
Sig
ns
and
sym
pto
ms
Rad
ial
Exte
nso
r p
olli
cis
bre
vis
Rad
ial
Exte
nso
r in
dic
is
Late
ral c
ord
Mu
scu
locu
tan
eou
s C
ora
cob
rach
ialis
Un
able
to
pro
nat
e an
d f
lex
the
fore
arm
. C
5 to
T1
Mu
scu
locu
tan
eou
s B
icep
sW
eakn
ess
in f
lexi
on
of
fore
arm
s an
d t
he
han
d a
t w
rist
.M
usc
ulo
cuta
neo
us
Bra
chia
lisW
eakn
ess
in f
lexi
on
of
dis
tal p
hal
ang
es o
f fi
ng
ers.
M
edia
n
Pro
nat
or
tere
sD
imin
ish
ed s
ensa
tio
n o
ver
the
late
ral f
ore
arm
an
d m
idd
le fi
ng
erM
edia
n
Flex
or
carp
i rad
ialis
Med
ian
Pa
lmar
is lo
ng
us
Med
ian
Fl
exo
r d
igit
oru
m
sup
erfi
cial
isM
edia
n a
nd
uln
ar
Flex
or
dig
ito
rum
p
rofu
nd
us
Med
ian
Fl
exo
r p
olli
cis
lon
gu
sPe
cto
ral
Pect
ora
lis m
ajo
rPe
cto
ral
Pect
ora
lis m
ino
r
Med
ial c
ord
Med
ian
Pa
lmar
is lo
ng
us
Wea
knes
s in
fle
xio
n o
f d
ista
l ph
alan
ges
of
fin
ger
s.
C6
to T
1M
edia
n
Flex
or
dig
ito
rum
W
eak/
abse
nt
abd
uct
ion
, fle
xio
n a
nd
op
po
siti
on
of
littl
e fi
ng
er t
ow
ard
s th
um
b.
sup
erfi
cial
isIn
abili
ty t
o a
dd
uct
ind
ex, r
ing
an
d li
ttle
fin
ger
s to
war
ds
mid
dle
fin
ger
.M
edia
n a
nd
uln
ar
Flex
or
dig
ito
rum
D
iffi
cult
y o
f ab
du
ctio
n o
f in
dex
, mid
dle
an
d r
ing
fin
ger
s fr
om
mid
dle
lin
e o
f m
idd
le
pro
fun
du
sfi
ng
er b
oth
rad
ial a
nd
uln
ar a
bd
uct
ion
.M
edia
nFl
exo
r p
olli
cis
lon
gu
sU
nab
le t
o a
dd
uct
th
e th
um
b in
bo
th u
lnar
an
d p
alm
ar d
irec
tio
ns.
Med
ian
Pro
nat
or
qu
adra
tus
Dec
reas
ed s
ensa
tio
n o
ver
the
vola
r su
rfac
e o
f th
e 1s
t to
3rd
an
d h
alf
of
the
Med
ian
A
bd
uct
or
po
llici
s b
revi
s4t
h fi
ng
ers
Med
ian
O
pp
on
ens
po
llici
sM
edia
n
Flex
or
po
llici
s b
revi
sU
lnar
Fl
exo
r ca
rpi u
lnar
isU
lnar
Pa
lmar
is b
revi
s
Tab
le 7
.1U
pp
er e
xtre
mit
ies
(co
nt’
d)
7 How to Plan Out the Examination 97
Co
rd le
sio
nC
ord
sN
erve
sM
usc
les
Sig
ns
and
sym
pto
ms
Uln
ar
Ab
du
cto
r d
igit
i min
imi
Uln
ar
Op
po
nen
s d
igit
i min
imi
Uln
ar
Flex
or
dig
iti m
inim
iU
lnar
Pa
lmar
inte
ross
eou
sU
lnar
D
ors
al in
tero
sseo
us
Uln
ar
Ad
du
cto
r p
olli
cis
Med
ian
an
d u
lnar
Lu
mb
rica
ls (
4)
Div
isio
n le
sio
nD
ivis
ion
sN
erve
sM
usc
les
Sig
ns
and
sym
pto
ms
Post
erio
r Su
bsc
apu
lar
Sub
scap
ula
ris
Wea
knes
s in
sh
ou
lder
RO
M a
nd
arm
ab
du
ctio
n, a
dd
uct
ion
, fle
xio
n, e
xten
sio
n,
div
isio
nSu
bsc
apu
lar
Tere
s m
ajo
rla
tera
l ro
tati
on
.C
5 to
C8
Axi
llary
D
elto
idW
eak
or
abse
nt
exte
nsi
on
of
fore
arm
at
elb
ow
.A
xilla
ry
Tere
s m
ino
rW
eak
or
abse
nt
exte
nsi
on
(d
ors
ifle
xio
n)
and
rad
ial a
bd
uct
ion
of
han
d a
t w
rist
.Th
ora
cod
ors
al
Lati
ssim
us
do
rsi
Un
able
to
su
pin
ate
and
ext
end
fin
ger
s at
MC
P.R
adia
l Tr
icep
sIn
abili
ty t
o d
ors
ifle
x th
e w
rist
an
d u
lnar
dev
iati
on
.R
adia
l A
nco
neu
sW
eak
or
abse
nt
exte
nsi
on
of
pro
xim
al a
nd
dis
tal p
hal
anx
of
thu
mb
.R
adia
l B
rach
iora
dia
lisD
imin
ish
ed s
ensa
tio
n o
ver
the
late
ral a
rm –
del
toid
pat
ch o
n u
pp
er a
rm, l
ater
al
Rad
ial
Exte
nso
r ca
rpi r
adia
lisfo
rear
m a
nd
firs
t 3
dig
its
Rad
ial
Sup
inat
or
Rad
ial
Exte
nso
r ca
rpi u
lnar
isR
adia
l Ex
ten
sor
dig
ito
rum
Rad
ial
Exte
nso
r d
igit
i min
imi
Rad
ial
Ab
du
cto
r p
olli
cis
lon
gu
s R
adia
l Ex
ten
sor
po
llici
s lo
ng
us
Rad
ial
Exte
nso
r p
olli
cis
bre
vis
Rad
ial
Exte
nso
r in
dic
is
Tab
le 7
.1U
pp
er e
xtre
mit
ies
(co
nt’
d)
Easy EMG98
Div
isio
n le
sio
nD
ivis
ion
sN
erve
sM
usc
les
Sig
ns
and
sym
pto
ms
An
teri
or
Mu
scu
locu
tan
eou
s C
ora
cob
rach
ialis
Wea
knes
s o
r ab
sen
t su
pin
atio
n o
f fo
rear
m a
nd
fle
xio
n o
f fo
rear
m a
t el
bo
w.
div
isio
n
Mu
scu
locu
tan
eou
s B
icep
sN
um
bn
ess/
tin
glin
g s
ensa
tio
n o
n t
he
vola
r su
rfac
e o
f th
e 1s
t to
3rd
an
d h
alf
of
the
C5
to T
1M
usc
ulo
cuta
neo
us
Bra
chia
lis4t
h fi
ng
ers.
Med
ian
Pr
on
ato
r te
res
Wea
k/ab
sen
t p
alm
ar a
bd
uct
ion
of
thu
mb
(p
erp
end
icu
lar
to p
lan
e o
f p
alm
).M
edia
n
Flex
or
carp
i rad
ialis
Wea
knes
s in
fle
xio
n o
f d
ista
l ph
alan
ges
of
fin
ger
s.
Med
ian
Pa
lmar
is lo
ng
us
Wea
k/ab
sen
t ab
du
ctio
n, f
lexi
on
an
d o
pp
osi
tio
n o
f lit
tle
fin
ger
to
war
ds
thu
mb
.M
edia
n
Flex
or
dig
ito
rum
In
abili
ty t
o a
dd
uct
ind
ex, r
ing
an
d li
ttle
fin
ger
s to
war
ds
mid
dle
fin
ger
.su
per
fici
alis
Dif
ficu
lty
of
abd
uct
ion
of
ind
ex, m
idd
le a
nd
rin
g fi
ng
ers
fro
m m
idd
le li
ne
of
mid
dle
M
edia
n a
nd
uln
ar
Flex
or
dig
ito
rum
fi
ng
er b
oth
rad
ial a
nd
uln
ar a
bd
uct
ion
.p
rofu
nd
us
Un
able
to
ad
du
ct t
he
thu
mb
in b
oth
uln
ar a
nd
pal
mar
dir
ecti
on
s.M
edia
nFl
exo
r p
olli
cis
lon
gu
sD
imin
ish
ed s
ensa
tio
n o
ver
the
late
ral f
ore
arm
, 3rd
, 4th
, an
d 5
th fi
ng
ers
Med
ian
Pro
nat
or
qu
adra
tus
Med
ian
A
bd
uct
or
po
llici
s b
revi
sM
edia
n
Op
po
nen
s p
olli
cis
Med
ian
Fl
exo
r p
olli
cis
bre
vis
Uln
ar
Flex
or
carp
i uln
aris
Uln
ar
Palm
aris
bre
vis
Uln
ar
Ab
du
cto
r d
igit
i min
imi
Uln
ar
Op
po
nen
s d
igit
i min
imi
Uln
ar
Flex
or
dig
iti m
inim
iU
lnar
Pa
lmar
inte
ross
eou
sU
lnar
D
ors
al in
tero
sseo
us
Uln
ar
Ad
du
cto
r p
olli
cis
Med
ian
an
d u
lnar
Lu
mb
rica
ls (
4)Pe
cto
ral
Pect
ora
lis m
ajo
rPe
cto
ral
Pect
ora
lis m
ino
r
Tab
le 7
.1U
pp
er e
xtre
mit
ies
(co
nt’
d)
7 How to Plan Out the Examination 99
Peri
ph
eral
ner
ve le
sio
nPe
rip
her
al n
erve
s R
oo
tsM
usc
les
Sig
ns
and
sym
pto
ms
Axi
llary
C
5, C
6,
Del
toid
Wea
knes
s in
sh
ou
lder
ran
ge
of
mo
tio
n a
nd
arm
ab
du
ctio
n, a
dd
uct
ion
, fle
xio
n,
C5,
C6
Tere
s m
ino
rex
ten
sio
n, l
ater
al r
ota
tio
n.
Dim
inis
hed
sen
sati
on
ove
r th
e la
tera
l arm
– d
elto
id p
atch
on
up
per
arm
Mu
scu
locu
tan
eou
s C
5, C
6, C
7C
ora
cob
rach
ialis
Wea
knes
s o
r ab
sen
t su
pin
atio
n o
f fo
rear
m a
nd
fle
xio
n o
f fo
rear
m a
t el
bo
w.
C5,
C6
Bic
eps
Dec
reas
ed s
enso
ry o
ver
the
late
ral f
ore
arm
C5,
C6
Bra
chia
lis
Rad
ial
C6,
C7,
C8
Tric
eps
Wea
k o
r ab
sen
t ex
ten
sio
n o
f fo
rear
m a
t el
bo
w.
C6,
C7,
C8
An
con
eus
Wea
k o
r ab
sen
t ex
ten
sio
n (
do
rsif
lexi
on
) an
d r
adia
l ab
du
ctio
n o
f h
and
at
wri
st.
C5,
C6
Bra
chio
rad
ialis
Un
able
to
su
pin
ate
and
ext
end
fin
ger
s at
MC
P.C
6, C
7Ex
ten
sor
carp
i rad
ialis
Inab
ility
to
do
rsif
lex
the
wri
st a
nd
uln
ar d
evia
tio
n.
C5,
C6
Sup
inat
or
Wea
k o
r ab
sen
t ex
ten
sio
n o
f p
roxi
mal
an
d d
ista
l ph
alan
x o
f th
um
b.
C7,
C8
Exte
nso
r ca
rpi u
lnar
isSe
nsa
tio
n is
dim
inis
hed
ove
r th
e w
eb s
pac
e b
etw
een
th
um
b a
nd
ind
ex fi
ng
erC
7, C
8Ex
ten
sor
dig
ito
rum
C7,
C8
Exte
nso
r d
igit
i min
imi
C7,
C8
Ab
du
cto
r p
olli
cis
lon
gu
sC
7, C
8Ex
ten
sor
po
llici
s lo
ng
us
C7,
C8
Exte
nso
r p
olli
cis
bre
vis
C7,
C8
Exte
nso
r in
dic
is
Med
ian
C
6, C
7Pr
on
ato
r te
res
Un
able
to
pro
nat
e th
e fo
rear
m a
nd
fle
x th
e h
and
at
wri
st.
C6,
C7
Flex
or
carp
i rad
ialis
Nu
mb
nes
s/ti
ng
ling
sen
sati
on
on
th
e vo
lar
surf
ace
of
the
1st
to 3
rd a
nd
hal
f o
f th
e C
7, C
8, T
1Pa
lmar
is lo
ng
us
4th
fin
ger
s.C
7, C
8, T
1Fl
exo
r d
igit
oru
m
Wea
k/ab
sen
t p
alm
ar a
bd
uct
ion
of
thu
mb
(p
erp
end
icu
lar
to p
lan
e o
f p
alm
).su
per
fici
alis
Un
able
to
do
th
e ‘O
K’ s
ign
. C
7, C
8, T
1Fl
exo
r d
igit
oru
m
Dec
reas
ed s
ensa
tio
n o
ver
the
dis
tal r
adia
l asp
ect
ind
ex fi
ng
erp
rofu
nd
us
C7,
C8,
T1
Flex
or
po
llici
s lo
ng
us
C7,
C8,
T1
Pro
nat
or
qu
adra
tus
C8,
T1
Ab
du
cto
r p
olli
cis
bre
vis
Tab
le 7
.1U
pp
er e
xtre
mit
ies
(co
nt’
d)
Easy EMG100
Peri
ph
eral
ner
ve le
sio
nPe
rip
her
al n
erve
s R
oo
tsM
usc
les
Sig
ns
and
sym
pto
ms
C8,
T1
Op
po
nen
s p
olli
cis
C8,
T1
Flex
or
po
llici
s b
revi
sC
8, T
1Lu
mb
rica
ls
Uln
ar n
erve
C8,
T1
Flex
or
carp
i uln
aris
Wea
k/ab
sen
t ab
du
ctio
n, f
lexi
on
an
d o
pp
osi
tio
n o
f lit
tle
fin
ger
to
war
ds
thu
mb
.C
8, T
1Fl
exo
r d
igit
oru
m
Inab
ility
to
ad
du
ct in
dex
, rin
g a
nd
litt
le fi
ng
ers
tow
ard
s m
idd
le fi
ng
er.
pro
fun
du
sD
iffi
cult
y o
f ab
du
ctio
n o
f in
dex
, mid
dle
an
d r
ing
fin
ger
s fr
om
mid
dle
lin
e o
f m
idd
le
C8,
T1
Palm
aris
bre
vis
fin
ger
bo
th r
adia
l an
d u
lnar
ab
du
ctio
n.
C8,
T1
Ab
du
cto
r d
igit
i min
imi
Un
able
to
ad
du
ct t
he
thu
mb
in b
oth
uln
ar a
nd
pal
mar
dir
ecti
on
s.C
8, T
1O
pp
on
ens
dig
iti m
inim
iD
ecre
ased
sen
sory
ove
r th
e 5t
h a
nd
hal
f o
f th
e 4t
h fi
ng
er o
n t
he
uln
ar s
ide
C8,
T1
Flex
or
dig
iti m
inim
iC
8, T
1Pa
lmar
inte
ross
eou
sC
8, T
1D
ors
al in
tero
sseo
us
C8,
T1
Ad
du
cto
r p
olli
cis
C8,
T1
Flex
or
po
llici
s b
revi
sC
8, T
1Lu
mb
rica
ls
Low
er e
xtre
mit
ies
Ro
ot
lesi
on
Ro
ots
Ner
ves
Mu
scle
sSi
gn
s an
d s
ymp
tom
s
L2Fe
mo
ral
Ilio
pso
asW
eakn
ess
in h
ip a
dd
uct
ion
an
d f
lexi
on
.Fe
mo
ral
Sart
ori
us
Wea
k o
r ab
sen
t th
igh
ad
du
ctio
n, f
lexi
on
, med
ial a
nd
late
ral r
ota
tio
n.
Fem
ora
l R
ectu
s fe
mo
ris
Wea
knes
s o
r in
abili
ty t
o e
xten
d t
he
leg
at
the
knee
.Fe
mo
ral
Vas
tus
late
ralis
Dim
inis
hed
sen
sati
on
ove
r th
e an
teri
or
and
med
ial a
spec
ts o
f th
e th
igh
an
d in
th
e Fe
mo
ral
Vas
tus
inte
rmed
ius
med
ial a
spec
t o
f th
e le
gFe
mo
ral
Vas
tus
med
ialis
Fem
ora
l Pe
ctin
eus
Ob
tura
tor
Ad
du
cto
r b
revi
sO
btu
rato
r A
dd
uct
or
lon
gu
sO
btu
rato
r G
raci
lisO
btu
rato
r A
dd
uct
or
mag
nu
s
Tab
le 7
.1U
pp
er e
xtre
mit
ies
(co
nt’
d)
7 How to Plan Out the Examination 101
Low
er e
xtre
mit
ies
Ro
ot
lesi
on
Ro
ots
Ner
ves
Mu
scle
sSi
gn
s an
d s
ymp
tom
s
L3Fe
mo
ral
Ilio
pso
asW
eakn
ess
in h
ip a
dd
uct
ion
an
d f
lexi
on
.Fe
mo
ral
Sart
ori
us
Wea
k o
r ab
sen
t th
igh
ad
du
ctio
n, f
lexi
on
, med
ial a
nd
late
ral r
ota
tio
n.
Fem
ora
l R
ectu
s fe
mo
ris
Wea
knes
s o
r in
abili
ty t
o e
xten
d t
he
leg
at
the
knee
.Fe
mo
ral
Vas
tus
late
ralis
Dim
inis
hed
sen
sati
on
ove
r th
e an
teri
or
and
med
ial a
spec
t o
f th
e th
igh
an
d k
nee
Fem
ora
l V
astu
s in
term
ediu
sFe
mo
ral
Vas
tus
med
ialis
Fem
ora
l Pe
ctin
eus
Ob
tura
tor
Ad
du
cto
r b
revi
sO
btu
rato
r A
dd
uct
or
lon
gu
sO
btu
rato
r G
raci
lisO
btu
rato
r A
dd
uct
or
mag
nu
s
L4Fe
mo
ral
Rec
tus
fem
ori
sW
eakn
ess
in h
ip a
dd
uct
ion
an
d a
bd
uct
ion
.Fe
mo
ral
Vas
tus
late
ralis
Wea
k o
r ab
sen
t th
igh
ad
du
ctio
n, a
bd
uct
ion
, fle
xio
n, m
edia
l an
d la
tera
l ro
tati
on
.Fe
mo
ral
Vas
tus
inte
rmed
ius
Wea
knes
s in
kn
ee f
lexi
on
, med
ial r
ota
tio
n a
nd
ext
ensi
on
. Fe
mo
ral
Vas
tus
med
ialis
Loss
of
do
rsif
lexi
on
(d
rop
fo
ot)
.O
btu
rato
r A
dd
uct
or
bre
vis
Lim
ited
inve
rsio
n o
f fo
ot.
Ob
tura
tor
Ad
du
cto
r lo
ng
us
Dim
inis
hed
sen
sati
on
ove
r th
e m
edia
l sid
e o
f th
e d
ista
l leg
an
d m
edia
l mal
leo
lus
Ob
tura
tor
Gra
cilis
area
Ob
tura
tor
Ad
du
cto
r m
agn
us
Sup
erio
r g
lute
al
Glu
teu
s m
ediu
sSu
per
ior
glu
teal
G
lute
us
min
imu
sSu
per
ior
glu
teal
Te
nso
r fa
scia
e la
tae
Dee
p p
ero
nea
l Ti
bia
lis a
nte
rio
rTi
bia
l Po
plit
eus
Tab
le 7
.1Lo
wer
ext
rem
itie
s (c
on
t’d
)
Easy EMG102
Low
er e
xtre
mit
ies
Ro
ot
lesi
on
Ro
ots
Ner
ves
Mu
scle
sSi
gn
s an
d s
ymp
tom
s
L5Su
per
ior
glu
teal
G
lute
us
med
ius
Wea
knes
s in
ad
du
ctio
n, a
bd
uct
ion
, fle
xio
n, e
xten
sio
n, m
edia
l an
d la
tera
l ro
tati
on
Su
per
ior
glu
teal
G
lute
us
min
imu
so
f th
igh
.Su
per
ior
glu
teal
Te
nso
r fa
scia
e la
tae
Wea
knes
s in
fle
xio
n a
nd
med
ial r
ota
tio
n o
f le
g.
Infe
rio
r g
lute
al
Glu
teu
s m
axim
us
Loss
of
do
rsif
lexi
on
(d
rop
fo
ot)
.Sc
iati
c Se
mit
end
ino
sus
Lim
ited
inve
rsio
n/e
vers
ion
of
foo
t.Sc
iati
c Se
mim
emb
ran
osu
sU
nab
le t
o e
xten
d a
ll to
es.
Scia
tic
Bic
eps
fem
ori
sW
eakn
ess
or
abse
nt
pla
nta
r fl
exio
n o
f th
e fo
ot/
toes
an
d f
lexi
on
of
the
knee
.D
eep
per
on
eal
Exte
nso
r d
igit
oru
m
Dim
inis
hed
sen
sati
on
ove
r th
e la
tera
l hal
f o
f th
e le
g a
nd
th
e d
ors
um
of
the
foo
t lo
ng
us
esp
ecia
lly t
he
big
to
e an
d t
he
seco
nd
to
eD
eep
per
on
eal
Tib
ialis
an
teri
or
Dee
p p
ero
nea
l Ex
ten
sor
hal
luci
s lo
ng
us
Dee
p p
ero
nea
l Pe
ron
eus
tert
ius
Dee
p p
ero
nea
l Ex
ten
sor
dig
ito
rum
bre
vis
Sup
erfi
cial
per
on
eal
Pero
neu
s lo
ng
us
Sup
erfi
cial
per
on
eal
Pero
neu
s b
revi
sTi
bia
l Po
plit
eus
Tib
ial
Tib
ialis
po
ster
ior
Tib
ial
Flex
or
hal
luci
s lo
ng
us
Tib
ial
Flex
or
dig
ito
rum
lon
gu
s
S1Su
per
ior
glu
teal
G
lute
us
med
ius
Wea
knes
s in
ad
du
ctio
n, a
bd
uct
ion
, fle
xio
n, e
xten
sio
n, m
edia
l an
d la
tera
l ro
tati
on
Su
per
ior
glu
teal
G
lute
us
min
imu
so
f th
igh
.Su
per
ior
glu
teal
Te
nso
r fa
scia
e la
tae
Wea
knes
s in
fle
xio
n a
nd
med
ial r
ota
tio
n o
f le
g.
Infe
rio
r g
lute
al
Glu
teu
s m
axim
us
Wea
knes
s o
r ab
sen
t p
lan
tar
flex
ion
of
the
foo
t/to
es a
nd
fle
xio
n o
f th
e kn
ee.
Scia
tic
Sem
iten
din
osu
sLo
ss o
f d
ors
ifle
xio
n (
dro
p f
oo
t).
Scia
tic
Sem
imem
bra
no
sus
Lim
ited
inve
rsio
n/e
vers
ion
of
foo
t.Sc
iati
c B
icep
s fe
mo
ris
Un
able
to
ext
end
all
toes
.D
eep
per
on
eal
Exte
nso
r d
igit
oru
m
Dim
inis
hed
sen
sati
on
ove
r th
e p
ost
erio
r, d
ista
l th
ird
of
the
leg
, lat
eral
hee
l, la
tera
l lo
ng
us
foo
t an
d li
ttle
to
e
Tab
le 7
.1Lo
wer
ext
rem
itie
s (c
on
t’d
)
7 How to Plan Out the Examination 103
Low
er e
xtre
mit
ies
Ro
ot
lesi
on
Ro
ots
Ner
ves
Mu
scle
sSi
gn
s an
d s
ymp
tom
s
Dee
p p
ero
nea
l Ex
ten
sor
hal
luci
s lo
ng
us
Dee
p p
ero
nea
l Pe
ron
eus
tert
ius
Dee
p p
ero
nea
l Ex
ten
sor
dig
ito
rum
bre
vis
Sup
erfi
cial
per
on
eal
Pero
neu
s lo
ng
us
Sup
erfi
cial
per
on
eal
Pero
neu
s b
revi
sTi
bia
l G
astr
ocn
emiu
sTi
bia
l Po
plit
eus
Tib
ial
Sole
us
Tib
ial
Tib
ialis
po
ster
ior
Tib
ial
Flex
or
hal
luci
s lo
ng
us
Tib
ial
Flex
or
dig
ito
rum
lon
gu
sTi
bia
l A
bd
uct
or
dig
iti m
inim
iTi
bia
l Q
uad
ratu
s p
lan
tae
Tib
ial
Flex
or
dig
iti m
inim
iTi
bia
l Lu
mb
rica
lsTi
bia
l A
dd
uct
or
hal
luci
sTi
bia
l A
bd
uct
or
hal
luci
sTi
bia
l Fl
exo
r d
igit
oru
m b
revi
sTi
bia
l Fl
exo
r h
allu
cis
bre
vis
S2In
feri
or
glu
teal
G
lute
us
max
imu
sW
eakn
ess
or
abse
nt
pla
nta
r fl
exio
n o
f th
e fo
ot/
toes
an
d f
lexi
on
of
the
knee
.Sc
iati
c Se
mit
end
ino
sus
Sen
sory
pro
ble
m o
ver
the
po
ster
ior
area
of
the
leg
Scia
tic
Sem
imem
bra
no
sus
Scia
tic
Bic
eps
fem
ori
sTi
bia
l G
astr
ocn
emiu
sTi
bia
l So
leu
sTi
bia
l Fl
exo
r h
allu
cis
lon
gu
sTi
bia
l Fl
exo
r d
igit
oru
m lo
ng
us
Tib
ial
Ab
du
cto
r d
igit
i min
imi
Tab
le 7
.1Lo
wer
ext
rem
itie
s (c
on
t’d
)
Easy EMG104
Low
er e
xtre
mit
ies
Ro
ot
lesi
on
Ro
ots
Ner
ves
Mu
scle
sSi
gn
s an
d s
ymp
tom
s
Tib
ial
Qu
adra
tus
pla
nta
eTi
bia
l Fl
exo
r d
igit
i min
imi
Tib
ial
Lum
bri
cals
Tib
ial
Do
rsal
inte
ross
eiTi
bia
l Pl
anta
r in
tero
ssei
Tib
ial
Ad
du
cto
r h
allu
cis
Tib
ial
Ab
du
cto
r h
allu
cis
Tib
ial
Flex
or
dig
ito
rum
bre
vis
Tib
ial
Flex
or
hal
luci
s b
revi
s
S3Ti
bia
l A
bd
uct
or
dig
iti m
inim
iW
eakn
ess
or
abse
nt
pla
nta
r fl
exio
n o
f th
e fo
ot/
toes
an
d f
lexi
on
of
the
knee
.Ti
bia
l D
ors
al in
tero
ssei
Dim
inis
hed
sen
sati
on
ove
r th
e p
eria
nal
are
aTi
bia
l Pl
anta
r in
tero
ssei
Tib
ial
Ad
du
cto
r h
allu
cis
Plex
us
lesi
on
Plex
us
Ner
ves
Mu
scle
sSi
gn
s an
d s
ymp
tom
s
Lum
bar
Ili
oh
ypo
gas
tric
Tr
ansv
ersu
s ab
do
min
isW
eakn
ess
in h
ip a
dd
uct
ion
an
d f
lexi
on
.p
lexu
sIli
oh
ypo
gas
tric
In
tern
al o
bliq
ue
mu
scle
sW
eak
or
abse
nt
thig
h a
dd
uct
ion
, fle
xio
n, m
edia
l an
d la
tera
l ro
tati
on
.T1
2, L
1 to
L4
Ilio
hyp
og
astr
ic
Exte
rnal
ob
liqu
e m
usc
les
Wea
knes
s o
r in
abili
ty t
o e
xten
d t
he
leg
at
the
knee
.Ili
oin
gu
inal
Tr
ansv
ersu
s ab
do
min
isD
imin
ish
ed s
ensa
tio
n o
ver
the
up
per
bu
tto
ck, s
cro
tum
or
lab
ium
, hyp
og
astr
ic
Ilio
ing
uin
al
Inte
rnal
ob
liqu
e m
usc
les
reg
ion
, an
teri
or,
med
ial a
nd
late
ral a
spec
t o
f th
e th
igh
, an
d t
he
med
ial a
spec
t o
f G
enit
ofe
mo
ral
Cre
mas
ter
the
leg
L1, L
2, L
3 Q
uad
ratu
s lu
mb
oru
mL1
, L2,
L3
Pso
as m
ino
rL1
, L2,
L3,
L4
Pso
as m
ajo
rFe
mo
ral
Ilio
pso
asFe
mo
ral
Sart
ori
us
Fem
ora
l R
ectu
s fe
mo
ris
Tab
le 7
.1Lo
wer
ext
rem
itie
s (c
on
t’d
)
7 How to Plan Out the Examination 105
Plex
us
lesi
on
Plex
us
Ner
ves
Mu
scle
sSi
gn
s an
d s
ymp
tom
s
Fem
ora
l V
astu
s la
tera
lisFe
mo
ral
Vas
tus
inte
rmed
ius
Fem
ora
l V
astu
s m
edia
lisFe
mo
ral
Pect
ineu
sO
btu
rato
r A
dd
uct
or
bre
vis
Ob
tura
tor
Ad
du
cto
r lo
ng
us
Ob
tura
tor
Gra
cilis
Ob
tura
tor
Ad
du
cto
r m
agn
us
Sacr
al p
lexu
s L4
, L5,
S1
Qu
adra
tus
fem
ori
sW
eakn
ess
in e
xten
sio
n, a
dd
uct
ion
, fle
xio
n a
nd
med
ial r
ota
tio
n o
f th
igh
.L4
to
S3
L4, L
5, S
1G
emel
lus
infe
rio
rW
eakn
ess
in f
lexi
on
an
d m
edia
l ro
tati
on
of
leg
.L5
, S1,
S2
Ob
tura
tor
inte
rnu
sW
eakn
ess
in a
nal
sp
hin
cter
.L5
, S1,
S2
Gem
ellu
s su
per
ior
Dim
inis
hed
sen
sati
on
ove
r th
e p
ost
erio
r th
igh
, lat
eral
hal
f o
f th
e le
g a
nd
th
e en
tire
S1
, S2
Piri
form
isfo
ot
Sup
erio
r g
lute
al
Glu
teu
s m
ediu
sSu
per
ior
glu
teal
G
lute
us
min
imu
sSu
per
ior
glu
teal
Te
nso
r fa
scia
e la
tae
Infe
rio
r g
lute
al
Glu
teu
s m
axim
us
Scia
tic
Ad
du
cto
r m
agn
us
Scia
tic
Sem
iten
din
osu
sSc
iati
c Se
mim
emb
ran
osu
sSc
iati
c B
icep
s fe
mo
ris
Peri
ph
eral
ner
ve le
sio
nPe
rip
her
al n
erve
s R
oo
tM
usc
les
Sig
ns
and
sym
pto
ms
Fem
ora
l L2
, L3
Ilio
pso
asW
eakn
ess
in h
ip a
dd
uct
ion
an
d f
lexi
on
.L2
, L3
Sart
ori
us
Wea
k o
r ab
sen
t th
igh
ad
du
ctio
n, f
lexi
on
an
d m
edia
l ro
tati
on
.L2
, L3,
L4
Rec
tus
fem
ori
sW
eakn
ess
or
inab
ility
to
ext
end
th
e le
g a
t th
e kn
ee.
L2, L
3, L
4V
astu
s la
tera
lisD
imin
ish
ed s
ensa
tio
n o
ver
the
ante
rio
r an
d m
edia
l asp
ect
of
the
thig
h a
nd
th
e L2
, L3,
L4
Vas
tus
inte
rmed
ius
med
ial a
spec
t o
f th
e le
g
Tab
le 7
.1Lo
wer
ext
rem
itie
s (c
on
t’d
)
Easy EMG106
Peri
ph
eral
ner
ve le
sio
nPe
rip
her
al n
erve
s R
oo
tM
usc
les
Sig
ns
and
sym
pto
ms
L2, L
3, L
4V
astu
s m
edia
lisL2
, L3
Pect
ineu
s
Ob
tura
tor
L2, L
3, L
4A
dd
uct
or
bre
vis
Wea
k o
r ab
sen
t th
igh
ad
du
ctio
n, f
lexi
on
, med
ial a
nd
late
ral r
ota
tio
n.
L2, L
3, L
4A
dd
uct
or
lon
gu
sD
imin
ish
ed s
ensa
tio
n o
ver
the
med
ial a
spec
t o
f th
e th
igh
L2, L
3, L
4G
raci
lisL2
, L3,
L4
Ad
du
cto
r m
agn
us
Sup
erio
r g
lute
al
L4, L
5, S
1G
lute
us
med
ius
Wea
knes
s in
ad
du
ctio
n, f
lexi
on
an
d m
edia
l ro
tati
on
of
thig
hL4
, L5,
S1
Glu
teu
s m
inim
us
L4, L
5, S
1Te
nso
r fa
scia
e la
tae
Infe
rio
r g
lute
al
L5, S
1, S
2G
lute
us
max
imu
sW
eakn
ess
in e
xten
sio
n, a
bd
uct
ion
an
d la
tera
l ro
tati
on
of
thig
h
Scia
tic
L5, S
1, S
2A
dd
uct
or
mag
nu
sW
eakn
ess
in e
xten
sio
n o
f th
e th
igh
.L5
, S1,
S2
Sem
iten
din
osu
sW
eakn
ess
in f
lexi
on
an
d m
edia
l ro
tati
on
of
leg
.L5
, S1,
S2
Sem
imem
bra
no
sus
Dim
inis
hed
sen
sati
on
ove
r th
e la
tera
l hal
f o
f th
e le
g a
nd
th
e en
tire
fo
ot
L5, S
1, S
2B
icep
s fe
mo
ris
– lo
ng
hea
dL5
, S1,
S2
Sho
rt h
ead
of
bic
eps
fem
ori
s
Dee
p p
ero
nea
l L5
, S1
Exte
nso
r d
igit
oru
m
Loss
of
do
rsif
lexi
on
(d
rop
fo
ot)
.lo
ng
us
Lim
ited
inve
rsio
n/e
vers
ion
of
foo
t.L4
, L5
Tib
ialis
an
teri
or
Un
able
to
ext
end
all
toes
.L5
, S1
Exte
nso
r h
allu
cis
lon
gu
sD
ecre
ased
sen
sati
on
ove
r th
e d
ors
um
of
the
foo
t es
pec
ially
th
e b
ig t
oe
and
th
e L5
, S1
Pero
neu
s te
rtiu
sse
con
d t
oe
L5, S
1Ex
ten
sor
dig
ito
rum
Sup
erfi
cial
per
on
eal
L5, S
1Pe
ron
eus
lon
gu
sW
eakn
ess
of
pla
nta
r fl
exio
n.
L5, S
1Pe
ron
eus
bre
vis
Lim
ited
eve
rsio
n o
f fo
ot.
Dim
inis
hed
sen
sati
on
ove
r th
e an
tero
late
ral p
art
of
the
leg
an
d t
he
do
rsu
m o
f th
e fo
ot
Tab
le 7
.1Lo
wer
ext
rem
itie
s (c
on
t’d
)
7 How to Plan Out the Examination 107
Peri
ph
eral
ner
ve le
sio
nPe
rip
her
al n
erve
s R
oo
tM
usc
les
Sig
ns
and
sym
pto
ms
Tib
ial
S1, S
2G
astr
ocn
emiu
sW
eakn
ess
or
abse
nt
pla
nta
r fl
exio
n o
f th
e fo
ot/
toes
an
d f
lexi
on
of
the
knee
.L4
, L5,
S1
Pop
liteu
sIn
abili
ty t
o in
vert
th
e fo
ot.
S1, S
2So
leu
sU
nab
le t
o c
up
so
le o
f fo
ot.
L5, S
1Ti
bia
lis p
ost
erio
rSe
nso
ry p
rob
lem
ove
r th
e p
ost
erio
r ar
ea o
f th
e le
gs.
L5
, S1,
S2
Flex
or
hal
luci
s lo
ng
us
L5, S
1, S
2Fl
exo
r d
igit
oru
m lo
ng
us
S1, S
2, S
3A
bd
uct
or
dig
iti m
inim
iS1
, S2
Qu
adra
tus
pla
nta
eS1
, S2
Flex
or
dig
iti m
inim
iS1
, S2
Lum
bri
cal
S2, S
3D
ors
al in
tero
ssei
S2, S
3Pl
anta
r in
tero
ssei
S1, S
2, S
3A
dd
uct
or
hal
luci
sS1
, S2
Ab
du
cto
r h
allu
cis
S1, S
2Fl
exo
r d
igit
oru
m b
revi
sS1
, S2
Flex
or
hal
luci
s b
revi
s
Tab
le 7
.1Lo
wer
ext
rem
itie
s (c
on
t’d
)
Easy EMG108
Muscle Nerves Roots
Common upper extremity – Cervical paraspinal C5 Rami C5– Cervical paraspinal C6 Rami C6– Cervical paraspinal C7 Rami C7– Cervical paraspinal C8 Rami C8– Cervical paraspinal T1 Rami T1– Deltoid Axillary C5–6– Biceps Musculocutaneous C5–6– Triceps Radial C6–7–8– Pronator teres Median C6–7– Abductor pollicis brevis Median C8–T1– 1st dorsal interosseous Ulnar C8–T1– Abductor digiti minimi Ulnar C8–T1
Common lower extremity– Lumbar paraspinal L3 Rami L3– Lumbar paraspinal L4 Rami L4– Lumbar paraspinal L5 Rami L5– Lumbar paraspinal S1 Rami S1– Gluteus maximus Inferior gluteal L5–S2– Biceps femoris (short head) Sciatic (peroneal) L5–S2– Med gastrocnemius anterior Tibial S1–2
tibialis Deep branch of peroneal L4–5– Rectus femoris Femoral L2–4– Biceps femoris (long head) Sciatic L5–S2– Peroneus longus Superficial branch of peroneal L5–S1
Other muscles frequently testedForearm– Flexor digitorum profundus Ulnar C8, T1
IV and V– Flexor pollicis longus Median (anterior interosseus) C7–8– Flexor digitorum superficialis Median C7–8– Flexor carpi radialis Median C6–7– Flexor carpi ulnaris Ulnar C7–T1– Extensor indicis Radial (posterior interosseus) C7–8– Extensor carpi ulnaris Radial (posterior interosseus) C7–8– Extensor carpi radialis Radial C6–7– Extensor digitorum communis Radial (posterior interosseus) C7–8– Brachioradialis Radial C5–6– Anconeus Radial C7–8– Pronator quadratus Median (anterior interosseus) C8, T1
Arm– Brachialis Musculocutaneous C5–6– Supinator Radial C5–6– Extensor pollicis longus Radial (posterior interosseus) C7–8– Abductor pollicis longus Radial (posterior interosseus) C7–8
Shoulder– Pectoralis major Pectoral C5–T1– Supraspinatus Suprascapular C5–6– Latissimus dorsi Thoracodorsal C6–8– Teres major Lower subscapular C5–6– Serratus anterior Long thoracic C5–7– Rhomboids Dorsal scapular C5– Levator scapulae Dorsal scapular C5– Infraspinatus Suprascapular C5–6– Trapezius Spinal accessory CN XI, C3–4
Table 7.2 EMG evaluation
7 How to Plan Out the Examination 109
Muscle Nerves Roots
Foot– Abductor hallucis Medial plantar S1–2– Abductor digiti quinti Lateral plantar S1–3
Leg– Tibialis posterior Tibial L5, S1– Soleus Tibial L5–S2
Thigh– Tensor fascia lata Femoral L4–5– Adductor longus Obturator L2–4– Vastus lateralis Femoral L2–4– Vastus medialis Femoral L2–4– Adductor magnus Obturator, sciatic L2–S1– Gracilis Obturator L2–4
Hip– Gluteus medius Superior gluteal L4–S1– Iliopsoas Femoral L2–3
Non-limb– Orbicularis oris Facial CN VII– Orbicularis oculi Facial CN VII– Diaphragm Phrenic C3–5– Anal sphincter Pudendal S2–4– Sternocleidomastoid Spinal accessory CN XI, C2–3
Table 7.2 EMG evaluation (cont’d)
8Pitfalls
Lyn Weiss, Jay Weiss, Rebecca Fishman
You’ve paid attention during EMG lectures and read about EMGs. You feel sufficientlyconfident to proceed with the study. However, you are not getting the response you wereanticipating. What went wrong? Before you start to doubt your abilities, review thepitfalls of EMG testing.
This chapter will emphasize the physiological and human sources of error that canbefall both the novice and the experienced electromyographer. These pitfalls arecommon and straight forward.
Pitfall 1: Not Performing a Good History and PhysicalExamination
You’ve heard it before and you’ll hear it again. Your history and physical examinationare the most important components of an accurate diagnosis – not the EMG. Forexample, a patient presents to you for electrodiagnostic testing with the diagnosis ofcarpal tunnel syndrome. On further questioning you discover the patient has neck painwith radiation to the hand and associated paresthesias. You suspect a cervicalradiculopathy and examine the patient. He has a positive Spurling’s test and upperextremity weakness with a decreased biceps deep tendon reflex. Although the originalconsultation requested an EMG for carpal tunnel syndrome, your history and physicalsuggests that you should also test for a possible cervical radiculopathy. This informationhelps to guide which nerves and muscles you will test during your EMG. Your historyand physical, as well as how you interpret your EMG findings, separate you as aphysician rather than simply a technician.
Pitfall 2: Technical Factors
Often people assume, when there is an abnormal or unexpected finding, that thisrepresents pathology. Much of the time however, unexpected findings are due to an errorby the electromyographer. The main reason for an unobtainable motor or sensory actionpotential (evoked response) is not stimulating the nerve and/or not recording from thenerve or muscle. This should be addressed methodically. Possible reasons for anunobtainable result are:
● Is a stimulus being delivered? Look for a visible muscle contraction. If there is nomuscle contraction:a. The stimulator is not working. Try turning down the intensity and stimulating
yourself to assess if you feel a shock.b. The location is incorrect. Relocate the stimulator. 111
!
!
orc. The stimulus may not be of a high enough intensity. This may be true especially if
there is an excess of adipose tissue. Try increasing the stimulus intensity orduration (pulse width).
● Is the preamplifier on?Most preamplifiers have a light indicating on/off. If the preamplifier is off, thepatient will feel the shock but no response will be recorded.
● Are the settings (gain and sweep) correct?Attempting to elicit a sensory nerve study at a motor setting will give a flat linebecause the gain on a motor setting will not be high enough.
● Are wires and electrodes properly connected?A sine wave usually indicates poor grounding or poor electrode contact.A large initial positive deflection indicates poor location of electrodes or evenreversal of electrodes.
Pitfall 3: Temperature
The temperature of the areas you are testing on your patient can affect the nerveconduction study. You should be aware that decreasing limb temperature could affectthe latency, amplitude, conduction velocity and duration of sensory nerve actionpotentials (SNAPs) and compound muscle action potentials (CMAPs) in the followingmanner:
● Latency prolonged (0.2 ms/degree centigrade)● Amplitude increased with cooling (sensory more than motor)● Conduction velocity decreased (1.8 to 2.4 m/s/degree centigrade)● Duration increased
You should also be aware that decreased temperature can affect the results of repetitivenerve studies and can cause normal test results in patients with neuromuscular junctiondisorders.
The limb being tested, ideally, should be continuously monitored for temperatureby a temperature probe placed on the limb. When performing nerve conductionstudies attempt to maintain the temperature of the upper limbs above 32°C and thelower limbs above 30°C. This can be achieved by warming the area to be tested. It isalways better to warm the limb rather than using correcting formulas, as describedabove (i.e., correct for a temperature of 30°C in the arms by decreasing the latency by0.4 msec). Tables 8.1 and 8.2 summarize the temperature corrections for nerveconduction studies.
Pitfall 4: Errors in Measurement
In general, the shorter the segment to be measured, the more likely an error inmeasurement will occur and the more dramatic change there will be in the calculatedconduction velocity. For example, a 0.5 cm error in measuring distance will significantlychange the conduction velocity if the measured distance is 5 cm (a 10% measurementerror). However, if the distance is 10 cm and there is a 0.5 cm error in measurement, thiswill result in a 5% error. You should try to use segments longer than 10 cm, as there isusually some error when measuring the length of the segment.
Easy EMG112
!
!
Another source of error in measurement is not measuring over the direct course ofthe nerve. It is impossible to exactly measure a nerve over the skin. However, measuringover the course of the nerve will minimize the error. This is especially true of the ulnarnerve across the elbow (Fig. 8.1). The ulnar nerve is slack when the elbow is extended,and taut when the elbow is bent. In order to measure the true length of the nerve, theelbow should be flexed to about 70–90 degrees both when the nerve is being stimulatedand when the nerve is being measured. Measuring the nerve in the extended elbowposition underestimates the true length. This will result in a calculated conductionvelocity that is erroneously slow. As all skin measurements are estimates of actual nervelength, the farther the measuring tape is from the actual nerve, the greater the potentialfor error. Therefore, measurements tend to be less accurate in obese patients.
8 Pitfalls 113
NCV corrected = factor × (measured skin temperature – 32°C) – NCV measured (m/sec)*
Measured Tibial Sural Peroneal Median Median Ulnar Ulnar temperature motor sensory motor motor sensory motor sensory
Factor for 1.1 1.7 2 1.5 1.4 2.1 1.6NCV change (m/sec/°C)
20°C –13.2 –20.4 –24 –18 –16.8 –25.2 –19.2
21°C –12.1 –18.7 –22 –16.5 –15.4 –23.1 –17.6
22°C –11 –17 –20 –15 –14 –21 –16
23°C –9.9 –15.3 –18 –13.5 –12.6 –18.9 –14.4
24°C –8.8 –13.6 –16 –12 –11.2 –16.8 –12.8
25°C –7.7 –11.9 –14 –10.5 –9.8 –14.7 –11.2
26°C –6.6 –10.2 –12 –9 –8.4 –12.6 –9.6
27°C –5.5 –8.5 –10 –7.5 –7 –10.5 –8
28°C –4.4 –6.8 –8 –6 –5.6 –8.4 –6.4
29°C –3.3 –5.1 –6 –4.5 –4.2 –6.3 –4.8
30°C –2.2 –3.4 –4 –3 –2.8 –4.2 –3.2
30.5°C –1.65 –2.55 –3 –2.25 –2.1 –3.15 –2.4
31°C –1.1 –1.7 –2 –1.5 –1.4 –2.1 –1.6
31.5°C –0.55 –0.85 –1 –0.75 –0.7 –1.05 –0.8
32°C 0 0 0 0 0 0 0
32.5°C 0.55 0.85 1 0.75 0.7 1.05 0.8
33°C 1.1 1.7 2 1.5 1.4 2.1 1.6
33.5°C 1.65 2.55 3 2.25 2.1 3.15 2.4
34°C 2.2 3.4 4 3 2.8 4.2 3.2
34.5°C 2.75 4.25 5 3.75 3.5 5.25 4
35°C 3.3 5.1 6 4.5 4.2 6.3 4.8
35.5°C 3.85 5.95 7 5.25 4.9 7.35 5.6
36°C 4.4 6.8 8 6 5.6 8.4 6.4
*Delisa J, Lee H, Baran E, Lai K, Spielholz N. Manual of Nerve Conduction Velocity andClinical Neurophysiology, 3rd Edn. New York: Raven Press, 1994, p. 17–19.
Table 8.1 Temperature correction for NCV study. Expected velocity deviation (m/sec)from 32°C
Easy EMG114
Median (or ulnar) motor or sensory NCV or distal latency corrected = –0.2 × (Tst – Tm) + obtained NCV or distal latency.*
Measured temperature –0.2 (Tst – Tm)†
20°C –2.6
21°C –2.4
22°C –2.2
23°C –2.0
24°C –1.8
25°C –1.6
26°C –1.4
27°C –1.2
28°C –1.0
29°C –0.8
30°C –0.6
31°C –0.4
32°C –0.2
33°C 0.0
34°C 0.2
35°C 0.4
36°C 0.6
*Delisa J, Lee H, Baran E, Lai K, Spielholz N. Manual of Nerve Conduction Velocity andClinical Neurophysiology, 3rd Edn. New York: Raven Press, 1994, p. 17–19.†Tst = 33°C for wrist. Tm is the measured skin temperature.
Table 8.2 Temperature correction for median and ulnar motor/sensory distal latency.Expected latency deviation from 33°C.
23
4 5 6 7 8 9 1
1 2 3 4 5 6 78
Figure 8.1 Inorder to measurethe true length ofthe ulnar nerve,the elbow shouldbe flexed toabout 70–90 degreesboth when thenerve is beingstimulated andwhen the nerve isbeing measured.
Pitfall 5: Anomalous Innervation
It is important to remember that human anatomy does not always follow the textbooksand that neurological anomalies exist. There are three anomalous innervations to beespecially aware of.
1. Martin–Gruber Anastomosis
This is a median to ulnar nerve anastomosis in the forearm (Fig. 8.2). Fibers from themedian nerve (usually the anterior interosseus nerve) cross the forearm and travel withthe ulnar nerve into the hand. They therefore do not have to traverse the carpal tunnel.This leads to three classic electrodiagnostic findings, which are more pronounced inpatients with carpal tunnel syndrome.
a. Positive Deflection of CMAP
The compound muscle action potential (CMAP) will have an initial positive (downward)deflection when stimulating the median nerve at the elbow and picking up over theabductor pollicis brevis (APB) muscle. The reason for this positive deflection is thatulnar fibers traveling with the median nerve stimulate the ulnar intrinsic hand muscles(specifically the adductor pollicis muscle). These fibers arrive at the adductor pollicismuscle before the median fibers arrive at the APB muscle, since they are not delayedacross the carpal tunnel as the median fibers are. Since the motor point of the adductormuscle is not over the recording electrode, a positive deflection will occur.
b. Increased Conduction Velocity or Negative Conduction Velocity
The median nerve is usually slowed somewhat as it traverses the carpal tunnel. (This iswhy the latency for the median nerve at the wrist is usually more than the ulnar nerve atthe wrist.) If a Martin–Gruber anastomosis exists, proximal stimulation will result in a‘normal’ latency because the fastest fibers (those upon which the latency is based) areactually ulnar fibers that do not have to travel through the carpal tunnel. The calculatedconduction velocity is therefore based on a proximal stimulation (which will be falsely
8 Pitfalls 115
Martin–Gruberanastomosis
Median nerve
Ulnar nerve
Figure 8.2Martin–Gruberanastomosis.
!
shortened by picking up over the ulnarly innervated adductor pollicis muscle) and thedistal stimulation (picking up over the median innervated APB muscle). With carpal tunnelsyndrome, the difference in these latencies will be exaggerated, and may actually lead to anegative conduction velocity (where the elbow latency is less than the wrist latency).
c. CMAP Amplitude Changes
With a Martin–Gruber anastomosis, the proximal CMAP amplitude will be larger thanthe distal amplitude (when stimulating the median nerve and picking up over the APB).This is because at the elbow, in addition to median fibers destined for the APB, ulnarfibers destined for the adductor pollicis muscle are stimulated. (These fibers will betraveling with the ulnar nerve because of the anastomosis). Since the adductor pollicismuscle is close to the APB, the two CMAPs summate to give the appearance of a largeramplitude CMAP with proximal stimulation. (Remember that this ‘larger amplitude’actually includes the response from the stimulated adductor muscle – an ulnarlyinnervated muscle that is not usually activated with pure median nerve stimulation.) Forthe same reason, this can also give larger amplitude on ulnar nerve studies whenstimulating the ulnar nerve at the wrist rather than at the elbow. The lost fibers in theelbow amplitude can be ‘found’ with median stimulation at the elbow.
2. Riche–Cannieu Anastomosis
This is a communication between the deep branch of the ulnar nerve and the recurrentbranch of the median nerve in the hand. With this anastomosis, the ulnar nerve mayinnervate the thenar muscles along with the median nerve.
If a patient with Riche–Cannieu anastomosis had a complete laceration of themedian nerve at the wrist; he or she may still retain thenar muscle function, as some ofthese muscles may be innervated by the ulnar nerve (via the anastomosis). On EMGevaluation, a median nerve injury at the wrist, which should result in fibrillationpotentials and positive sharp waves in median innervated hand muscles, may result in anormal study. Conversely, an ulnar nerve lesion at the elbow may result in spontaneousactivity in median innervated hand muscles.
3. Accessory Peroneal Nerve (Fig. 8.3)
The accessory deep peroneal nerve is a branch from the superficial peroneal nerve thattravels posterior to the lateral malleolus and can innervate the lateral portion of theextensor digitorum brevis (EDB) muscle. Therefore a patient may have a peroneal nerveinjury with loss of muscle function while still maintaining EDB function. This anomaly isusually picked up when the amplitude of the peroneal CMAP is larger on proximal (fibularhead) stimulation than on distal (ankle) stimulation. This results because fibers from theaccessory branch (posterior to the lateral malleolus) are not activated with anklestimulation but are activated with fibular head stimulation. Usually, stimulation posteriorto the lateral malleolus (with pickup over the extensor digitorum brevis) will produce awaveform that (in amplitude) along with the ankle stimulation summates to the amplitudeof the proximal (fibular head) stimulation (Fig. 8.4):
Accessory peroneal nerve amplitude (posterior to lateral malleolus) + ankle peroneal amplitude = fibular head amplitude
Pitfall 6: Stimulating Over Subcutaneous or Adipose Tissue
While performing NCS, you must be aware that placing the stimulator over areas ofincreased adipose or subcutaneous tissue can cause submaximal stimulation. This may
Easy EMG116
!
result in decreased amplitude of the CMAP. To correct this, press deeply with thestimulator until the desired results are obtained. You can also increase the pulse width.Care must be taken so as not to stimulate a different nerve located nearby.
Pitfall 7: Anatomy Error
Obviously, if you are stimulating or placing a needle in the incorrect nerve or muscle,your results will be inaccurate. To help identify the correct muscles have the patientactivate the muscle first and palpate for correct placement.
8 Pitfalls 117
Lateral malleolus Ankle
Fibular head
Popliteal fossa
Superficialperoneal nerve
Accessoryperoneal nerve
Deepperoneal nerve
orExtensorum brevisdigitor
Figure 8.3Accessoryperoneal nerve.
Figure 8.4Stimulationposterior to thelateral malleolus(with pickup overthe extensordigitorum brevis)will produce awaveform that (inamplitude) alongwith the anklestimulationsummates to theamplitude of theproximal (fibularhead)stimulation.
Fibular head
Popliteal fossa
Ankle
Lateral malleolus
!
Pitfall 8: Physiologic Factors
Human physiology presents various factors that can significantly affect NCS. Toprofessionally and appropriately conduct EMG examinations the relevant factors mustbe considered.
Age
Age affects electrodiagnostic studies in both the very young and the very old patient. Theeffect of age is most significant from birth to one year when myelination is incomplete. Inthe newborn, nerve conduction velocities are approximately 50% of adult values.1 By oneyear of age the velocities reach 75% and by 3–5 years myelination is complete andchildren’s values can be compared to adult normative data.
In adults, NCS values also change as people age. Typically, the older you get, theslower your nerves will conduct. Although these changes are fairly insignificant in themiddle-aged adult, they do become more pronounced in the older adult. For example, amedian motor conduction velocity of 46 meters/second in a 90-year-old patient would benormal even though generally the lower limit of normal is 50 meters/second.2 The usualcorrective factor is about one to two meters/second slowing per decade of life after age 60.3
In NCS, the amplitude of the SNAP and CMAP may also be affected by age. It isestimated that the SNAP amplitude may decrease by as much as 50% in a 70-year-oldpatient. This means that very low or even absent sensory nerve responses in the elderlyshould be interpreted with caution, as they may be normal given the patient’s advancedage. It is important to review the entire study, including the different technical factorsthat may affect the results, before arriving at a conclusion.
In the elderly, when dropout of motor units occurs due to normal aging, the bodycompensates with axonal sprouting leading to reinnervation. These reinnervated fibersare more likely to fire asynchronously. Therefore, during the EMG portion of the test, inthe older adult, the MUAP duration may increase with age. In childhood, the MUAPduration increases due to physiologic growth of the muscle fiber and motor unit size.
In summary, age affects NCS in babies with marked slowing of the velocities, due toincomplete myelination. In the elderly, NCS are slower with reduced amplitudes andEMG findings reveal increased duration of the MUAP.
Height
If you can remember that nerve conduction studies are normally faster in the arms thanin the legs, then the effect of height will make sense to you. Basically, the longer theextremity, the slower the nerves conduct. So, in the arms they conduct more quickly andin shorter people they conduct more quickly. This is probably due to the fact that there isdistal tapering of the nerve. The longer the limb, the more tapering and therefore, theslower the conduction velocity will be. Also, longer limbs are probably cooler and thistoo will slow the conduction velocity.
Weight
Weight is not a well-appreciated physiologic factor. However, in obese individuals, itmay be difficult to stimulate the nerve directly. Additional stimulus intensity or durationmay be required. This is due to the electrical stimulation having to pass throughadditional adipose tissue before reaching the nerve. During the EMG portion of the test,technical difficulties may arise when the needle is not long enough to be easily insertedinto the muscle.
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Pitfall 9: Non-physiologic Factors (Machine or EnvironmentallyRelated)
Noise
Noise is exactly what it says – noise. Noise is any electrical signal that is not the desiredbiological signal you are studying. When you have a lot of noise, it is difficult to hearwhat you need to hear (and to see what you need to see on the screen). Electrical noise ispresent to some degree in all electrodiagnostic labs. The most frequent form of noise is60 Hz interference, which is due to ubiquitous electrical appliances (e.g., lights,computers, fans and heaters). In order to minimize noise, check all of your equipment:
● Wires should be intact (not frayed or damaged). ● Electrodes, including the ground, should be securely attached.● The ground should be between the recording and stimulating electrodes.● The skin should be properly cleaned (usually with alcohol).● Electrode gel needs to be applied.● The closer the electrodes are to each other, the less likely there will be noise.● Unplug equipment (e.g., exam tables) that you are not using while performing the
study. ● Turning off fluorescent lights will cut down on the interference from unwanted
signals.
Many EMG machines have a 60-cycle notch filter that will filter out only electricalresponse firing at 60 Hz. This can be beneficial in eliminating 60 Hz interference. Onetheoretical downside is you can eliminate a potential whose frequency is 60 cycles, i.e. afib or positive sharp wave that is firing at 60 Hz.
In summary, there are a number of factors that may result in an abnormal finding.Before you decide that this is true pathology you must consider the possible pitfallsdiscussed in this chapter.
● Remember to do a thorough history and physical examination.● Know your anatomy.● Be aware of anomalous innervations and temperature changes.● Keep the limb appropriately warm● Measure correctly.● If abnormalities are encountered – check and recheck your stimulating electrodes,
wires and placement.
REFERENCES
1. Preston DC, Shapiro BE. Electromyography and Neuromuscular Disorders. Newton,Massachusetts: Butterworth-Heinemann, 1998, p. 86.
2. Preston DC, Shapiro BE. Electromyography and Neuromuscular Disorders. Newton,Massachusetts: Butterworth-Heinemann, 1998, p. 87.
3. Dumitru D. Electrodiagnostic Medicine. Philadelphia, PA: Hanley & Belfus, Inc.,1995, p. 39.
8 Pitfalls 119
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9Carpal Tunnel Syndrome
Lyn Weiss
Carpal tunnel syndrome (symptomatic median neuropathy at the wrist) is the mostcommon focal nerve entrapment, and a frequent reason for electrodiagnostic consultation.Electrodiagnostic testing is the only available method to assess the physiologic changesthat occur in carpal tunnel syndrome.
Clinical Presentation
Classic symptoms of carpal tunnel syndrome (CTS) include paresthesias and numbnessin the thumb, index and long fingers, and radial half of the ring finger (Fig. 9.1). Pain inthe hand may also be present, and radiation proximally is not uncommon. The symptomsare frequently more prominent at night. The patient may complain of an inability toperform fine motor tasks and/or weakness of the hand. Certain medical and/or physicalconditions predispose patients to CTS. These include diabetes, pregnancy, thyroiddisorders, repetitive strain, rheumatoid arthritis, gout, peripheral neuropathy, and edema.A good history is therefore important.
On physical examination, there may be a sensory deficit in the radial three and a halfdigits. Weakness of pinch strength may also be noted. In severe cases of carpal tunnelsyndrome, wasting of the thenar eminence may be present. Provocative tests mayreproduce the symptoms. These include Tinel’s test (percussion of the median nerve aboutthe wrist) and Phalen’s test (maximum flexion of the wrist, which is maintained for one totwo minutes). Since CTS can be confused with other disorders, a thorough physicalexamination is always important.
Anatomy
The carpal tunnel is a fixed space that includes nine tendons (four flexor digitorumsuperficialis tendons, four flexor digitorum profundus tendons, and the flexor pollicis
121
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Figure 9.1Median nervesensorydistribution (A),palmar (B).
A B
longus tendon), and the median nerve (Fig. 9.2). The carpal tunnel is bound dorsally bythe carpal bones and volarly by the transverse carpal ligament (flexor retinaculum).When the space in the tunnel becomes restricted, the median nerve can becomecompressed.
Electrodiagnostic Findings
In order to do a complete electrodiagnostic assessment of the median nerve, the affectedextremity must be compared to the unaffected side and to another nerve in the samehand, usually the ulnar nerve. Sensory and motor studies should be performed, as well asneedle testing. When performing nerve conduction studies, it is imperative that thedistance from the active electrode to the stimulation site be recorded. If a person has alarge hand, and the distance for the distal latency for motor nerve conduction studies isnot the standard 8 cm, an increased latency will have no real meaning (Fig. 9.3).
Sensory Nerve Conduction Studies
Sensory nerve action potentials (SNAPs) are usually the first potentials affected incarpal tunnel syndrome. A useful technique is to compare SNAPs recorded at mid palmand across the carpal tunnel. Usually, a distance of 7 cm from the ring electrode on thesecond digit to mid palm and then another 7 cm to the carpal tunnel (14 cm total) is used.However, since it is important to stimulate across the carpal tunnel, a larger distance canbe used and recorded. Although every lab has its own standards of normal, in general avelocity of less than 44 meters/second across the carpal tunnel indicates slowing.
Normal mid palm SNAPs confirm that the slowing is only across the carpal tunnel,although in moderate or severe cases, Wallerian degeneration may occur and affect thesedistal SNAPs as well. Median SNAPs may also be compared to ulnar SNAPs on thesame finger. A greater than 0.5 milliseconds difference between the two sensory latenciesindicates CTS. Decreased amplitude on the affected side could indicate either an axonallesion of the median nerve (not specific as to where along the course of the nerve) or aconduction block across the carpal tunnel (if proximal amplitude is less than 50% of
Easy EMG122
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Figure 9.2Anatomy of thecarpal tunnel.
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distal mid palm amplitude). An amplitude difference of more than 50% (as compared tothe median sensory amplitude on the non-affected side) is considered significant.
Motor Nerve Conduction Studies
The distal latency of the compound muscle action potential (CMAP) is an importantparameter in assessing for motor fiber involvement in CTS. As in sensory studies, thedistance from the active electrode to the stimulation site must be standardized. Manylaboratories use a distance of 8 cm. With this distance, a latency of more than 4.2 milliseconds usually indicates CTS. The ulnar nerve must also be assessed to ensurethat there is not a generalized motor neuropathy present. A median to ulnar distal latencydifference of more than 1 millisecond also indicates CTS, as with sensory conductionstudies. Decreased amplitude on the affected side could indicate either an axonal lesionof the median nerve (not specific as to where along the nerve) or a conduction blockacross the carpal tunnel.
Late Responses
Late responses (F-waves and H-reflexes) are generally not helpful in the evaluation ofCTS because they are non-specific and the area of greatest interest is not being assesseddirectly. The areas of interest are easily directly assessed by conventional motor andsensory studies.
EMG
EMG testing should be performed to provide evidence of axonal damage (fibrillationpotentials or positive sharp waves), and/or reinnervation. Testing should include theabductor pollicis brevis (APB) muscle. If spontaneous activity is present in this muscle,other muscles should be tested to ensure that the diagnosis is indeed CTS, as CTS cancoexist with other conditions. Specifically, a more proximal median muscle should betested to be sure there is not a median neuropathy elsewhere along the nerve’s course. Inaddition, a non-median innervated C8 muscle should be tested. Finally, especially ifthere is any indication of a neck problem, the cervical paraspinal muscles may be tested
9 Carpal Tunnel Syndrome 123
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Easy EMG124
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to rule out a cervical radiculopathy. If there is conduction block in the median nerve,recruitment may be decreased in the APB without evidence of spontaneous potentials.
Written Report
The written conclusion should include the following:
1. Whether or not carpal tunnel syndrome is present electrodiagnostically.2. The severity of the CTS (mild, moderate or severe).1 As a general guideline:
a. Mild – median sensory nerve conduction slowing and/or median sensoryamplitude decreased but more than 50% of reference value (no motorinvolvement).
b. Moderate – Median sensory and motor slowing, and/or SNAP amplitude lessthan 50% of the reference value.
c. Severe – Absence of median SNAP with motor slowing or median motorslowing with decreased median motor amplitude or CMAP abnormalities withevidence of axonal injury on needle testing of the thenar muscles.
3. Whether sensory and/or motor fibers are affected.4. If spontaneous activity is noted in the abductor pollicis brevis (fibrillation potentials
and/or positive sharp waves).
Summary
The classic electrodiagnostic findings in carpal tunnel syndrome may include:
1. slowing of median sensory nerve conduction velocity across the carpal tunnel2. prolonged distal latency of the median motor nerve3. low amplitude of the median SNAP4. low amplitude of the median CMAP5. spontaneous potentials (fibs and/or PSWs) in the abductor pollicis brevis muscle.
For a summary of NCS/EMG findings in median neuropathy, see Table 9.1.
REFERENCE
1. O’Young B, Young M, Stiens S. PM&R Secrets. Philadelphia, PA: Hanley & Belfus,Inc., 1997, p. 188.
9 Carpal Tunnel Syndrome 125
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10Ulnar Neuropathy
Lyn Weiss
Clinical Presentation
Ulnar neuropathy is the second most frequent entrapment neuropathy of the upperextremity (carpal tunnel syndrome being the most common). The ulnar nerve can becompressed at several locations along its course. Most commonly, compression occursin its superficial location at the elbow. Often this occurs when someone leans on his orher elbow (e.g., at a desk at work) or when the elbow is repetitively flexed and extended(e.g., carpenter or assembly worker). Scarring of the ulnar collateral ligament, arthritiswithin the ulnar groove, traction at a compression site or valgus overload in throwingathletes may all contribute to the injury. Patients typically report paresthesias, pain andnumbness in the little and ring fingers, which can worsen with elbow flexion. Pain maybe experienced throughout the arm (Fig. 10.1).
Ulnar neuropathy at the wrist is less common and occurs in a canal formed by thehamate and its hook and the pisiform. These are connected by an aponeurosis, whichforms the roof of Guyon’s canal. This canal contains the ulnar artery, vein and nerve.People who put a lot of pressure on their wrists, particularly in extension (e.g., cyclistsand cane users) are at risk for this injury.
On physical examination in patients with ulnar neuropathy at the elbow, the ulnarnerve may be palpable in the post-condylar groove, especially with elbow flexion. Theremay be a sensory deficit in the fifth digit and the ulnar half of the fourth digit. Anyaltered sensation should be distal to the wrist, as the medial antebrachial cutaneousnerve supplies sensation above the wrist. An important clinical clue as to whether anulnar lesion is at the elbow or the wrist is assessment of the dorsal ulnar cutaneousbranch of the ulnar nerve. This nerve usually branches before the wrist so it is spared inulnar nerve lesions at the wrist. This nerve provides sensation to the dorsal lateral aspectof the hand. With ulnar neuropathy at either the wrist or elbow, hand intrinsic muscleweakness may be evident, and in severe cases clawing of the fourth and fifth digits (withattempted hand opening) and atrophy of the intrinsic muscles (particularly the firstdorsal interosseous muscle) may be obvious (Fig. 10.2).
Wartenberg’s sign (abduction of the 4th and 5th digits) may occur, especially if thepatient is asked to put his or her hands in the pants’ pocket. Froment’s sign may also bepresent. This is seen when a patient is asked to grasp a piece of paper between the thumband radial side of the second digit. When the examiner tries to pull the paper out of thepatient’s hand, the patient will use the flexor pollicis longus muscle (innervated by the intactmedian nerve) to substitute for the adductor pollicis muscle (innervated by the affectedulnar nerve) (Fig. 10.3).
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On physical examination of ulnar neuropathy at the wrist there are three basic typesof lesions that can occur which affect the presentation significantly.
Type I affects the trunk of the ulnar nerve proximally in Guyon’s canal and typicallyinvolves both the motor and the sensory fibers. This means that clinically the patientpresents with numbness, pain, paresthesias and weakness in an ulnar distribution. There
Easy EMG128
A
B
Figure 10.1(A) Ulnar nerve:cutaneousdistribution. (B) Detail ofhand.
may be a notable sensory loss and the hand intrinsic muscles may show wasting in severecases.
In Type II only the deep motor branch is affected distally in Guyon’s canal. Sensationis typically spared and the abductor digiti quinti as well as the hypothenar muscles may ormay not be spared.
In Type III only the superficial branch of the ulnar nerve is affected. The superficialbranch provides sensation to the volar aspect of the fourth and fifth fingers and thehypothenar eminence. Strength is generally preserved throughout, as is sensation of thedorsal aspect of the hand.
Anatomy
Anatomy of the ulnar nerve renders it vulnerable to compression at two main locations –the elbow and the wrist (Fig. 10.4).
At the elbow (the most common site for ulnar nerve compression), the ulnar nerve isrelatively superficial. The nerve can be compromised by pressure (such as repetitiveleaning on the elbow), bony deformity (such as tardy ulnar palsy – ulnar neuropathyafter a distal humeral fracture with development of a cubital valgus deformity), chronicsubluxation, or in the cubital tunnel.
10 Ulnar Neuropathy 129
Figure 10.2Atrophy of theintrinsic muscles –particularly thefirst dorsalinterosseousmuscle.
Figure 10.3Froment’s sign.
Muscle atrophy
Abnormal Normal
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Cubital tunnel syndrome is compression of the ulnar nerve at or beneath theproximal edge of the flexor carpi ulnaris aponeurosis and the arcuate ligament (alsoreferred to as the humeroulnar arcade – HUA). With elbow flexion, the distance betweenthe olecranon process and the medial epicondyle decreases. Elbow flexion stretches andtightens the arcuate ligament, which can compress the ulnar nerve. The volume of thecubital tunnel is maximal in extension, and can decrease by 50% with elbow flexion.
The ulnar nerve is also vulnerable to compression at Guyon’s canal. This is a fibro-osseous compartment in the wrist where the ulnar nerve is bound by the transversecarpal ligament, the volar carpal ligament, the pisiform bone and the hook of thehamate. When compression occurs at Guyon’s canal, the superficial and the deepbranches of the ulnar nerve may be affected, but again, the dorsal ulnar cutaneous nervewould not be affected.
Electrodiagnostic Findings
Electrodiagnostic testing of the ulnar nerve can help to establish the existence of alesion, localize the injury, prognosticate, and exclude other conditions that may mimican ulnar neuropathy. In severe cases of ulnar neuropathy, when surgery is beingconsidered, electrodiagnostic testing can direct the surgeon to the area of entrapment.Moreover, C8 radiculopathy can present with symptoms similar to an ulnar neuropathy,and electrodiagnostic testing can help differentiate the two conditions.
While different causes of ulnar neuropathy at the elbow may benefit from differentsurgical procedures, electrodiagnostic studies cannot reliably and consistently differentiatebetween tardy ulnar palsy, retrocondylar compression and cubital tunnel entrapment.Nevertheless, these studies can be very helpful in distinguishing ulnar neuropathy at theelbow from other pathology.
Sensory Nerve Conduction Studies
Sensory nerve action potentials (SNAPs) can be affected in ulnar neuropathy since thelesion is distal to the dorsal root ganglion (see Chapter 12, Radiculopathy). This is incontrast to a C8 radiculopathy, where the lesion is proximal to the dorsal root ganglion
Easy EMG130
Flexor carpiulnaris
Flexor digitorumprofundis
Palmaris brevis3rd & 4th lumbricals
Adductor pollicis &flexor pollicis brevis(deep)
Palmar & dorssalinterossei
Figure 10.4Anatomy of theulnar nerve.
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and the SNAPs are not affected. If an ulnar lesion affects the sensory fibers, SNAPamplitudes will usually be reduced. A side-to-side difference of more than 50% issignificant for sensory axonal loss. It should be noted that a Type II lesion at the wrist, asdescribed above, would affect the ulnar nerve, but spare the sensory fibers.
In an ulnar neuropathy, it is important to test not only the SNAP to the 5th digit, butalso the dorsal ulnar cutaneous nerve. This sensory branch of the ulnar nerve is given off5–10 cm proximal to the wrist and supplies sensation to the dorsum of the 5th and ulnarside of the 4th digit. A lesion distal to the branching of the dorsal ulnar cutaneous nerve(e.g., at the wrist) should yield a normal dorsal ulnar cutaneous response, but anabnormal ulnar sensory response to the 5th digit. By contrast, an ulnar neuropathy at theelbow would affect both the dorsal ulnar cutaneous response and the ulnar sensoryresponse to the 5th digit.
Motor Nerve Conduction Studies
Slowing of latency and/or conduction velocity can indicate a demyelinating process inthe ulnar nerve. In general, a prolonged distal latency of the compound muscle actionpotential (CMAP) indicates slowing of the ulnar nerve across the wrist, provided thereare no other indications of a generalized condition (i.e., the median distal motor latencyis normal and conduction throughout the rest of the ulnar nerve is normal). Slowing ofthe ulnar nerve across the elbow is quite common. Slowing of proximal conductionvelocity of more than 10 meters/second is considered significant (compared to the distalconduction velocity on the same side).
Assessment of amplitude can be tricky, especially if a conduction block is present.Low CMAP amplitude throughout the nerve indicates an axonal lesion. However, anamplitude drop when stimulating over a portion of a nerve indicates a conduction block.(Provided there is no anomalous innervation, and ample stimulation is applied directlyover the nerve.) A drop in amplitude from the distal to the proximal site of more than20–30% usually indicates either a conduction block or a Martin–Gruber anastomosis.Evaluating the median nerve CMAP morphology can check for the presence of aMartin–Gruber anastomosis (see Chapter 8, Pitfalls).
When performing nerve conduction studies of the ulnar nerve, position andmeasurement across the elbow is very important. The elbow should be held in a flexedposition of 70–90 degrees. The main reasons for this are:
1. The ulnar nerve is redundant in the extended position. Therefore, measurement inextension does not measure the nerve’s true anatomical length. The conductionvelocity will be falsely slowed since the distance will be under-estimated and thenumerator will be decreased in the equation for velocity:
velocity = distance / time
2. Maintaining the elbow in a flexed position is more likely to reproduce the symptomsof ulnar entrapment at the elbow, if it exists.
If an ulnar neuropathy is expected from the patient’s clinical presentation, but theCMAPs are normal, consider using the first dorsal interosseus (FDI) muscle for the activeelectrode instead of the abductor digiti quinti. In some patients, the FDI is more affected,and therefore more likely to yield a positive result.
Inching is a useful technique for localizing entrapment along the course of a nerve(Fig. 10.5). It is particularly useful in ulnar neuropathy across the elbow when surgery isbeing considered, as it localizes entrapment more precisely than conventional studies.
10 Ulnar Neuropathy 131
With the elbow flexed, segments of 1 cm are marked on the patient’s skin both proximaland distal to the elbow. The ulnar nerve is then stimulated at 1 cm intervals, and theresulting CMAPs compared. An increase in latency of ≥ 0.4 milliseconds/cm is indicativeof focal slowing. A substantial amplitude drop from one segment to a more proximalsegment indicates a conduction block across that area. One must interpret these resultswith caution, as the margin of error is high with a small distance. Therefore, an amplitudechange is much more significant than a latency change.
When performing nerve conduction studies across the elbow, a distance of at least10 cm should be used in order to decrease the margin of error.
Late Responses
Late responses (F-waves and H-reflexes) are generally not helpful in the evaluation of anulnar neuropathy, because they are non-specific.
EMG
EMG testing in cases of ulnar neuropathy can be difficult to interpret because of themuscles innervated by the ulnar nerve and their location. The abductor digiti minimi(ADM) (sometimes referred to as the abductor digiti quinti – ADQ) and the first dorsalinterosseous (FDI) are the most commonly tested ulnar innervated hand muscles. If thereis an axonotmetic lesion, these are more likely to be positive than the forearm muscles. Theflexor carpi ulnaris (FCU) and FDP IV/V are the only ulnar proximal muscles to the wrist.However, in ulnar nerve lesions at the elbow, the FCP and FDP muscles are usuallyspared. This may be due to:
1. the FCU and FDP receiving their innervation proximal to the medical epicondyle or 2. the fibers to the FCU being situated more medially and therefore are more protected.
Consequently, if the needle examination of the FCU and FDP is negative, an ulnar nervelesion proximal to the wrist cannot be ruled out. For this reason, frequently theconduction studies are the most important tests in localizing an ulnar lesion.
If an axonal lesion is present anywhere along the course of the nerve, spontaneousactivity (fibrillation potentials and positive sharp waves) may be present in musclesdistal to the lesion.
Easy EMG132
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10 Ulnar Neuropathy 133
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trap
men
t at
wri
st
arm
(re
tro
con
dyl
ar
(cu
bit
al t
un
nel
(G
uyo
n’s
can
al)*
g
roo
ve)
syn
dro
me)
Fore
arm
Flex
or
carp
i uln
aris
Uln
ar✓
✓Fl
exo
r d
igit
oru
m p
rofu
nd
us
(to
dig
its
4 an
d 5
)U
lnar
✓✓
Palm
aris
bre
vis
Uln
ar✓
✓H
and
Ab
du
cto
r d
igit
i min
imi
Uln
ar✓
✓✓
Op
po
nen
s d
igit
i min
imi
Uln
ar✓
✓✓
Flex
or
dig
iti m
inim
iU
lnar
✓✓
✓Pa
lmar
inte
ross
eou
sU
lnar
✓✓
✓D
ors
al in
tero
sseo
us
(th
e fi
rst
on
e)U
lnar
✓✓
✓A
dd
uct
or
po
llici
s U
lnar
✓✓
✓Lu
mb
rica
ls (
two
med
ial o
nes
)U
lnar
✓✓
✓
Clin
ical
sig
nPa
rest
hes
ia, p
ain
, or
nu
mb
nes
s fr
om
4th
an
d 5
th d
igit
s an
d
Up
to
th
e el
bo
w,
Up
to
(o
r sl
igh
tly
Vo
lar
asp
ect
on
ly o
f h
ypo
then
ar e
min
ence
exac
erb
ated
by
dis
tal t
o)
the
elb
ow
, d
igit
s 4
and
5p
rolo
ng
ed e
lbo
w
exac
erb
ated
by
flex
ion
pro
lon
ged
elb
ow
fle
xio
nLo
ss o
f se
nsa
tio
n o
ver
the
uln
ar d
ors
al s
urf
ace
of
the
han
dY
esY
esN
oC
law
han
dM
ay o
ccu
rM
ay o
ccu
rM
ay o
ccu
rW
eakn
ess
of
the
flex
or
carp
i uln
aris
an
d f
lexo
r d
igit
oru
m
Yes
Var
iab
leN
op
rofu
nd
us
(dig
its
4 an
d 5
)W
eakn
ess
of
firs
t d
ors
al in
tero
sseo
us
mu
scle
: Fro
men
t’s
sig
nM
ay o
ccu
r M
ay o
ccu
rM
ay o
ccu
r
*In
or
abo
ut
Gu
yon
’s c
anal
th
e u
lnar
ner
ve d
ivid
es in
to a
su
per
fici
al a
nd
dee
p b
ran
ch. T
he
sup
erfi
cial
bra
nch
of
the
uln
ar n
erve
inn
erva
tes
the
pal
mar
is b
revi
sm
usc
le. T
he
dee
p b
ran
ch o
f th
e u
lnar
ner
ve t
rave
ls b
etw
een
th
e ab
du
cto
r d
igit
i min
imi a
nd
fle
xor
dig
iti m
inim
i mu
scle
s.
Tab
le 1
0.1
Uln
arly
inn
erva
ted
mu
scle
s an
d e
lect
rom
yog
rap
hy
for
the
foca
l uln
ar n
erve
inju
ry
Summary
In summary, the classic electrodiagnostic findings in ulnar neuropathy at the elbow mayinclude:1. slowing of the ulnar motor nerve conduction velocity across the elbow2. decreased amplitude of the ulnar motor CMAP with stimulation above the elbow
(conduction block)3. decreased amplitude of the ulnar SNAP4. spontaneous potentials (fibs and PSWs) in ulnarly innervated muscles5. decreased amplitude of the dorsal ulnar cutaneous SNAP.
See Table 10.1 for a summary of electrodiagnostic findings in ulnar neuropathy.
Easy EMG134
!
11Radial Neuropathy
Julie Silver
Clinical Presentation
As with any nerve, the radial nerve is at risk for injury in a number of locations and from anumber of factors, including trauma such as a humeral fracture or compression due to anextrinsic force. The most common sites of injury are at the spiral groove (honeymooner’spalsy or Saturday night palsy) and in the forearm where the nerve penetrates the supinatormuscle. Less common sites include the axilla (due to crutches), elbow (in radiusdislocation injuries) and the wrist (due to handcuffs). The recurrent epicondylar branchmay be associated with tennis elbow. If only the posterior interosseous nerve is affected,patients will complain of weakness without sensory symptoms. Injury to the antebrachialcutaneous nerve or the superficial radial sensory nerve (e.g., from lacerations at the wristor even a watchband that is too tight) can cause numbness and paresthesias in a radialdistribution (Fig. 11.1). There may or may not be associated pain. When pain is present, itcan mimic or be associated with tenosynovitis (e.g., De Quervain’s syndrome) of thethumb.
The physical examination is consistent with sensory and strength deficits that are inthe distribution of the radial nerve or one of its branches. It is important to know theanatomy of the radial nerve in order to perform a competent physical examination. Usuallythe most obvious physical deficit is wrist drop.
Anatomy
The radial nerve branches from the posterior cord of the brachial plexus (Fig. 11.2) andin the proximal arm gives off the following sensory branches:
1. posterior cutaneous nerve of the arm 2. lower lateral cutaneous nerve of the arm and 3. posterior cutaneous nerve of the forearm.
Also in the proximal arm, the radial nerve supplies motor branches to the triceps andanconeus. The radial nerve then wraps around the humerus in the spiral groove (oneof the most common sites of injury) and supplies motor branches to thebrachioradialis, the long head of the extensor carpi radialis and the supinator. Justdistal to the lateral epicondyle, the radial nerve splits into the posterior interosseousnerve (motor) and the superficial radial sensory nerve (sensory). The superficialradial sensory nerve supplies the lateral dorsum of the hand. The posteriorinterosseous nerve enters the supinator muscle under the arcade of Frohse (anothercommon site of compression) and supplies motor nerves to the wrist, thumb andfinger extensors. 135
!
!
Easy EMG136
A
B
Figure 11.1Radial nerve –cutaneousdistribution.
Radial nerve injuries can be classified into injuries:
● around the axilla ● associated with the spiral groove ● of the posterior interosseous nerve or ● of the superficial radial sensory nerves.
It may also help to remember that the radial nerve is responsible for the so-called Saturdaynight palsy which is classically compression of the radial nerve when someone whoperhaps is very fatigued or intoxicated lies with the arm draped over the back of a chairor some other fixed object.
Electrodiagnostic Findings
Sensory Nerve Conduction Studies
If the superficial radial sensory nerve is affected, in demyelinating lesions there will be aprolonged distal latency if the lesion is distal to the site of stimulation. In axonal lesionsthere will be reduced amplitude of the sensory nerve action potential (SNAP) regardlessof the location of the lesion (as long as it is distal to the dorsal root ganglion). In caseswhere the SNAP is normal but the patient clinically has a radial sensory deficit, this maybe because: the study was done too early (it takes 4–7 days for Wallerian degeneration tooccur); the lesion may be proximal to the dorsal root ganglion (i.e., root level); or thelesion may be proximal to the site of stimulation.
11 Radial Neuropathy 137
Triceps
Triceps &anconeus
Brachioradialis
Posterior cutaneous of arm
Posterior cutaneous of forearm
Extensor carpiradialis brevis
Extensordigitorum
Extensordigiti quinti
Extensorcarpi ulnaris
Extensor carpiradialis longus
Abductor pollicislongus
Extensor pollicislongus
Extensor pollicisbrevis
Extensor digital nerves
Extensorindicis
Posteriorinterosseous
Supinator
Lower lateral cutaneous
Figure 11.2 Branches of the radial nerve.
!
Easy EMG138
Loca
tio
nM
usc
les
inn
erva
ted
by
rad
ial
Ner
veM
usc
les
sho
win
g
Mu
scle
s sh
ow
ing
M
usc
les
sho
win
g
ner
ve f
rom
pro
xim
al t
o d
ista
l n
euro
gen
ic c
han
ge
neu
rog
enic
ch
ang
e in
n
euro
gen
ic c
han
ge
in
up
per
ext
rem
ity
in t
he
cru
tch
pal
sy
the
Sat
urd
ay n
igh
tp
ost
erio
r in
tero
sseo
us
(po
ster
ior
cord
inju
ry)
pal
sy (
spir
al g
roo
ve
ner
ve s
ynd
rom
ein
jury
)
Sho
uld
er(D
elto
id)*
(Axi
llary
)*✓
Tric
eps
Rad
ial
✓
Arm
An
con
eus
Rad
ial
✓✓
Fore
arm
Bra
chio
rad
ialis
Rad
ial
✓✓
Exte
nso
r ca
rpi r
adia
lisR
adia
l✓
✓Su
pin
ato
rPI
N†
✓✓
✓Ex
ten
sor
carp
i uln
aris
PI
N†
✓✓
✓Ex
ten
sor
dig
ito
rum
co
mm
un
isPI
N†
✓✓
✓Ex
ten
sor
dig
iti m
inim
iPI
N†
✓✓
✓A
bd
uct
or
po
llici
s lo
ng
us
PIN
†✓
✓✓
Exte
nso
r p
olli
cis
lon
gu
sPI
N†
✓✓
✓Ex
ten
sor
po
llici
s b
revi
sPI
N†
✓✓
✓Ex
ten
sor
ind
icis
PIN
†✓
✓✓
Clin
ical
sig
ns
Dec
reas
ed d
ista
l rad
ial s
ensa
tio
nY
esY
esN
oW
eakn
ess
of
abd
uct
ion
of
sho
uld
erY
esN
oN
oW
eakn
ess
of
exte
nsi
on
of
sho
uld
erY
esN
oN
oW
eakn
ess
of
exte
nsi
on
of
elb
ow
Yes
Yes
No
Wea
knes
s o
f ex
ten
sio
n o
f w
rist
Yes
Yes
Dep
end
s o
n t
he
loca
tio
n o
f le
sio
nW
eakn
ess
of
exte
nsi
on
of
MC
PY
esY
esY
esW
eakn
ess
of
DIP
/PIP
ext
ensi
on
Yes
Yes
Yes
Wea
knes
s o
f su
pin
atio
n o
f fo
rear
mY
esY
esD
epen
ds
on
th
e lo
cati
on
of
lesi
on
*Del
toid
wh
ile n
ot
rad
ially
inn
erva
ted
, is
inn
erva
ted
by
the
axill
ary
ner
ve, w
hic
h a
rise
s fr
om
th
e p
ost
erio
r co
rd w
ith
th
e ra
dia
l ner
ve.
† Post
erio
r in
tero
sseo
us
ner
ve is
a m
oto
r b
ran
ch o
f ra
dia
l ner
ve.
Tab
le 1
1.1
Rad
ial n
erve
inn
erva
ted
mu
scle
s an
d e
lect
rod
iag
no
sis
for
the
foca
l rad
ial n
erve
inju
ry
Motor Nerve Conduction Studies
Radial motor studies can be very helpful in diagnosing radial nerve injuries. In axonalinjuries, there is a reduction in the compound muscle action potential (CMAP)amplitude after 4–7 days. This can be compared to the contralateral (unaffected) side.Radial conduction velocities may appear to be abnormally fast (e.g., more than 75 meters/second), but the value of doing this study is to look for a focal conduction block ordecreased amplitude. In primarily demyelinating lesions at the spiral groove, the CMAPsrecorded at the elbow, forearm and below can be normal. However, stimulation proximalto the spiral groove may reveal marked temporal dispersion or a decrease of amplitudeor area (evidence of conduction block).
Late Responses
Late responses are non-specific and not typically done in suspected radial neuropathy.
EMG
The EMG will typically be abnormal in motor axonal radial nerve lesions. It maydemonstrate the usual findings in any neuropathy (spontaneous activity, large motor unitaction potentials (MUAPs) with long duration, possibly polyphasic in chronic cases,etc.). Since the extensor indicis muscle is the most distal muscle innervated by the radialnerve, it is often tested first. The crux of the EMG study in a radial neuropathy is tolocate the lesion by knowing the anatomy.
Table 11.1 is a summary of NCS/EMG findings in radial neuropathy. A muscleinnervated by C7, but not by the radial nerve (such as the pronator teres or flexor carpiradialis muscle), should be tested. Such muscles would be normal in a radial nerveinjury, but may be abnormal in a C7 radiculopathy. If the radial nerve injury is in theaxilla, the triceps muscle may be abnormal, but the deltoid muscle (innervated by theaxillary nerve) should be normal. It should also be noted that in patients with a supinatorsyndrome, the supinator muscle itself would be normal. This is because the radial nerveinnervation to the supinator muscle occurs proximally. The radial nerve is compressed inthe supinator muscle after the supinator has received its innervation.
Summary
In summary, electrodiagnostic findings in radial neuropathy may include (depending onthe location of the lesion):
1. decreased amplitude of the radial SNAP2. decreased amplitude of radial CMAP3. slowing of radial motor conduction velocity across the affected segment4. a drop in radial CMAP amplitude across the affected segment (conduction block)5. spontaneous potentials (fibs and PSWs in radially innervated muscles distal to lesion)6. if the posterior interosseous nerve (a motor branch) is affected, the radial CMAP
may be abnormal, but the radial SNAP should be normal (this may be seen in thesupinator syndrome).
7. if the superficial radial sensory nerve (a pure sensory nerve) is affected, the radialSNAP may be abnormal, but the radial CMAP should be normal.
11 Radial Neuropathy 139
!
12Radiculopathy
Lyn Weiss, Nancy Fung
Radiculopathy is a lesion of a specific nerve root and is generally caused by rootcompression. It is second only to carpal tunnel syndrome (CTS), as the reason for referralfor electrodiagnostic study. The diagnosis of radiculopathy is based on a patient’s history,physical examination, and electrodiagnostic study. Imaging studies are also helpful. Thediagnosis of radiculopathy is contingent upon motor and sensory symptoms and/orfindings in a distribution consistent with a nerve root. In certain clear-cut clinical pictures,electrodiagnosis may not be necessary.
Often however, in the case of a radiculopathy or possible radiculopathy, electro-diagnostic studies are quite helpful in making or confirming the diagnosis, as well as indetermining the prognosis. Whereas an MRI may be helpful in anatomically localizing alesion it is basically only a snapshot in time. On the other hand, although an EMG doesnot reveal the anatomy in the same way that imaging studies do, it provides physiologicalinformation about what is actually occurring to the nerves and muscles. Therefore, bothimaging studies (usually an MRI) and electrodiagnostic studies are extremely helpful inconfirming the diagnosis of a radiculopathy.
Clinical Presentation
Patients with radiculopathy will frequently complain of neck pain radiating to the arm(cervical radiculopathy) or back pain radiating to the leg (lumbosacral radiculopathy).There may also be numbness or tingling in the distribution of a sensory nerve root, referredto as a dermatomal distribution (see Fig. 18.2). Thoracic radiculopathies, while rare, wouldradiate pain and/or numbness in the distribution of the nerve root. In addition, if the motorfibers are affected, there will be weakness of muscles innervated by that nerve root, referredto as a myotomal distribution (Tables 12.2 and 12.3). For example, a patient with a right L5radiculopathy may complain of back pain radiating to the right leg, numbness along thelateral aspect of the right leg into the dorsum of the foot, and foot slap with walking.
On physical examination, the patient described above may have normal reflexes,decreased sensation on the lateral aspect of the right leg and dorsum of the right foot,and weakness of the ankle dorsiflexors. It is important to remember that not all patientsexperience the same symptoms. In addition, dermatomal and myotomal distributionsmay vary amongst individuals. It is possible for a radiculopathy to affect predominantlysensory fibers, motor fibers, or both. Physical findings that may suggest a radiculopathyinclude the following:
● decreased reflexes in muscles innervated by that nerve root● weakness in muscles innervated by that nerve root● sensory symptoms in a dermatomal distribution. 141
!
The physical examination has several limitations that may make electromyography anecessary adjunct in the diagnosis of radiculopathy. A mild weakness can be easily missedon manual muscle testing. If the patient is stronger than the examiner, subtle weaknessin the upper extremities may not be apparent. The examination is not quantitative anda loss of 10 pounds of biceps strength, for example, may be imperceptible. Lowerextremity muscles such as the quadriceps can exert forces greater than the total bodyweight and only severe weakness will be apparent. In many cases of clinically missedweakness, electromyography will be positive. For instance a 10% loss of motor axonsmay reveal no perceptible weakness on physical examination. However, EMG testing islikely to be sensitive enough to detect the abnormality.
Anatomy
Electrodiagnostic evaluation of a radiculopathy requires a thorough knowledge of theanatomy of the spine. There are 31 pairs of spinal nerves attached to the spinal cord byventral and dorsal roots. The spinal nerve is a mixed sensory and motor nerve that isformed by the fusion of ventral and dorsal roots in the intervertebral foramina (seeFig. 1.1).
● The ventral roots are axons with cell bodies in the anterior horn cells in the ventralgray matter of the spinal cord. These roots are from motor neurons whose axonsterminate in a neuromuscular junction.
● The dorsal roots are axons with cell bodies in the dorsal root ganglia in the vertebralforamina, outside the spinal cord. These are sensory axons.
The cell body of sensory fibers is outside the spinal cord, as opposed to motor fibers wherethe cell body is within the spinal cord. In a radiculopathy there is usually continuitybetween the sensory cell body and the digits, as the lesion is proximal to the dorsal rootganglia. Although sensation may be altered, electrodiagnostically the sensory nerveaction potential (SNAP) will not be affected (see Fig. 1.1).
All the muscles that are innervated by a single ventral root define a myotome. Adermatome is the sensory distribution of a single nerve root. Except for the rhomboidmuscle, which is predominantly innervated by the C5 root, almost every muscle isinnervated by multiple roots and is therefore part of multiple myotomes. It should be
Easy EMG142
EMG diagnosis: Mildly Moderately suggestive Strongly suggestive/suggestive definitive
Muscles with Early change in Early change in . Acute denervation neurogenic paraspinals or paraspinals and two or and/or chronic change one root more same root change in two
innervated innervated muscles muscles from two muscle without without motor/sensory different peripheral motor/sensory NCS change nerves but same NCS change Acute denervation myotome as well as
and/or chronic paraspinal change on involvementparaspinals and any one spinal root innervated muscle
Table 12.1 Levels of confidence in diagnosis of cervical or lumbosacral radiculopathy
!
kept in mind when performing a physical examination that dermatomes (the skin areainnervated by a single dorsal root) also overlap.
Electrodiagnostic Medicine Evaluation
Sensory Nerve Conduction Studies
Pain, numbness, and tingling are common complaints in patients with radiculopathy.However, in the majority of radicular processes, the SNAP should be normal, both inamplitude and latency. Latency is contingent on the speed of the fastest fibers. Amplitudeis contingent on the number of fibers firing. Damage to the myelin sheath of an axon wouldgenerally cause slowing or conduction block. This would be apparent on nerve studies ifthe lesion were between the area of stimulation and the pickup electrodes.
In radiculopathy, any demyelination is proximal to the area being stimulated andtherefore conduction block or slowing will not be seen. Basically this means that sensoryNCS are always normal unless there is alternate or coexisting pathology, e.g., carpaltunnel syndrome. When there is axonal damage and the distal parts of the axon are nolonger contiguous with the cell body, the axon will die back, a process known asWallerian degeneration. In a radiculopathy any damage to the dorsal (sensory) fibers isgenerally proximal to the dorsal root ganglion. Therefore as the axon is still in contactwith its cell body, no sensory denervation will occur. Even in severe lesions that wouldresult in anesthesia, normal sensory studies can be seen. If SNAP abnormalities arefound, it is important to rule out other lesions such as a brachial plexopathy, anentrapment neuropathy or a peripheral neuropathy.
Motor Nerve Conduction Studies
Compound muscle action potential (CMAP) amplitudes reflect the actual number ofmotor fibers activated upon stimulation. The latency is a function of the speed of the fastestfibers. In general, both the sensory and motor NCS will be normal in an isolated case ofradiculopathy. However, in a severe radicular lesion (which is distal to the anterior horncell) axonal loss can result in Wallerian degeneration distal to the lesion. Therefore the
12 Radiculopathy 143
Motor H
35 mA
CathodeAnode
GroundG1G2
30 mA25 mA22 mA18 mA15 mA12 mA8 mA5 mA
Figure 12.1Assessment for S1radiculopathy byperforming an H-reflex.
!
CMAP amplitude might be reduced. On the other hand, if it is a focal demyelinatinglesion, the amplitude will be normal.
Nonetheless even with a lesion that causes axonal degeneration, the CMAP amplitudecould still be normal. This is because the muscles have input from multiple nerve rootsand motor units. The radicular lesion may impinge on nerve fibers that do not innervatethe muscle being tested, or fibers from other nerve roots may contribute moresignificantly and therefore the amplitude will not be significantly affected. For example,if the C8 nerve root is affected, the amplitude of a CMAP recorded from the abductorpollicis brevis (APB) muscle is usually not affected. In addition to receiving fibers fromC8, the APB receives innervation from T1 and is probably more heavily innnervated byT1 than C8. Since the lesion is proximal to the area being stimulated, no slowing orconduction block should be present on motor nerve studies.
From these discussions, it should be apparent that motor and sensory studies are oflimited use in radiculopathies. When abnormalities occur they are likely to be of motornerve (CMAP) amplitude. Increased distal latencies and slowing or conduction block ordecreased SNAP amplitude would not suggest radiculopathy but would suggest analternate diagnosis. In fact, the main value of nerve conduction studies in testing forradiculopathy is to rule out other diagnoses such as a peripheral or entrapment neuropathy.
Late Responses
The H-reflex is a monosynaptic or oligosynaptic spinal reflex involving both motor andsensory fibers. It electrically tests some of the same fibers as are tested in the ankle jerkreflexes. In fact it is rare to be unable to obtain an H-reflex in the presence of an ankle jerkreflex. If this occurs, technical factors should be considered. In theory it is a sensitivemeasure in assessing radiculopathy because: it helps to assess proximal lesions, it becomesabnormal relatively early in the development of radiculopathy, and it incorporates sensoryfiber function proximal to the dorsal root ganglion. The H-reflex primarily assessesafferent and efferent S1 fibers. Clinically, L5 and S1 radiculopathies may appear similaron EMG due to the overlap of myotomes. The H-reflex’s primary value is indistinguishing S1 from L5 radiculopathies.
When assessing for S1 radiculopathy, the H-reflex latency is recorded from thegastrocnemius-soleus muscle group upon stimulating the tibial nerve in the poplitealfossa (Fig. 12.1). The H-reflex is elicited with a submaximal stimulation with the cathodeproximal to the anode. As the stimulation is gradually increased from peak H-amplitude,we generally see a diminishment of the H-amplitude with a concurrent increase in the M-wave amplitude. With supramaximal stimulation, the H-reflex is usually absent.
The H-reflex can also be used in C6/C7 radiculopathy by recording over the flexorcarpi radialis muscle and stimulating the median nerve at the elbow. The median H-reflexis less commonly performed and clinically is less likely to be helpful for radiculopathythan a lower extremity H-reflex. Generally, gastrocnemius-soleus H-reflex latency side-to-side differences of greater than 1.5 ms are suggestive of S1 radiculopathy.
Although the H-reflex is sensitive, it has certain limitations. First, patients with anS1 radiculopathy can have a normal H-reflex. Second, an abnormal H-reflex is onlysuggestive, but not definitive for radiculopathy because the abnormality may originate inother components of the long pathway involved, such as the peripheral nerves, plexuses,or spinal cord. Third, once the H-reflex becomes abnormal, it usually does not returnto normal, even over time. Finally, the H-reflex is often absent in otherwise normalindividuals over the age of 60 years. The reflexes therefore can be considered a sensitive,but not specific indicator of pathology. Latency of the H-reflex is dependent on the age
Easy EMG144
and leg length of the patient (see Table 4.1). A side-to-side amplitude difference of 60%or more may also indicate pathology.
F-waves are low amplitude late responses thought to be due to antidromic activationof motor neurons (anterior horn cells) following peripheral nerve stimulation, whichthen cause orthodromic impulses to pass back along the involved motor axons. Someelectromyographers have called this a ‘backfiring’ of axons. It is called the F-wavebecause it was first noted in intrinsic foot muscles. The F-wave has small amplitude, avariable configuration, and a variable latency. Generally F-wave amplitudes are on theorder of 1% of the orthodromically generated motor response (M-response). The mostwidely used parameter is the latency of the shortest reproducible response. The F-wave can be found in many muscles of the upper and lower extremities. UnfortunatelyF-waves have not turned out to be as sensitive a test as initially hoped. The reasons forthis are:
1. the pathways involve only the motor fibers 2. as with the H-reflex, it involves a long neuronal pathway so that if there is a focal
lesion it might be obscured 3. if an abnormality is present, the F-wave will not pinpoint the exact cause because
any lesion, from the anterior horn cell to the muscle being tested, can affect the F-wave similarly
4. since muscles have multiple root innervations, the shortest latency may reflect thehealthy fibers in the non-affected root and
5. the latency and amplitude of an F-wave is variable so that multiple stimulationsmust be performed to find the shortest latency.
If not enough stimulations are done (usually more than 10), the shortest latency may notbe apparent. Thus, use of F-waves in evaluating for radiculopathy are extremely limited andshould not be the basis upon which a diagnosis is made. See Table 4.2 for a comparison ofH-reflex and F-waves.
EMG
EMG still is the most useful procedure in localizing radiculopathy and predictingprognosis. In cases of radiculopathy causing axonal damage, Wallerian degeneration willoccur. Muscle fibers supplied by these axons will begin to fire spontaneously. Thisspontaneous activity in the form of fibrillation potentials and positive sharp waves initiallyoccurs proximally, and extends distally with time. These potentials have a characteristicappearance and sound.
The presence of spontaneous activity is the most objective evidence of acutedenervation. Lesser lesions can cause increased insertional activity although the subjectivenature in determining these lowers the confidence level in diagnosis. In reinnervation andwith sprouting of collateral axons, motor unit abnormalities such as long durationpolyphasic motor units may be present. The diagnosis of radiculopathy should not bemade based solely on polyphasicity. Much of the work on polyphasicity was based onstudies with concentric electrodes that record from a smaller area than monopolarelectrodes and are less likely to see polyphasic potentials.
Recruitment abnormalities, if seen, would be typical of a neuropathic recruitmentincluding few motor units firing at a high rate (higher than 20 Hz) as described inChapter 5.
Spontaneous activity as seen by EMG begins in the proximal paraspinal muscles,within 5–7 days of compression. Most limb muscles show spontaneous activity within
12 Radiculopathy 145
3 weeks, but 5–6 weeks may be required in the distal portions of the limb.1 Similarly,reinnervation occurs proximally first, with paraspinal muscle reinnervation thought tooccur after 6–9 weeks, followed by the proximal muscles at 2–5 months, and the distalmuscles at 3–7 months.2 One should keep in mind that EMG in general will be able toassess only axonal injury to motor fibers.
The selection of muscles to be tested is of critical importance. The needle examinationshould be sufficiently detailed to distinguish between lesions at the root, plexus, andperipheral nerve level. The muscles noted to be weak on examination, or muscles withabnormal reflexes, should be examined in order to maximize the yield of the study. In fact,the physical examination serves as the foundation upon which the electrodiagnosticstudy is performed. Without an adequate history and physical exam, the yield of theelectrodiagnostic studies is significantly lowered. There is not enough time and it wouldbe unkind to your patient to attempt to examine every possible muscle. Therefore thestudy needs to be tailored to fit the specific clinical circumstances.
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Root Muscle group Clinical signlevel
C5 Rhomboid (dorsal scapular nerve) 1. Positive neck distraction/Supraspinatus/infraspinatus compression test(suprascapular nerve) 2. Decreased/absent biceps tendon Deltoid/teres minor (axillary nerve) reflex Biceps brachii/brachialis 3. Decreased/absent sensation to (musculocutaneous nerve) the lateral arm (axillary nerve)
4. Weakness of shoulder abduction
C6 Extensor carpi radialis longus and 1. Decreased/absent brachioradialis brevis (radial nerve) reflexPronator teres/flexor carpi radialis 2. Decreased/absent sensation to (median nerve) the lateral forearm Deltoid/teres minor (axillary nerve) (musculocutaneous nerve)
3. Weakness of wrist extension
C7 Triceps/extensor digitorum 1. Decreased/absent triceps reflexcommunis/extensor indicis proprius 2. Decreased/absent sensation to digiti minimi (radial nerve) the middle fingerFlexor carpi radialis (median nerve) 3. Weakness of wrist flexionFlexor carpi ulnaris (ulnar nerve)
C8 Flexor carpi ulnaris (ulnar nerve) 1. Decreased/absent sensation to Flexor pollicis longus/flexor the ring and little fingers of the digitorum superficialis (median hand and to the distal half of the nerve) forearm’s ulnar side (ulnar nerve)Flexor digitorum profundus (median 2. Weakness of finger flexionor ulnar nerve) 3. Intrinsic weakness and atrophyExtensor indicis proprius/extensor pollicis brevis (radial nerve)First dorsal interosseous (ulnar nerve)
T1 Abductor pollicis brevis (median 1. Decreased/absent sensation nerve) to medial side of the upper half of Abductor digiti minimi/dorsal the forearm and the arm (medial interosseous (ulnar nerve) brachial cutaneous nerve)
2. Weakness of finger abduction/adduction
Table 12.2 Clinical picture – cervical radiculopathy3,4
In order to have a definitive diagnosis of radiculopathy, a paraspinal muscle and twomuscles from different peripheral nerves innervated by the same root should havepositive findings. If only some (but not all) of the criteria are met, the diagnosis ofradiculopathy is only suggestive (see Table 12.2). It is also important to note that if thepatient only has sensory involvement, the NCS/EMG test may be completely normal.Remember that the SNAP will not be affected, and the EMG only assesses motor fibers.In these cases the EMG may be performed to rule out other causes for the patient’ssymptoms. The report should specify that while the study is normal, radiculopathycannot be ruled out, and it may be appropriate to refer for other diagnostic tests.
12 Radiculopathy 147
Root level Muscles Clinical sign
L2, 3,4* Iliacus/vastus medialis (femoral nerve) L2, 3 Pain in the thighAdductor longus/gracilis (obturator nerve) Weakness in hip L2, 3,4 flexion, adduction
(L4) Vastus lateralis, rectus femorus Decreased/absent Tibialis anterior (deep peroneal nerve) patellar reflex**L4–L5 Pain in the medial side Vastus medialis and lateralis (L2–4) of the leg
Knee extension weakness
L5 Gluteus medius/tensor fasciae latae Pain & paresthesias in (superior gluteal nerve L4–S2, posterior) lateral aspect of leg and Flexor hallucis longus/flexor digitorum dorsum of footlongus/lateral gastrocnemius/tibialis Ankle dorsiflexor posterior (tibial nerve, L5–S2)/tibialis weaknessanteriorExtensor hallucis longus/extensor digitorumlongus (deep peroneal nerve, L5)
S1*** Medial gastrocnemius/soleus/ flexor Decreased/absent ankle hallucis brevis (tibial nerve, L5–S2) reflexPeroneus longus and brevis (superficial Pain & paresthesias to peroneal nerve, L5, S1)/tensor fascia the lateral border of lata/gluteus maximus (superior/inferior the foot gluteal nerve L4–S1/ L5–S2) Weakness of foot Extensor hallucis longus, extensor plantar flexion and toe digitorum (deep peroneal nerve, extensionL4, L5, S1)
*Lesions of L2, L3, and L4 are best considered collectively because they have suchextensive myotomal overlap. Consequently, it is frequently impossible to distinguishisolated lesions involving one of them. It can be difficult to diagnose an L2 or an L3radiculopathy: The L2–L3 myotomes have limited limb representation. All the musclesinnervated by the L2–L3 myotomes are located proximally in the lower extremity andthey are reinnervated sooner than muscles located more distally. There is no reliablesensory NCS available for evaluating the L2–L4 fibers. In L4 radiculopathies similarchanges may be found in the tibialis anterior muscle, but their absence never excludes alesion of that root.**The patellar reflex is a deep tendon reflex, mediated through nerves emanating fromthe L2, L3, and L4 nerve roots, but predominantly from L4. For clinical application, thepatellar reflex is considered an L4 reflex; however, even if the L4 nerve root is totallycut, the reflex can still be present in significantly diminished form.***H-reflex may confirm diagnosis and distinguish S1 from L5 radiculopathy.
Table 12.3 Clinical picture – lumbosacral radiculopathy3,4
Summary
In summary, electrodiagnostic findings in radiculopathy may include:
1. normal SNAP amplitudes2. normal CMAP (predominantly)3. spontaneous potentials (fibs and PSWs) in the paraspinal muscles and two muscles
from different peripheral nerves innervated by the same affected root level.
See Tables 12.2 and 12.3 for a summary of clinical findings in radiculopathy.
REFERENCES
1. Dumitru D, Zwarts MJ. Radiculopathies. In Dumitru D, Amato AA, Zwarts M, eds.Electrodiagnostic Medicine, 2nd Edn. Philadelphia: Hanley & Belfus, 2002, pp. 713–776.
2. Johnson EW. Electrodiagnosis of Radiculopathy. In Johnson EW, ed. PracticalElectromyography, 2nd Edn. Baltimore: Williams and Wilkins, 1988, pp. 229–245.
3. Wilbourn AJ. AAEM mimimonograph #32: The electrodiagnostic examination inpatients with radiculopathies. Muscle & Nerve 1998; 21: 1612–1631.
4. Dumitru D. In Dumitru D, Amato AA, Zwarts M, eds. Electrodiagnostic Medicine,2nd Edn. Philadelphia: Hanley & Belfus, 2002, pp. 523–584.
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13Spinal Stenosis
Lyn Weiss
Clinical presentation
Spinal stenosis can be defined as narrowing or restriction of the vertebral canal, and canaffect any spinal level. The spinal cord, cauda equina, and/or nerve root structures maybe involved.
Patients with spinal stenosis usually complain of back or neck pain with radiation toone or both extremities. Patients with lumbar stenosis usually complain of a dull ache inthe hip and thigh region. The pain is typically relieved with sitting, which tends to flexthe spine and therefore increases the diameter of the spinal canal. This is referred to asneurogenic claudication. (In true vascular claudication, the patient only has to stop andrest to relieve the symptoms, not necessarily sit down.)
Anatomy
The lumbar spinal canal usually has an anteroposterior diameter of about 15 mm or more.Any decrease in the diameter of the canal beyond 12 mm is considered significant forspinal stenosis. The condition may be due to congenital or acquired factors. These factorscan include spondylolisthesis, enlargement of the soft tissues in and around the canal,hypertrophy of the facet joints, intervertebral disc herniation, or ligamentum flavumhypertrophy or laxity.
Electrodiagnostic findings
Although electrodiagnostic testing in spinal stenosis may be non-specific, testing ishelpful to rule out other causes for the patient’s symptoms, including radiculopathy,peripheral neuropathy or entrapment neuropathy. It is important to note that electro-diagnostic studies are not typically done as a means of diagnosing spinal stenosis. Thisdiagnosis is usually made with information from the history, physical examination andimaging studies.
Sensory Nerve Conduction Studies
Sensory nerve conduction studies and amplitudes should be normal in spinal stenosis.This is due to the fact that the sensory (dorsal) root ganglion is located outside the spinalcanal and therefore usually not affected in spinal stenosis. In summary, similar toradiculopathies, sensory and motor NCS are typically normal with the exception of severeaxonal loss, in which case you may see decreased amplitude of the CMAP.
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Motor Nerve Conduction Studies
Motor nerve studies should demonstrate normal distal latencies, as the distal aspect ofthe nerve is not affected. Velocities and amplitudes are usually unaffected, unless thedisease has progressed to the point that there is significant axonal damage and motoraxon collateral sprouting cannot keep pace with axonal damage. In such cases, you maysee decreased amplitude of the CMAP on nerve conduction studies.
Late Responses
H-reflexes may be prolonged or absent bilaterally if the S1 nerve root is affected by thespinal stenosis. F-waves are generally not helpful in the evaluation of spinal stenosis asthey are non-specific.
EMG
If neural compression is significant, you may see multilevel bilateral abnormalities,including fibrillations and positive sharp waves (in acute neural compression), and largeamplitude, polyphasic, increased duration motor unit action potentials (in chronic neuralcompression). It is important to test multiple bilateral paraspinal levels as well as multiplemyotomal levels in both extremities.
Summary
The classic electrodiagnostic findings in spinal stenosis may include:
1. Normal SNAP amplitudes and conduction velocities2. Normal CMAP latency, amplitude and conduction velocities3. EMG findings of bilateral multilevel nerve root involvement.
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14Peroneal Neuropathy
Julie Silver
Clinical Presentation
Peroneal neuropathy is the most common mononeuropathy in the legs and occurs due tocompression, entrapment, ischemia or direct trauma. The most likely site of compressionis at the fibular neck (or head), where the nerve is very superficial (Fig. 14.1). The patienttypically presents with foot drop that is usually acute but may be gradual. There may be ahistory of recent falls or trips as well. Paresthesias and numbness in the lower lateral legand dorsum of the foot may be present. Pain is typically absent.
A thorough history can help determine the cause of the symptoms (e.g., a plaster castthat was too tight, a habit of crossing the legs, a brace that doesn’t fit well, occupationalsquatting such as in a carpenter, etc.). Peroneal neuropathy can easily be confused withlumbar radiculopathy (usually L5), sciatic neuropathy or lumbosacral plexopathy.Electrodiagnostic studies can be crucial to determining the location and extent of damage.
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Common peronealnerve
Superficial peronealnerve
Deep peronealnerve
Figure 14.1Peroneal nerve.
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In peroneal neuropathy, both the deep and superficial peroneal nerves are usuallyaffected. In cases where only one branch is affected, deep peroneal neuropathy is morecommon than superficial peroneal neuropathy. The physical examination will varydepending on the affected nerve(s) (Fig. 14.2). Since the deep peroneal nerve providessensation to the first dorsal web space, assessment of sensory deficits in this region canhelp localize the lesion. Strength deficits are usually most notable in ankle dorsiflexion andgreat toe extension. There may be a foot slap or steppage gait when the patient ambulates.Reflexes are typically normal. Tinel’s sign may be present over the fibular neck.
Anatomy
The common peroneal nerve arises from the L4–S1 nerve roots that travel through thelumbosacral plexus and then through the sciatic nerve. Within the sciatic nerve, thefibers that eventually form the common peroneal nerve run separately from those thatdistally become the tibial nerve (separation of these nerves usually occurs at the level ofthe popliteal fossa). The common peroneal nerve branches, giving rise to the lateralcutaneous nerve of the knee and then winds around the fibular neck and passes throughthe ‘fibular tunnel’ between the peroneus longus muscle and the fibula. It then dividesinto superficial and deep branches. The superficial peroneal nerve innervates theperoneus longus and brevis and terminates in sensory branches that supply the lateralaspect of the lower leg and the dorsum of the foot and toes. In 15–25% of people, thesuperficial peroneal nerve also gives rise to the accessory peroneal nerve. This providesan anomalous innervation of the extensor digitorum brevis (see Chapter 8, Pitfalls).
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Common peronealnerve
Superficial peronealnerve
Deep peronealnerve (first web space)
Figure 14.2Sensorydistribution ofperoneal nerve.
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The deep peroneal nerve (also called the anterior tibial nerve) supplies the tibialisanterior, extensor digitorum longus, extensor hallucis longus, peroneus tertius andextensor digitorum brevis. The terminal sensory branches supply the skin over the firstweb space.
The peroneal division of the sciatic nerve innervates the short head of the bicepsfemoris. This is important electrodiagnostically as it is the only muscle proximal to theknee that is innervated by the peroneal nerve. In peroneal neuropathy at the fibular neck,the short head of the biceps femoris muscle should not be affected.
Electrodiagnostic Findings
Sensory Nerve Conduction Studies
The superficial sensory peroneal nerve study is not significantly more technicallydemanding than the sural sensory study; however, it is often not done. Nevertheless,when there is a question of a peroneal neuropathy, it is an important study to perform. Inlesions that are axonal or mixed axonal and demyelinating, the superficial peronealSNAP amplitude is low or absent. However, in purely demyelinating lesions at thefibular neck, the distal superficial peroneal sensory response remains normal.
Motor Nerve Conduction Studies
In demyelinating lesions, focal slowing or conduction block can be noted in peronealmotor studies across the fibular neck. Proximal slowing of more than 10 meters persecond compared to the distal conduction velocity is considered significant. A drop inamplitude of the peroneal CMAP of more than 20% suggests conduction block.
If axonal loss is predominantly present, then peroneal CMAP amplitudes will bereduced at all stimulation sites (e.g., ankle, below the fibular head and lateral poplitealfossa). The motor nerve conduction velocity and the distal latency may be slightlyslowed or normal – depending on whether the fastest conducting axons have been lost.Often there is a combination of demyelination and axonal loss in the same patient.
The extensor digitorum brevis (EDB) is usually the site of recording for motorstudies. However, it is not unusual for the EDB to be atrophied for non-pathologicreasons (e.g., due to wearing tight shoes). Therefore, although the EDB is the usual siteof recording, it may be worthwhile to consider recording over the tibialis anterior muscle(TA). If you do the study over the EDB and it does not show focal slowing or conductionblock, then consider repeating the study using the active electrode over the tibialisanterior, which may pick up the deficit. Of course, if there is any question of anabnormal study, you can compare it to the contralateral side as well.
Late Responses
In peroneal neuropathy at the fibular neck, F-wave responses may be prolonged orabsent on the affected side and normal on the unaffected side. However, these responsesare non-specific and should not be used to diagnose peroneal neuropathy. H-reflexes areusually done to rule out an alternate diagnosis and should be normal in peronealneuropathy.
EMG
EMG is abnormal in axonal peroneal lesions when a significant axonotmesis is present.Abnormalities will be found in peroneal-innervated muscles. In axonal lesions, therewill be evidence of spontaneous activity, positive sharp waves and fibrillation potentials,
14 Peroneal Neuropathy 153
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and decreased recruitment of motor unit action potentials (MUAPs). In chronic axonallesions there may be evidence of decreased recruitment of MUAPs and the morphologyof the MUAPs may be long duration, high-amplitude and polyphasic. In predominantlydemyelinating lesions, only decreased MUAP recruitment will occur and the MUAPmorphology will be normal. The EMG is important in order to rule out other nervelesions. Therefore, proximal leg and paraspinal muscles are often tested (to rule out aradiculopathy) and tibial-innervated muscles are sampled below the knee. It is importantto note that the tibial nerve supplies the hamstring muscles, with the exception of theperoneal innervated short head of the biceps femoris muscle.
The short head of the biceps femoris can be very helpful in distinguishing aperoneal nerve injury at the fibular head from a sciatic nerve injury affectingpredominantly peroneal fibers. Due to the anatomy of the sciatic nerve (as noted above)the peroneal fibers can be more susceptible to injury than the tibial (especially in thesciatic notch and buttock region). In instances where insults could have occurred to thebuttock region as well as the fibular head (i.e., trauma, foot drop after hip surgery) the short head of the biceps femoris may be the main distinguishing factor between theselesions.
Summary
The classic electrodiagnostic findings in a peroneal neuropathy at the fibular neck mayinclude:
1. Reduced peroneal CMAP amplitude compared to the contralateral side2. Peroneal motor nerve conduction block or focal slowing across the fibular neck3. Reduced superficial peroneal SNAP amplitude4. Absent or prolonged peroneal F-response on the affected side5. Normal sural sensory, tibial motor and H-reflexes6. EMG findings of spontaneous activity and/or reinnervation in muscles supplied by
the deep and superficial peroneal nerves7. Normal EMG findings in the short head of the biceps femoris, paraspinal muscles
and tibially innervated muscles.
See Table 14.1 for a summary of electrodiagnostic findings in peroneal neuropathy.
14 Peroneal Neuropathy 155
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15Tarsal Tunnel Syndrome
Julie Silver
Clinical Presentation
Tarsal tunnel syndrome is an entrapment neuropathy of the tibial nerve behind the medialmalleolus. The syndrome is much less common than other neuropathies such as carpaltunnel syndrome or peroneal neuropathy. This neuropathy is nearly always unilateral.Conditions that may lead to tarsal tunnel syndrome include trauma, space-occupyinglesions, biomechanical problems causing joint deformity and systemic diseases. Somecases are idiopathic as well.
Patients with tarsal tunnel syndrome generally complain of pain around the ankle(especially medially) and/or paresthesias typically accompanied by numbness over thesole of the foot. Weakness in the foot is not very common in this neuropathy.
On physical examination there may be a positive Tinel’s sign over the tibial nerve atthe medial ankle (Fig. 15.1). Sensory exam might be abnormal over the plantar surfaceof the foot. Subtle weakness is not well appreciated because it is often difficult to isolatethe muscles supplied by the involved nerve(s).
Anatomy
Tarsal tunnel syndrome involves entrapment of the tibial nerve or any of its branches inthe region beneath the flexor retinaculum at the medial ankle. In addition to the tibialnerve, the tibial artery and tendons of the flexor hallucis longus, flexor digitorum longus
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Figure 15.1Tinel’s sign overthe tibial nerve.
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and tibialis posterior muscles pass through the tarsal tunnel (see Fig. 15.2). The tibialnerve divides into two sensory branches (medial and lateral calcaneal sensory nerves)and two mixed motor and sensory branches (medial and lateral plantar nerves). Thesenerves supply the medial and lateral sole of the foot respectively.
Both plantar nerves innervate the intrinsic muscles of the foot. The medialplantar nerve typically supplies the first three toes and the medial half of the fourthtoe, while the lateral plantar nerve supplies the lateral fourth toe and the entire fifth toe.
Electrodiagnostic Findings
Sensory Nerve Conduction Studies
In tarsal tunnel syndrome, the medial and lateral plantar sensory nerve action potential(SNAP) may be affected or absent. However, this should be interpreted with cautionsince pure SNAPs are difficult to obtain in the foot and frequently require averaging.Also, the foot is very sensitive to temperature changes. It is important to note that medialand lateral plantar sensory nerves are often hard to obtain even in normal patients.
Mixed and Motor Nerve Conduction Studies
These are the most common and important studies done in tarsal tunnel syndrome. Thedistal latency of the medial plantar nerve or the lateral plantar nerve, or both, may beincreased in tarsal tunnel syndrome if demyelination is present. Since motor latenciesare less temperature sensitive than sensory latencies, you can compare medial and laterallatencies and compare both latencies to the contralateral (unaffected) side. If axonal lossis prominent, then the compound muscle action potential (CMAP) will be reduced andthe distal latencies will be normal or just slightly prolonged.
Late Responses
F-waves may be abnormal but are non-specific and not typically done in tarsal tunnelsyndrome studies. H-reflexes should be normal in tarsal tunnel syndrome.
Easy EMG158
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Figure 15.2Anatomy of thetibial nerve.
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15 Tarsal Tunnel Syndrome 159
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l pla
nta
r n
erve
✓✓
Clin
ical
sig
nN
oct
urn
al p
ares
thes
ias
Var
iab
leC
om
mo
n
Bu
rnin
g in
th
e so
le o
f th
e fo
ot
Var
iab
leC
om
mo
n
Tin
el’s
sig
n o
ver
the
tars
al t
un
nel
No
Co
mm
on
Inab
ility
of
pla
nta
r fl
exio
nV
aria
ble
No
Dec
reas
ed s
ensa
tio
n in
pla
nta
r as
pec
t o
f th
e fo
ot
Co
mm
on
Co
mm
on
*Tar
sal t
un
nel
syn
dro
me
is c
ause
d b
y co
mp
ress
ion
of
the
tib
ial n
erve
or
its
bra
nch
es a
t th
e ta
rsal
tu
nn
el.
Tab
le 1
5.1
Mu
scle
invo
lvem
ent
in f
oca
l tib
ial n
erve
inju
ry
EMG
EMG of the foot is usually quite difficult in part because patients tolerate this exam poorly(due to pain). Additionally many patients have difficulty isolating specific muscles foractivation. Even in normal people there is often evidence of spontaneous activity as wellas long duration and large amplitude MUAPs in foot muscles. Nevertheless, it isrecommended that you perform an EMG in tibial innervated muscles both above andbelow the level of the tarsal tunnel, and that you check peroneal innervated muscles as partof the differential diagnosis. If a positive finding is noted, be sure to check the unaffectedfoot to rule out the possibility of a normal variant.
Summary
In summary, electrodiagnostic findings in tarsal tunnel syndrome may include:
1. prolonged or low amplitude medial or lateral plantar sensory or mixed nervesresponses
2. prolonged distal latency of the medial or lateral plantar motor nerve3. decreased amplitude of the medial or lateral plantar motor nerve4. spontaneous potentials (fibs and PSWs) in muscles innervated by lateral or medial
plantar nerve.
See Table 15.1 for a summary of NCS/EMG findings in tarsal tunnel syndrome.
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16Peripheral Neuropathy
Lyn Weiss
Peripheral neuropathies occur when there is a generalized dysfunction of nerves. This isreally a collection of disorders that all have the common characteristic of affecting theperipheral nerves. When doing electrodiagnostic testing on patients with suspectedperipheral neuropathy, it is possible to state if a peripheral neuropathy exists, how severeit is, and what the characteristics of the neuropathy are. Based on the characteristics ofthe neuropathy (axonal, demyelinating, sensory, motor, etc.) the electromyographer candirect the referring clinician towards suspected causes for the neuropathy (Table 16.1).
Clinical Presentation
Symptoms of peripheral neuropathy usually begin in the feet with numbness and/orpain/paresthesias. As the disease progresses, patients may report that they feel weaker orthat they are tripping more frequently. When the hands are affected, all activities of dailyliving may be affected. It is important to note that regardless of the strength present, loss ofsensation will markedly affect function making it difficult to walk, button a shirt, make aphone call, write a letter, etc. Peripheral neuropathies are commonly seen in diabetics andindividuals who drink alcohol excessively. There are many other medical conditions thatare associated with peripheral neuropathy as well. A good history should include askingabout symptoms in family members, as some neuropathies are hereditary.
On physical examination, the patient may have findings consistent with the specifictype of neuropathy. For example, a patient with a motor axonal neuropathy may haveweakness in the distal muscles with decreased deep tendon reflexes. Patients with apredominantly sensory neuropathy may have diminished sensation to light touch, pinprick,temperature and vibration. If the feet and hands are predominantly affected, the patientis referred to as having a ‘stocking–glove’ distribution of symptoms. It is important toremember that many patients have a neuropathy that may affect both sensory and motorfibers or that affect both the axon and the myelin.
Anatomy
Peripheral neuropathies are classified as affecting primarily motor fibers, sensory fibers,or both. They are also classified as to what part of the nerve is predominantly affected –axon, myelin, or both (Fig. 16.1). Finally, neuropathies are classified as segmental(affecting only certain areas of the nerve) or uniform (affecting the entire length of thenerve). Most neuropathies affect the distal segment of the nerve more than the proximalsegment. Therefore the longer the nerve, the more it is usually affected. This explains thepredominance of findings in the feet in patients with neuropathy. 161
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Easy EMG162
EMG
fin
din
g:
Un
ifo
rm
Seg
men
tal
Axo
n lo
ss
Sen
sory
A
xon
loss
M
ixed
axo
nal
d
emye
linat
ing
d
emye
linat
ing
m
oto
r >
ax
on
loss
m
ixed
lo
ss &
m
ixed
m
eter
>se
nso
ry
neu
rop
ath
y se
nso
rim
oto
r d
emye
linat
ing
se
nso
rim
oto
r se
nso
ry
po
lyn
euro
pat
hy
po
lyn
euro
pat
hy
sen
sori
mo
tor
po
lyn
euro
pat
hy
po
lyn
euro
pat
hy
po
lyn
euro
pat
hy
CM
AP
No
rmal
Dec
reas
ed
Dec
reas
ed
No
rmal
Dec
reas
edD
ecre
ased
amp
litu
de
seco
nd
ary
to
dis
per
sio
n o
r co
nd
uct
ion
blo
ck
Mo
tor
late
ncy
Incr
ease
dIn
crea
sed
No
rmal
No
rmal
No
rmal
Incr
ease
d
Mo
tor
Dec
reas
edD
ecre
ased
No
rmal
No
rmal
No
rmal
Dec
reas
edco
nd
uct
ion
ve
loci
ty
Dis
per
sio
n
No
Yes
No
No
No
Yes
(m
ild)
of
CM
AP
SNA
P N
orm
alN
orm
al o
r D
ecre
ased
(u
sual
ly)
Dec
reas
edD
ecre
ased
Dec
reas
ed
amp
litu
de
dec
reas
ed
SNA
P D
ecre
ased
Dec
reas
ed
No
rmal
No
rmal
No
rmal
Dec
reas
edco
nd
uct
ion
(s
om
ewh
at)
velo
city
Nee
dle
EM
G
No
(N
orm
al)
No
(N
orm
al)
Yes
No
(N
orm
al)
Yes
Yes
Wo
uld
fib
s* &
PS
Ws*
* lik
ely
be
no
ted
?
Tab
le 1
6.1
Poly
neu
rop
ath
y
16 Peripheral Neuropathy 163
EMG
fin
din
g:
Un
ifo
rm
Seg
men
tal
Axo
n lo
ss
Sen
sory
A
xon
loss
M
ixed
axo
nal
d
emye
linat
ing
d
emye
linat
ing
m
oto
r >
ax
on
loss
m
ixed
lo
ss &
m
ixed
p
oly
neu
rop
ath
y se
nso
ry
neu
rop
ath
y se
nso
rim
oto
r d
emye
linat
ing
se
nso
rim
oto
r p
oly
neu
rop
ath
y p
oly
neu
rop
ath
y se
nso
rim
oto
r p
oly
neu
rop
ath
y p
oly
neu
rop
ath
y
Co
mm
on
1.
Her
edit
ary
mo
tor
1. A
IDP† : G
uill
ain
–1.
Par
aneo
pla
stic
1. P
aran
eop
last
ic1.
Alc
oh
olic
1.
Dia
bet
ic
dis
ease
sse
nso
ry n
euro
pat
hy
Bar
ré s
ynd
rom
e m
oto
r (s
enso
ry, p
ain
ful
po
lyn
euro
pat
hy
po
lyn
euro
pat
hy
(dis
tal
typ
e I,
III, V
I (d
ista
l (a
scen
din
g
neu
ron
op
ath
y in
dis
tal
(dis
tal s
ymm
etri
c sy
mm
etri
c w
eakn
ess)
w
eakn
ess
wit
h
pro
xim
al w
eakn
ess)
(d
ista
l wea
knes
s)
extr
emit
ies)
w
eakn
ess)
2.
Ure
mia
(d
ista
l lit
tle
atro
ph
y)
2. C
IDP‡
(wea
knes
s 2.
Po
rph
yria
2.
Her
edit
ary
2. V
itam
in (
thia
min
e,
sym
met
ric
wea
knes
s)
2. M
etac
hro
mat
ic
of
asym
met
ric
low
3.
Axo
nal
Gu
illai
n–
sen
sory
B
12)
defi
cien
cy
leu
kod
ystr
op
hy
extr
emit
ies)
B
arré
syn
dro
me
neu
rop
ath
y (d
ista
l sym
met
ric
3. K
rab
be’
s 3.
Ost
eosc
lero
tic
4. H
ered
itar
y m
oto
r ty
pes
I–IV
w
eakn
ess)
le
uko
dys
tro
ph
y m
yelo
ma
sen
sory
3.
Fri
edre
ich
’s
3. G
ou
ty n
euro
pat
hy
4. A
dre
no
mye
lo-
4. L
epro
sy
neu
rop
ath
y ty
pes
at
axia
4.
Met
al
neu
rop
ath
y 5.
Acu
te a
rsen
ic
II an
d V
4.
Sp
ino
cere
bel
lar
neu
rop
ath
y 5.
Co
ng
enit
al
po
lyn
euro
pat
hy
5. L
ead
neu
rop
ath
y d
egen
erat
ion
(m
ercu
ry, t
hal
lium
, h
ypo
mye
linat
ing
6.
Ph
arm
aceu
tica
ls
6. D
apso
ne
5. A
bet
alip
o-
go
ld, e
tc.)
n
euro
pat
hy
(Am
iod
aro
ne
neu
rop
ath
y p
rote
inem
ia
5. S
arco
ido
sis
6. T
ang
ier
dis
ease
Pe
rhex
ilin
e)
(Bas
sen
–6.
Co
nn
ecti
ve t
issu
e 7.
Co
ckay
ne’
s H
igh
do
se A
ra-C
K
orn
zwei
g
dis
ease
s (r
heu
mat
oid
sy
nd
rom
e C
arci
no
ma,
AID
Sd
isea
se)
arth
riti
s, S
LE, e
tc.)
8.
Cer
ebro
ten
din
ou
s 6.
Pri
mar
y b
iliar
y 7.
Gas
trec
tom
y,
xan
tho
mat
osi
s ci
rrh
osi
s g
astr
ic r
estr
icti
on
7.
Acu
te
surg
ery
for
ob
esit
y se
nso
ry
8. C
hro
nic
live
r n
euro
no
pat
hy
dis
ease
neu
rop
ath
y C
is-p
lati
nu
m
of
chro
nic
illn
ess
toxi
city
9.
Hyp
oth
yro
idis
m
8. L
ymp
ho
mat
ou
s 10
.M
yoto
nic
dys
tro
ph
y se
nso
ry
11.
AID
S 12
. Lym
e d
isea
se
13.
Vin
cris
tin
e n
euro
pat
hy,
Tab
le 1
6.1
Poly
neu
rop
ath
y (c
on
t’d
)
Easy EMG164
EMG
fin
din
g:
Un
ifo
rm
Seg
men
tal
Axo
n lo
ss
Sen
sory
A
xon
loss
M
ixed
axo
nal
d
emye
linat
ing
d
emye
linat
ing
m
oto
r >
ax
on
loss
m
ixed
Lo
ss &
m
ixed
m
oto
r >
se
nso
ry
neu
rop
ath
y se
nso
rim
oto
r d
emye
linat
ing
se
nso
rim
oto
r se
nso
ry
po
lyn
euro
pat
hy
po
lyn
euro
pat
hy
sen
sori
mo
tor
po
lyn
euro
pat
hy
po
lyn
euro
pat
hy
po
lyn
euro
pat
hy
neu
ron
op
ath
y et
c.
Ch
ron
ic id
iop
ath
ic
14. T
oxi
c n
euro
pat
hy
atax
ic n
euro
pat
hy
(acr
ylam
ide,
car
bo
n
9. S
jög
ren
’s
dis
ulfi
de,
car
bo
nsy
nd
rom
e m
on
oxi
de)
10. F
ish
er v
aria
nt
Gu
illai
n–B
arré
sy
nd
rom
e 11
. Par
apro
tein
emia
s 12
. Pyr
ido
xin
e to
xici
ty
13. A
myl
oid
osi
s
*fib
s:fi
bri
llati
on
po
ten
tial
s.**
PSW
s: p
osi
tive
sh
arp
wav
es.
† AID
P: a
cute
infl
amm
ato
ry d
emye
linat
ing
po
lyn
euro
pat
hy.
‡ CID
P: c
hro
nic
infl
amm
ato
ry d
emye
linat
ing
po
lyn
euro
pat
hy.
Tab
le 1
6.1
Poly
neu
rop
ath
y (c
on
t’d
)
Electrodiagnostic Findings
In order to adequately assess for a peripheral neuropathy, sensory and motor nerves mustbe tested in at least two extremities. Since temperature can affect latency, amplitude andconduction velocity (see Chapter 8, Pitfalls), limb temperature should be maintained at32°C for the upper extremities and 30°C for the lower extremities. Table 16.1 will helpyou identify the type of neuropathy based on the electrodiagnostic findings.
Sensory Nerve Conduction Studies
If a peripheral neuropathy involves the sensory fibers, sensory nerve action potentials(SNAPs) may be reduced. If the sensory neuropathy is axonal in nature, the amplitude ofthe SNAP will be affected, or the response may be unobtainable. If the sensory neuropathyis demyelinating, the SNAP responses can have a decreased conduction velocity. Aprofound demyelinating process can also result in the loss of SNAPs.
Motor Nerve Conduction Studies
If a peripheral neuropathy involves motor fibers, the compound motor action potential(CMAP) may be affected. If the motor neuropathy is axonal in nature, the amplitudeof the CMAP may be affected, or it may be unobtainable. If the motor neuropathy isdemyelinating, the CMAP response may have an increased distal latency and/orslowed conduction velocity. Conduction velocity less than 80% of the lower limit ofnormal suggests a demyelinating neuropathy.
It should be noted whether conduction velocity slowing is uniform throughout thenerve (uniform demyelination), or only affects certain segments of the nerve (segmentaldemyelination). In segmental demyelination, some of the fibers are traveling slower thanother fibers. The CMAP that is generated will be dispersed, meaning it will have a longerduration and lower amplitude (temporal dispersion) (see Fig. 6.1).
When performing motor studies on the peroneal nerve, the active electrode is overthe extensor digitorum brevis (EDB) muscle. In many normal people, this muscle isatrophied. Therefore, if the CMAP amplitude is decreased on stimulation of the peronealnerve with pickup over the EDB, try moving the active electrode to the tibialis anteriormuscle. If the amplitude is still low, the findings are significant (i.e., indicate axonal loss).
16 Peripheral Neuropathy 165
Normal nerve and distribution of myelin
Injury to myelin
Injury to axon
Figure 16.1Classification ofperipheralneuropathies.
!
If the amplitude is decreased in the EDB bilaterally, together with the abductor hallucis,this indicates an axonal peripheral neuropathy.
Late Responses
Since late responses (F-waves and H-reflexes) assess the peripheral nerve along itsentire course, these responses are usually affected in peripheral neuropathy. In diseasessuch as Guillain–Barré syndrome, F-waves can be the earliest indication of a problem,since the proximal segment of the nerve is tested. It should be remembered, however,that these responses are not specific. Therefore, the information generated can help, butnot make, the diagnosis.
EMG
EMG findings are usually negative in peripheral neuropathy, unless an axonal motorneuropathy is present. In such cases, affected muscles may demonstrate spontaneousactivity (fibrillation potentials and positive sharp waves). Complex repetitive discharges(CRDs) may be noted in chronic neurogenic disorders. Both proximal and distalmuscles should be tested. EMG testing is helpful, even when negative, as it helps to ruleout other disorders, such as a focal neuropathy or myopathy. In addition, if an axonal lesionis present, the time course of the disease can be assessed by evaluating for the presence ofchronic changes in the motor unit action potentials (MUAPs) such as increased duration,polyphasicity or large amplitude (see Chapter 5, Electromyography).
Summary
In summary, electrodiagnostic findings in peripheral neuropathy may include:
1. decreased latency and/or conduction velocity in demyelinating neuropathies (decreaedmotor latency and/or conduction velocity in motor demyelinating neuropathies anddecreased sensory latency and/or conduction velocity in sensory demyelinatingneuropathies)
2. decreased amplitude of the CMAP or SNAP in axonal neuropathies (decreaseddCMAP amplitude in motor axonal neuropathies and decreased SNAP amplitudes insensory axonal neuropathies)
3. abnormal spontaneous activity may be found on needle study in motor axonalneuropathies
See Table 16.1 for a summary of NCS/EMG findings in peripheral neuropathy.
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17Myopathy
Julie Silver
Clinical Presentation
A myopathy is simply a disorder of the muscles. This can take various forms and thecommon myopathic disorders are listed in Table 17.1. The primary symptom inmyopathies is weakness. It is important to note that most myopathies affect the proximal
167
CongenitalCentronuclear myopathyMyotubular myopathyNemaline rod myopathyFiber-type disproportion
InflammatoryPolymyositisDermatomyositisInclusion body myositisViral myopathy (e.g., HIV associated myopathy/polymyositis and human T-cell
lymphotropic virus-I myopathy)Sarcoid myopathy
InfectiousTrichinosis
AtrophicToxicColchicine, azidothymidine (AZT), alcohol, chloroquine, hydroxychloroquine,
pentazocine, clofibrate, steroids
EndocrineThyroid myopathyParathyroid myopathyAdrenal/steroid myopathyPituitary myopathy
MetabolicAcid maltase deficiency myopathyCarnitine deficiency myopathyDebrancher deficiency myopathy
Dystrophies Dystrophin deficiency (Duchenne and Becker’s)Facioscapulohumeral muscular dystrophyMyotonic muscular dystrophyEmery–Dreifuss muscular dystrophyOculopharyngeal muscular dystrophyLimb girdle muscular dystrophy
Table 17.1 Common myopathic disorders
!
muscles more than the distal muscles. This means that the first symptom a patient maycomplain about is difficulty rising from a chair or walking up stairs.
The weakness is constant but may be more noticeable when someone is fatigued. Inconditions where distal weakness is more prominent (e.g., hereditary distal myopathies)patients may complain of foot drop, unstable ankles, difficulty opening jars or carrying anobject in the hand, etc. Pain, when present, is usually not well localized and is an aching orcramping feeling.
Myopathies present as pure motor conditions, so the classic presentation is weaknesswithout sensory symptoms. On physical examination it is important to assess strength andmuscle atrophy. Most myopathies present with symmetrical proximal weakness. In somemyopathies, ocular and bulbar muscles are affected, and this should be noted if present.Sensation should be normal and reflexes become increasingly diminished as weaknessprogresses. Contractures of the joints may develop due to loss of strength.
The usual tests ordered to confirm the diagnosis of myopathy include creatine kinase(CK) serum levels (typically elevated), EMG and muscle biopsy.
Classification
Myopathies can be generally classified as congenital, inflammatory, metabolic, atrophic,or muscular dystrophies (Table 17.1).
Congenital myopathies. Congenital myopathies typically present in the first fewyears of life, but occasionally there are people who are diagnosed as an adult. Theclinical symptoms are usually non-specific. Most of the myopathies in this category havefairly typical histochemical findings when stained, so muscle biopsy is generally needed toconfirm the diagnosis.
Inflammatory myopathies. Most inflammatory myopathies are presumably due tosome type of immunologic attack of the muscles. However, there are some inflam-matory myopathies that are known to be due to infection caused by parasites, virusesor bacteria.
Metabolic myopathies. These are caused by inherited enzyme deficiencies that areessential for intracellular energy production. These may present as a typical non-specificmyopathy with proximal weakness as the only clue, or with cramps and myoglobinuria.In some cases metabolic myopathies are part of a more diffuse neurologic syndrome thatmay involve the central nervous system (CNS). Patients may become symptomatic onlyafter exercise. CK levels are typically very elevated.
Muscular dystrophies. These are inherited muscular disorders, often with an earlyonset and very progressive course. Some muscular dystrophies can now be identified bya specific chromosomal abnormality or gene product (e.g., Duchenne and Becker’sdystrophy).
Electrodiagnostic Findings
EMG plays an important role in the diagnosis of myopathy and is frequently done inconjunction with a muscle biopsy. EMG not only helps to determine the diagnosis andextent of the disease, but can also be an important indicator of where the muscle biopsyshould be obtained.
Some electrodiagnosticians perform just the EMG portion of the test if myopathy isthe suspected diagnosis, because the nerve conduction studies should be normal.However, if there is a concurrent neuropathy, this likely will be missed with only EMG
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!
studies. So, it is useful to perform at least one motor and one sensory nerve conductionstudy as a screen when testing for myopathy.
Sensory Nerve Conduction Studies
Sensory nerve conduction studies should be normal in patients with myopathy.
Motor Nerve Conduction Studies
Motor nerve conduction studies are typically normal in myopathy, since the activeelectrode is usually over a distal muscle. However, if the myopathy is severe enough toaffect both distal and proximal muscles or is one of the less common myopathies thatpreferentially affect distal muscles, then the motor nerve conduction studies may beabnormal. In these cases there may be evidence of reduced compound muscle actionpotential (CMAP) amplitude. The distal latencies and conduction velocities will benormal, as the myelin is not affected.
Late Responses
Late responses are not usually helpful in myopathies as they are non-specific.
EMG
Myopathies present with characteristic findings on EMG. Myopathic motor units areusually of short duration, small amplitude, polyphasic and have early recruitment (seeFig. 5.14). This would be seen as a large number of small motor units firing for aminimal contraction. The motor unit action potential (MUAP) is typically smaller due todropout or dysfunction of individual muscle fibers. This leads to a decreased size of themotor unit. The number of motor units usually remains the same except in severe caseswhere every single fiber drops out and thus eliminates that motor unit.
Spontaneous activity is frequently noted in myopathies. Many myopathies presentwith positive sharp waves and fibrillation potentials (fibs). Less commonly myopathiesmay reveal myotonic discharges (see Chapter 5, Electromyography). It is not uncommonin chronic myopathies to note complex repetitive discharges (CRDs). Rarely there isevidence of contracture, which is the complete absence of electrical activity in thecontracted state.
The EMG study should first focus on the weakest muscles. Typically these are themore proximal muscles. In some instances, the only abnormalities may be in theparaspinal muscles. If these show the typical findings consistent with myopathy, thenstronger muscles should be tested as well in order to determine the extent of the disease.If the clinically weakest muscles are normal, then testing the stronger muscles will notbe useful and is not advised. In cases where the muscles show neuropathic instead ofmyopathic changes, the electromyographer needs to reconsider the scope of the study andexpand it to rule out other conditions. In this instance, nerve conduction testing woulddefinitely be indicated. It should also be noted that steroid myopathies predominantlyaffect Type II fibers. Since EMG testing evaluates Type I fibers, EMG testing is oftennormal in steroid myopathy.
There are three additional considerations when performing an EMG in a suspectedmyopathic patient. First, it is not a good idea to order a CK blood test shortly after theEMG as the levels may be falsely elevated. Second, when determining which muscle tobiopsy it is wise to choose a muscle that is affected but not completely atrophic. Third,do not test all affected muscles, because once they have been needled, they should not be
17 Myopathy 169
used for a biopsy. The EMG report should clearly identify which muscles have not beentested so that an appropriate decision can be made for which muscle to biopsy.
Summary
In summary, electrodiagnostic findings in myopathy may include:
1. normal SNAP2. normal CMAP3. spontaneous potentials (PSWs and fibs) in affected muscles4. short duration small amplitude polyphasic motor units with early recruitment in
affected muscles on EMG.
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18Brachial Plexopathies
Walter Gaudino
Clinical Presentation
Evaluation of the brachial plexus is one of the most challenging examinations that theelectromyographer will encounter. This is due to the complexity of the anatomy and itsrelative inaccessibility. Moreover, standard nerve conduction protocols do not test manyparts of the brachial plexus. A thorough understanding of the anatomy of the brachialplexus is integral to performing an accurate electrodiagnostic study.
Clinical presentations vary according to the area of the brachial plexus that isinvolved. Most brachial plexus lesions are due to trauma, either obstetrical or accidentale.g., motor vehicle, knife or projectile injuries. The majority of brachial plexus lesions inadults are unilateral and affect the dominant limb more commonly than the non-dominantlimb. Obstetric palsies affect the right side more than the left. The history and physicalexamination varies with the type of lesion to the brachial plexus. One useful way toclassify the varied brachial plexus lesions is on the basis of their anatomic location.Brachial plexus lesions can be classified into supraclavicular, infraclavicular and panplexus lesions (Table 18.1).
The clinical presentation of the lesions of the brachial plexus varies according to thesite of the brachial plexus involved. Injuries to the lateral cord may present with numbnessin the lateral aspect of the forearm below the elbow extending just above the thumb. This isthe distribution of the lateral cutaneous nerve of the forearm. This may be associated withnumbness in the distribution of the median nerve (the 1st, 2nd and 3rd digits), andweakness of the biceps, brachioradialis and pronator teres muscles. A lesion affecting themedial cord may damage the medial antebrachial cutaneous nerve and present with
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Supraclavicular Infraclavicular Pan plexus
Roots/upper trunks Radiation related TraumaIncomplete traction injury Gunshot wound Severe traction injuryErb’s palsy Humeral fracture/dislocation Late metastatic diseaseC5, C6 root avulsions Dislocation Late radiation palsyAxillary nerve blockLower plexus(Roots/lower trunk)Metastatic tumorPancoast syndromePost sternotomyThoracic outlet syndromeKlumpke’s palsy (C8, T1)
Table 18.1 Brachial plexus lesions
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numbness of the medial aspect of the forearm. This may be associated with weakness ofthe flexor carpi ulnaris (FCU), abductor pollicis brevis (APB), opponens pollicis, flexordigitorum indicis (FDI), abductor digit minimi (ADM), and adductor pollicis muscles.
Brachial plexopathy due to carcinomatous spread usually presents with pain.These lesions may present as a result of spread from an adjacent breast or lung mass.These plexopathies have a predilection for the lower trunks, but can also involve a morediffuse pattern. Brachial plexopathy may develop from months to years after radiationtreatment of breast, lung, and mediastinal cancer. These plexopathies typically are notpainful, but present with paresthesias and sensory loss that progress slowly. They tend tobe more prominent in the upper trunk distribution. Figures 18.1 and 18.2 review thecutaneous innervation of the extremities.
Anatomy
The brachial plexus (Fig. 18.3) is an intricate neural web that provides the innervation tothe neck and the upper extremities. Most commonly the plexus arises from the anterior
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C4
T2
C5
T1
C6
C8C7
Supraclavicular
Intercostobrachial
Radial
Axilla
ry
Med
ial c
utan
eous
M
Ulnar
Med
ian
M,musculocutaneous
Supraclavicular
Intercostobrachial
C6
C7C8
Axillary
Radial
Ulnar
Ulnar
Radial
Med
ian
Musculocutaneous
Figure 18.1Cutaneousinnervation.
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A
B
rami of the C5 through the T1 nerves. There are variants on the theme with somepatients having contributions from the C4 level or the T2 levels. These are known as pre-fixed and post-fixed plexi respectively. The following discussion will focus on the mostcommon pattern of innervation (i.e., C5 to T1).
There are many methods to help learn the anatomy of the plexus. The anatomy neednot be intimidating. You can remember the section of the brachial plexus using themnemonic ‘Robert Taylor Drinks Coors Beer’ along with three parallel lines; an X, a Y andan M. The mnemonic stands for the five sections of the brachial plexus, which are theroots, trunks, divisions, cords, and branches.
18 Brachial Plexopathies 173
C2
C3
C4C5T2T3T4T5
T1
C6
C8C7
T6
T7
T8T9
T10
T11
T12
L1
L2
L3
L4
L4L5S1
C2
C3
C4
C5
T1
C6C7
C8 T2
T4
T6
T8
T10
T12
L2
L4
C6
C7C8
S1 S2
S1 L5 L4
T5
T7T9
T11
L1
L3
L5
S5S4
S3
S2
S1
Figure 18.2Cutaneousinnervation.
Figure 18.3 Thebrachial plexus.
Ulnaar nerveMeddian nerve
Radial nerveAxillary nerve
Musculocutaneous nerve C5C6C7C8T1
Start the drawing of the brachial plexus by representing the C5–T1 nerve roots byfive down-sloping horizontal lines and label them C5, C6, C7, C8, and T1. The roots ofthe plexus originate at the anterior rami of C5 through the T1 nerves (Fig. 18.4). Theroots run through the anterior and posterior scalene muscles (Fig. 18.5). It is at this levelthat the C5 and C6 roots converge to form the upper trunk, the C7 root forms the middle
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Brachial plexusRoots
C5
C6
C7
C8
T1
Figure 18.4 Theroots of thebrachial plexus.
Figure 18.5 Thestructure of thebrachial plexus.
Posterior scaleneAnterior scalene
Axillaryartery
C5C6
C7
C8T1
trunk and the C8 and T1 roots form the lower trunk. Then connect the roots to the threeparallel lines as in Figure 18.6. These represent the roots and the trunks of the brachialplexus.
The trunks slope down and divide to form the anterior and posterior divisions(Fig. 18.7). The divisions are found deep under the middle section of the clavicle. Theyrun along a parallel course to the subclavian artery. They then weave around the axillaryartery. At this point the posterior divisions of the upper and lower trunks join the middle
18 Brachial Plexopathies 175
Brachial plexus
C5
Upper
Middle
Lower
C6
C7
C8
T1
TrunksRoots
Figure 18.6 Thestructure of thebrachial plexus.
Figure 18.7 Thestructure of thebrachial plexus.
Brachial plexus
Roots
C5
C6
C7
C8
T1
Trunks
Upper
Middle
Lower
Divisions
Anterior
Anter
ior
Posterior
Post
erio
r
Posterior
Anterior
trunk to form the posterior cord. The anterior division of the middle trunk joins theupper trunk fibers to become the lateral cord. At this level the brachial plexus is dividedinto lateral, posterior and medial cords that are named in their relationship to the axillaryartery (Fig. 18.8). The brachial plexus then goes on to divide into the terminal nervebranches (Fig. 18.9). The posterior cord becomes the radial nerve, but also gives off theaxillary nerve. The lateral cord terminates in the musculocutaneous nerve as well as abranch that merges with a branch from the medial cord to form the median nerve. Themedial cord and terminates in the ulnar nerve.
Along its course, the brachial plexus gives off collateral nerves. These nerves arehelpful in that they can be used to help localize lesions either proximal or distal to thebrachial plexus. Some of the clinically more important nerves include the dorsal scapularnerve to the rhomboids (involvement will localize the lesion above the level of the trunks).The suprascapular nerve to the supraspinatus and infraspinatus comes off at the trunklevel. For example, plexopathies involving the upper trunk can usually be distinguished
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Brachial Plexus
Roots
C5
C6
C7
C8
T1
Trunks Divisions Cords
Lateral
Posterior
Medial
Figure 18.8 Thestructure of thebrachial plexus.
Figure 18.9 Thestructure of thebrachial plexus.
Brachial plexus
Roots Trunks Divisions Cords Branches NervesLateral pectoral
nerve
Dorsal scapularSuprascapular
Subclaviusmuscle nerve
Longthoracicnerve
Medialpectoralnerve
Lower subscapular nerveThoracodorsal nerve
Upper subscapular nerve
Medialbrachialcutaneousnerve
Medialantebrachialcutaneousnerve
Axillarynerve
Musculocutaneousnerve
Radialnerve
Median nerve
Ulnar nerve
C5
C6
C7
C8
T1
from lesions of the lateral cord. Although both will have reduced amplitudes of themusculocutaneous compound muscle action potentials (CMAPs), lateral antebrachialsensory nerve action potential (SNAP), and median SNAP, only the upper trunk lesionwill have a decreased amplitude of the axillary nerve CMAP recorded from the deltoidmuscle and suprascapular CMAP recorded from supraspinatus muscle. Only the uppertrunk lesion may have spontaneous potentials in the deltoid, brachial radialis,infraspinatus, or supraspinatus muscles. These relationships will be further reviewed inthe next section.
Electrodiagnosis
A properly planned and technically correct brachial plexus electrodiagnostic examinationcan give more information than a physical examination alone. The electrodiagnosticexamination is the most sensitive physiologic examination of the brachial plexus. Thistest can help to localize the site of the lesion and provide the electromyographer with anestimate of the prognosis of the lesion. When performing an examination to rule out abrachial plexus lesion it is important to use the unaffected limb as a control and comparenerve responses from the two sides tested.
Examination of the brachial plexus will require learning many non-standard nervetests. Standard ulnar and median motor and sensory nerve evaluation examines only themedial cord and lower trunk. Median sensory nerve studies are testing the upper trunk orlateral cord. A brachial plexus lesion is proximal to the segments of these nerves that arebeing tested. Extensive electromyography is essential to localize the area of the brachialplexus that is affected, and to rule out possible radiculopathies and mononeuropathies asthe source of the patient’s symptoms.
Aside from localizing the lesion, the electrodiagnostic test can also establish theseverity of nerve damage. Axon loss plexopathy is the most likely type of pattern seen inthe electrodiagnostic lab. The electrophysiologic changes depend upon the severity ofthe axonal loss.
Sensory Nerve Conduction Studies
The sensory nerve conduction study is a more sensitive indicator of injury to thebrachial plexus than the motor nerve response. The sensory nerve distal latency andconduction velocity are usually normal in brachial plexus lesions. This is because thelesion is usually axonal. However, the sensory nerve action potential amplitude (SNAP)may be decreased in lesions affecting the brachial plexus. With mild lesions of thebrachial plexus the SNAP amplitude may be unaffected. With increasing severity ofinjury to the brachial plexus the amplitude of the appropriate SNAP may be decreased orabsent. The SNAP amplitude reflects the number of functioning axons in continuity withthe sensory root cell body. This is also called the dorsal root ganglion (Fig. 18.10).Lesions that are proximal to this cell body, such as radiculopathies and nerve rootavulsions, do not interfere with the function of the cell body on the sensory nerves derivedfrom that root. Therefore lesions proximal to the dorsal root ganglion have intact sensorynerve electrical function, even though sensation may be affected clinically.
Lesions proximal to the dorsal root ganglion have a normal SNAP amplitude. Lesionsdistal to the dorsal root ganglion disconnect the sensory nerve cell body from its axons. Thisresults in deprivation of the axons from their nutritional source. Depending on the severityof the lesion this may result in a decrement or absence of the SNAP potential. Thedifferentiation between pre- and postganglionic lesions is extremely important. Although
18 Brachial Plexopathies 177
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both lesions may present with numbness and sensory loss in a defined distribution, thenerve root avulsion (preganglionic lesion) usually portends a dismal prognosis. Suchinjuries do not undergo spontaneous regeneration and are poorly amenable to surgicalrepair. The postganglionic lesions have a much more favorable prognosis.
Motor Nerve Conduction Studies
The compound muscle action potential amplitudes (CMAP) are not affected unless thebrachial plexus injury is severe. With severe injuries to the brachial plexus there may bea reduction in the appropriate CMAP amplitudes. When they are affected, the CMAP isgenerally a better indication of the extent of axonal loss than SNAP amplitudes. Whenlooking for a decrease in the amplitude, consider the nerve you are testing and the levelaffected in the brachial plexus. (CMAPs from ADM and APB should be equallyreduced.)
Stimulating at Erb’s point may reveal decreased amplitude if a conduction block ispresent distal to that point. The motor latencies and conduction velocities are usuallyunaffected by a brachial plexus lesion because they are a function of the fibers that areintact and do not reflect abnormal conduction across the brachial plexus. However,stimulation across Erb’s point may reveal slowing if there is a demyelinating lesion inthe brachial plexus.
Late Responses
Most lesions of the brachial plexus are incomplete and have normal conduction across thebrachial plexus. The lesion may be so localized that the effect of the lesion is ‘diluted’along the neural path of transmission of the F-wave. Therefore, F-wave prolongation is anon-specific finding.
EMG
Your findings on the history and physical examination will help you decide which musclesto examine electromyographically. The EMG testing should be mapped out based on areview of the brachial plexus (Fig. 18.9) before the test is started. Electrodiagnosticfindings with acute mild plexopathies are usually limited to fibrillations and positive sharpwaves in an appropriate pattern. For example, a lesion of the lateral cord may have positivesharp waves noted in the biceps, pronator teres, flexor carpi radialis (FCR) and thepectoralis muscles. The supraspinatus, infraspinatus and levator scapulae muscles would
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Dorsal root
Dorsal root ganglion
Dorsal ramus
Ventral ramus
Ventral root
Figure 18.10SNAP amplitudemay be decreasedin lesionsaffecting thebrachial plexus.
be normal. In lesions where reinnervation has occurred, long duration, high amplitude orpolyphasicity may be noted in the MUAPs.
The clinical manifestations of an injury to the brachial plexus are maximal at onsetbut the electrodiagnostic findings may take up to three weeks to develop. It is importantthat the electrodiagnostic test be delayed three weeks after the onset of the injury, so thatsufficient Wallerian degeneration of the distal parts of the injured nerves can occur. Thisallows for the development of fibrillation potentials and positive sharp waves. Testing priorto that time frame may yield confusing and misleading data. Cervical paraspinals areexpected to be normal in brachial plexus lesions because the paraspinal muscles areinnervated by the posterior rami and the brachial plexus is innervated by the anteriorrami of the spinal nerve. Table 18.2 maps out the electrodiagnosis of the brachial plexus.
18 Brachial Plexopathies 179
Anatomical Affected sensory Affected motor Positive findings area of Injury NCS NCS EMG
Radiculopathy Normal CMAPs decreased Cervical paraspinals Myotomal pattern
Upper trunk Lateral antebrachial Musculocutaneous SupraspinatusMedian nerve to nerve to biceps Biceps1st digit Suprascapular Pronator teresRadial nerve to Deltoid
supraspinatus Brachial radialisAxillary nerve to deltoid
Middle trunk Median nerve to Radial nerve to Latissimus dorsi 3rd digit and extensor digitorum Teres major4th digit communis Extensor digitorum
communisPronator teresFlexor carpi radialis
Lower trunk Ulnar nerve to Ulnar nerve to Flexor digitorum 5th digit abductor digiti superficialisMedial antebrachial minimi Abductor digitorum
Median nerve to minimiabductor pollicis Flexor carpi ulnarisbrevis Flexor superficialis
Flexor digitorum profundus
Lateral cord Lateral antebrachial Musculocutaneous BicepsMedian nerve to nerve to biceps Pronator teres1st digit Flexor carpi radialis
Posterior cord Radial Axillary nerve to Latissimus dorsideltoid Teres majorRadial nerve to Deltoidextensor Radial musclescarpi ulnaris
Medial cord Ulnar nerve to Ulnar nerve to Ulnar muscles5th digit abductor digiti Flexor digitorum Medial antebrachial minimi superficialisnerve Median nerve to Flexor pollicis
abductor pollicis longusbrevis Abductor pollicis
brevis
Table 18.2 Localization of lesions in the brachial plexus
By reviewing the table, you can localize the lesions to the roots or areas of the brachialplexus.
Summary
In summary, the electrodiagnostic findings in brachial plexopathy may include (seeTable 18.2):
1. Decreased SNAP amplitude2. Decreased CMAP amplitude3. Slowing of conduction velocity with stimulation across Erb’s point4. Normal EMG findings in the paraspinal muscles5. Spontaneous activity (fibs and PSWs) in muscles distal to the level of the injury.
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19Lumbosacral Plexopathies
Walter Gaudino
Electrodiagnostic evaluations of the lumbar and sacral plexus (LSP) can be challengingexaminations. This is due to the complexity of the anatomy and its relative inaccessibility.Moreover, standard nerve conduction protocols do not test many parts of these areas. Athorough understanding of the anatomy is integral to performing an accurate electro-diagnostic study.
Clinical Presentation
Neurologic damage to the lumbar and sacral plexus is less common than in the brachialplexus. This is due to the relatively protected position of these neural structures and theirdecreased accessibility to injury. Lumbosacral plexopathies can be caused by anatomicinjury and abnormalities, such as tumors, hematomas, surgical damage and trauma. TheLSP can also be damaged by metabolic insults such as diabetes mellitus, infection,vasculitis, or paraneoplastic syndromes. The presentation of the plexopathy variesaccording to the structures involved.
Anatomy
The anatomy of the lumbar and sacral plexi will be discussed separately. The lumbarplexus (Fig. 19.1) is an intricate neural web that provides innervations to the abdominal
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Lumbar plexxus erve rootT12 ne
rve rootL1 ne
rve rootL2 ne
rve rootL3 ne
rve rootL4 ne
rve rootL5 ne
bosacralLumbktrunk
Subcostal neerveGenitofemorralnerve
IlioinguinalnerveLateral femooralcutaneous nerveTo psoas &IliacusFemoral nervveObturatornerve
Iliohypogastricnerve
Figure 19.1Anatomy of thelumbar plexus.
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wall and the anterior-medial aspect of the thigh. The lumbar plexus is formed in thepsoas muscle from the anterior rami of the upper four lumbar nerves L1, L2, L3 andL4. There is sometimes a contribution from T12, but this is variable. The branches of the plexus emerge from the lateral, medial and anterior borders of the muscle. Theiliohypogastric, ilioinguinal, femoral and lateral femoral cutaneous nerves arise fromthe lateral aspect of the psoas muscle. The obturator nerve arises from the medial aspectof the psoas muscle. The genitofemoral nerve arises from the anterior aspect of the psoasmuscle (Fig. 19.2).
The lumbar plexus has a much simpler pattern than the brachial plexus, because itlacks the distinct subdivisions such as trunks and cords that is characteristic of the brachialplexus. The lumbar plexus consists of anterior primary rami, and these rami divide intoanterior and posterior divisions.
Nerve roots from L1, L2, L3 and L4 transverse through the psoas muscle and thencoalesce, to divide into anterior and posterior divisions. The lumbar plexus then terminatesinto seven major branches. The first three provide motor and sensory innervation to theabdominal wall and groin. These are the iliohypogastric, ilioinguinal and genitofemoralnerves respectively. The next three go on to innervate the thigh’s anterior and medialaspects. These are the lateral femoral cutaneous, femoral and obturator nerves. The 7thbranch is a contribution from L4 to the sacral plexus. The obturator nerves derive fromthe anterior divisions. The lateral femoral cutaneous and the femoral nerves arise from theposterior divisions. The femoral nerve terminates into the saphenous nerve that providessensation to the medial aspect of the leg. Table 19.1 summarizes the nerves of the lumbarplexus and their respective neural innervation pathways.
The sacral plexus (Figs 19.3 and 19.4) is similar to the lumbar plexus in that it isprimarily a collection of ventral primary spinal nerves that divide into anterior and
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Lumbar plexus
Kidneyerve rootT12 ne
ve rootL1 nerv
ve rootL2 nerv
ve rootL3 nerv
ve rootL4 nerv
ve rootL5 nervosacralLumbo
trunkIliacus
Bladder
Inguinalligament
Aorta
Psoas
Subcostal nerve
Genitofemoral nnerve
Iliohypogastric nnerve
Ilioinguinal nerve
Lateral femoralcutaneous nerve
Femoral nerve
Obturator nerve
Rectum
To psoas & iliacus
Femoral artery
Figure 19.2 The lumbar plexus is formed in the psoas muscle from the anterior ramiof the upper four lumbar nerves L1, L2, L3 and L4.
19 Lumbosacral Plexopathies 183
Peripheral nerve Root Division Sensation Muscle
Iliohypogastric L1,2 Superior gluteal Noneregion
Genitofemoral L1,2 Scrotal skin/adjacent Nonethigh and labia
Lateral femoral L2,3 Posterior Anterolateral thigh Nonecutaneous
Femoral L2,3,4 Posterior Anterior thigh, Sartoriousanteromedial thigh IliacusMedial leg/foot via Pectinousthe saphenous Quadriceps division of the femoral nerve
Obturator L2,3,4 Anterior Medial thigh Adductor longus, GracilisAdductor brevisObturator internusAdductor magnus
Table 19.1 The lumbar plexus
Figure 19.3 The sacral plexus.
L4
L5
S1
Superior gluteal
Inferior glutealVisceral branch S2
Visceral branch S3Posterior femoral cutaneousObturator internus & superior gemmellus
Coccygeal Pudendal Perforating cutaneous
Levator ani, coccygeus & rectal sphincterQuadratus femoris & inferior gemellus
Piriformis
S2
S3
S4
S5
Tensor fascia lata
Gluteusminimus
Gluteus maximus
Tibial
Commonperoneal
Sciatic
Gluteus medius
posterior divisions. These, in turn, divide into multiple peripheral nerves. The sacralplexus provides sensation, muscular and articular innervation to the posterior hip girdle,thigh and anterior and posterior leg regions. The sacral plexus is composed of primaryventral rami from the L4–S3 levels. Although the sacral plexus appears intimidating it isactually quite simple to learn. The plexus is formed in the posterior aspect of the pelvisand lies in the back of the pelvis between the piriformis muscle and the pelvic fascia(Fig. 19.4).
In front of the sacral plexus are the hypogastric vessels, the ureter and the sigmoidcolon. The superior gluteal and the inferior gluteal vessels run between the 1st, 2nd and3rd sacral nerves respectively. The close anatomic relationship to these blood vesselsmakes this structure vulnerable to trauma, which may lead to bleeding.
The sacral plexus is formed from the ventral primary rami from the L4 through theS3 nerves. All of the nerves (except the S3 root) then divide into an anterior and posteriordivision. The plexus gives off a number of branches, five of which are important toremember for electrodiagnostic testing of this area. The five essential nerves are thesuperior and inferior gluteal, the posterior femoral cutaneous, sciatic and the pudendal.The sciatic nerve divides into the common peroneal and tibial divisions in the thigh. Thegluteal, posterior femoral cutaneous and the common peroneal division of the sciatic nervearise from the posterior components of the sacral plexus. The tibial division of the sciaticnerve, pudendal and muscular branches to the quadratus femoris, gemellus inferior,obturator internus, and gemellus superior muscles arise from the anterior components ofthe sacral plexus. Table 19.2 reviews the main contents of the sacral plexus.
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Aorta
l IliaclInternanal IliacnExtern
L4
L5
S1
S2S3S4S5
BladderBProstate
Rectum
Figure 19.4 Theplexus is formedin the posterioraspect of thepelvis and lies inthe back of thepelvis betweenthe piriformismuscle and thepelvic fascia.
Electrodiagnostic Findings
The electrodiagnostic examination is the most sensitive physiologic examination of thelumbosacral plexus. This test can help to localize the site of the lesion and prognosticate.When performing an examination to rule out a lumbar or sacral lesion, it is important touse the unaffected limb as a control and compare nerve responses from the two sides.
Examination of the lumbosacral plexus may necessitate a few non-standard nerve tests.For example, the lumbar plexus may require evaluation of the saphenous portion of thefemoral nerve, the lateral femoral cutaneous nerve of the thigh and the femoral nerve. Thesacral plexus may require evaluation of the superficial peroneal and sural sensory nerves.The peroneal motor response from both the extensor digitorum brevis and the tibialisanterior muscles may be required. The tibial response may be recorded from the abductorhallucis and the abductor digiti quinti. Extensive needle electromyography is essential tolocalize the area of the plexus that is affected, and to rule out possible radiculopathies ormononeuropathies as the source of the patient’s symptoms. Aside from localizing the lesion,the electrodiagnostic test can also establish the severity of nerve damage.
19 Lumbosacral Plexopathies 185
Peripheral nerve Root Division Sensation Muscle
Superior gluteal L4,5, S1 Posterior None Gluteus minimus, & medius Tensor fascia lata
Inferior gluteal L5, S1,2 Posterior None Gluteus maximus
Posterior femoral L2,3,4 Posterior Posterior thigh, Nonecutaneous Scrotum/labia
Proximal calf, lower border of gluteus maximus
Sciatic (peroneal) L4,5, Posterior Posterolateral leg, Short head of S1,2 web space between biceps
1st and 2nd toes Femoris, tibialis dorsal/medial leg anterior
Extensor digitorum brevis (EDB) Peroneus tertius, brevis and longus
Sciatic (tibial) L4,5, Anterior Posterior leg, lateral Long head of S1,2,3 foot, sole foot biceps,
Semi-membranous, SemitendinosusAdductor magnus, Plantaris,Popliteus, Gastrocnemius, Tibialis posterior Soleus, Flexor digitorum longus, Flexor, hallucis longus
Table 19.2 The sacral plexus
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Sensory Nerve Conduction Studies
The sensory nerve is a more sensitive indicator of injury to the plexus than the motornerve response. The sensory nerve distal latency and conduction velocity are usuallynormal in plexus lesions; however, the sensory nerve action potential (SNAP) amplitudemay be decreased in lesions affecting the plexus. With mild lesions of the lumbar orsacral plexus, the SNAP amplitude may be unaffected. With increasing severity of injuryto the plexus the amplitude of the appropriate SNAPs may be decreased or absent. TheSNAP amplitude is a summation of individual functioning sensory axons. In order foran axon to function it must be in contact with the sensory root cell body. This is alsocalled the dorsal root ganglion (Fig. 19.5).
Lesions that are proximal to this cell body, such as radiculopathies and nerve rootavulsions, do not interfere with the trophic function of the cell body on the sensorynerves derived from that root. Therefore lesions proximal to the dorsal root ganglionhave intact sensory nerve electrical function. This results in normal SNAP parameters evenin the presence of sensory loss. Lesions distal to the dorsal root ganglion disconnect thesensory nerve cell body from its axons. This results in death of the disconnected axonsbecause they are deprived of the nutrition that they need to survive. Depending on theseverity of the lesion this may result in a decrement or absence of the SNAP amplitude.The differentiation of preganglionic and postganglionic lesions is extremely important.Although both lesions may present with numbness and sensory loss in a defineddistribution, the nerve root avulsion usually portends a poorer prognosis because theseinjuries do not undergo spontaneous regeneration and are usually not amenable tosurgical repair. The postganglionic lesions have a more favorable prognosis.
Motor Nerve Conduction Studies
In general, with lumbosacral plexopathies, the motor latencies and velocities are withinnormal limits. The compound muscle action potential (CMAP) amplitudes are usuallynot affected unless the injury is severe. With severe injuries to the plexus there may be areduction in the amplitude of the corresponding CMAP. As with the brachial plexus, whenCMAP amplitudes are affected, they are generally a better indicator of the extent of axonalloss than SNAP abnormalities. Side to side amplitude differences can give an approx-imation of the degree of axonal injury during the first few months following injury. Forexample, a 70% decrement in CMAP amplitude roughly correlates to a 70% axon loss.The motor latencies and conduction velocities are usually unaffected by a lumbar or sacral
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Dorsal root
Dorsal root ganglion
Dorsal ramus
Ventral ramus
Ventral root
Figure 19.5 Inorder for an axonto function itmust be incontact with thesensory root cellbody (also calledthe dorsal rootganglion).
lesion, because they are a function of the fibers that are intact and do not reflect abnormalconduction across the plexus. One should be cautioned that due to normal wear and tearand day-to-day trauma, atrophy of intrinsic foot muscles and side-to-side amplitudedifferences are not that unusual, even in asymptomatic individuals. For this reason,amplitude differences of less than 50% may not be significant, depending on the clinicalpicture.
Late Responses
Most lesions of the lumbosacral plexus are incomplete and have many areas of normalconduction across the lumbosacral plexus. The lesion may be so localized that the affect ofthe lesion is ‘diluted’ along the neural path of transmission of the H-reflex and F-wave.Therefore, H-reflexes and F-waves are usually not helpful in the diagnosis of plexopathies.
EMG
Your findings on the history and physical examination will help guide you in deter-mining which muscles to examine electromyographically. Refer to Tables 19.1 and 19.2to help design your study. Electrodiagnostic findings in plexopathies may include fibril-lations and positive sharp waves in all muscles innervated distal to the lesion. In chroniclesions, motor unit action potentials may demonstrate long duration, high amplitude,and polyphasic potentials. Recruitment is usually decreased in all affected muscles.
The clinical manifestations of an injury to the plexus are apparent at onset but theelectromyographic findings may take up to three weeks to develop. It is important thatthe test be delayed three weeks after the onset of injury so that Wallerian degeneration ofthe distal parts of the injured nerves occurs – this allows for the development of fibril-lation potentials and positive sharp waves. Testing prior to that time-frame can yieldconfusing and misleading data. Lumbar paraspinals are expected to be normal in lumbarand sacral plexus lesions because the paraspinal muscles are innervated by the posteriorrami, and the plexus is innervated by the anterior rami of the spinal nerve.
A classic lumbar plexus injury may have decreased saphenous, femoral and lateralfemoral cutaneous amplitudes, with intact latencies and conduction velocities. In addition,EMG would reveal muscle membrane instability in the vastus medialis obliquus, adductorbrevis, sartorius and iliopsoas. The lumbar paraspinal muscles would test normal in a purelumbar plexopathy. By using these guidelines, a thorough electrodiagnostic evaluation ofthe lumbosacral plexus can be planned and carried out with a minimum of discomfort tothe patient.
Summary
In summary, the electrodiagnostic findings in lumbosacral plexopathy may include:
1. Decreased SNAP amplitude2. Decreased CMAP amplitude3. Normal EMG findings in the paraspinal mucles4. Abnormal spontaneous activity (fibs and PSWs) in muscles distal to the level of the
injury
19 Lumbosacral Plexopathies 187
20Motor Neuron Diseases
Lyn Weiss
Motor neuron diseases represent a group of diseases with the primary pathology locatedin the spinal cord and affecting both upper and/or lower motor neurons. They includepoliomyelitis, amyotrophic lateral sclerosis (ALS), progressive muscular atrophy, pro-gressive lateral sclerosis and progressive bulbar palsy. Although many of these diseasesaffect both upper and lower motor neurons, only the injury to the lower motor neuronscan be assessed with electrodiagnostic testing.
The diagnosis of motor neuron disease is based on the electrodiagnostic findings inconjunction with the physical examination, neuroimaging, and laboratory studies. Thegoal of electrodiagnostic studies is to assess for lower motor neuron dysfunction inclinically affected regions as well as in regions that are clinically unaffected.1 The gravityand significance of a diagnosis of motor neuron disease is of such magnitude that if thisdiagnosis is suspected, referral to a physician with significant experience in this area isrecommended.
Clinical Presentation
Patients with motor neuron diseases typically present with findings of both upper andlower motor neuron abnormalities on physical examination. The exceptions to this wouldbe poliomyelitis and progressive muscular atrophy, which affect only the lower motorneurons, and progressive lateral sclerosis, which affects only the upper motor neurons.Signs and symptoms of upper motor neuron involvement may include spasticity, stiffnessand impaired motor control. Signs and symptoms of lower motor neuron involvementmay include muscle atrophy, weakness, flaccidity, fasciculations and cramps.
Anatomy
As stated above, motor neuron diseases can affect either the upper and/or the lower motorneuron. These disorders are specific for the motor system affecting the motor cortex,corticospinal (motor) tracts and the anterior horn cells. There is usually no significantsensory or cognitive effect.
Electrodiagnostic Findings
Sensory Nerve Conduction Studies
Because motor neuron diseases affect the anterior horn cell and not the dorsal rootganglion, sensory nerve action potentials should show normal amplitude and conductionvelocities. 189
!
!
!
Motor Nerve Conduction Studies
Compound muscle action potential (CMAP) latencies and conduction velocities shouldbe normal, as the myelin is intact. Because of axon loss, the amplitude of the CMAPsmay be markedly reduced. If there is severe axonal loss, some of the fastest fibers maybe lost. Therefore, one may see mildly increased latency and decreased conductionvelocity, but the amount of slowing should not exceed about 20% of normal.
Late Responses
F-waves and H-reflexes are generally not helpful in the diagnosis of motor neuron diseaseas they are non-specific, however they can be beneficial in ruling out other diagnoses.
EMG
In order to diagnose a disease of the anterior horn cells, three limbs, or two limbs andbulbar muscles should show spontaneous potentials (fibs or positive sharp waves). Bothproximal and distal muscles corresponding to various myotomal distributions should betested. Fasciculation potentials as well as complex repetitive discharges (CRDs) may beobserved. Motor unit action potentials (MUAPs) may be of long duration, increasedpolyphasicity and large amplitude, indicating reinnervation. Decreased recruitment shouldbe noted.
Summary
The electrodiagnostic findings in motor neuron diseases may include the following:
1. Normal SNAP amplitude and conduction velocity.2. CMAPs have decreased amplitude with normal (or mildly increased) latency and
normal (or mildly decreased) conduction velocity.3. EMG will demonstrate spontaneous potentials (fibs and PSWs) in affected muscles.
Fasciculations and CRDs may also be noted. MUAPs may show increased duration,large amplitude polyphasic potentials if reinnervation has occurred. There will bedecreased recruitment as well. Remember to test at least three limbs, or two limbsand bulbar muscles.
REFERENCE
1. Misulis K. Essentials of Clinical Neurophysiology. London: Butterworth-Heinemann,1997.
Easy EMG190
!
!
21How to Write a Report
Lyn Weiss
Writing a meaningful report will help convey your findings to the referring physician.Most reports contain the following information:
1. Patient’s name, identification number (if applicable), date of test, name of physicianperforming the test, and referring physician.
2. Brief history and physical. 3. Table of findings (usually printed out from the tabular data). This is important in case
the test needs to be repeated at a later date. Results can be compared for electro-physiological improvement or progression.
4. Findings. The pertinent findings should be discussed. Specific nerve or muscleabnormalities can be discussed.
5. Conclusion. The conclusion should be written with the referring physician’s reasonfor the testing kept in mind.
Findings
For each motor nerve tested, the latency, amplitude (and/or area under the curve) andconduction velocity should be reported. Since the tabular data is usually included as partof the report, specific numbers are usually not necessary in this section of the report. It ishelpful if the tabular printout flags abnormal values or alternatively labels individualnerves as increased, decreased or normal. Abnormal findings should be highlighted inthis area. Abnormalities can be recorded as increased or decreased. In instances ofsevere abnormalities, when a number is far outside the normal range, (i.e. median distalmotor latency of 8.2 msec or an amplitude decrement of 80%) it would be appropriate tomention it.
For each sensory nerve tested, amplitude and distal latency or conduction velocityshould be recorded. Once again, if this is a tabular printout these do not need to be listedagain. Abnormalities, however, should be noted. These can be reported as increased,decreased, or normal. Note that since the sensory response contains no myoneuraljunction, the latency reflects the conduction velocity. In motor nerves, this myoneuraljunction must be ‘factored out’ by obtaining two latencies (proximal and distal). If asensory latency is reported instead of a velocity, the distance that was used (and whetherthat latency was measured to peak or onset) must be specified.
Since we are usually determining the sensory conduction velocity based on thelatency, it is imperative to accurately measure the distance from the stimulator to theactive electrode.
191
!
EMG Findings
For EMG findings, report on insertional activity, activity at rest, MUAP (motor unitaction potential) morphology and recruitment.
Insertional Activity
Increased insertional activity exists when there is a run of fibrillation potentials orpositive sharp waves that only briefly persist beyond needle movement. (In order to beconsidered true fibrillation potentials or positive sharp waves, the waves shouldpersist.) This is a somewhat subjective component and its accurate determination isdependent on the experience of the electromyographer. Myotonic discharges may alsobe noted on insertional activity. These are discharges that wax and wane in frequencyand amplitude.
Spontaneous Activity
There are a variety of potentials that may be noted when the needle is at rest in themuscle. These potentials (and their significance) are described in Chapter 5.
Easy EMG192
Motor nervesA. LatencyB. AmplitudeC. Conduction velocity
Sensory nervesA. AmplitudeB. Conduction velocity or distal latency
Needle studyA. Insertional activity
Increased (denervated muscle, myotonic discharges)Decreased (atrophy)Normal
B. Spontaneous activityMuscle generated
Fibrillation potentialsPSWsMyotonic dischargesComplex repetitive discharges
Neurally generatedFasciculations
Myokymic dischargesCramps Neuromyotonic dischargesTremorMultiples
C. MUAP morphologyDurationPolyphasicityAmplitude
D. RecruitmentIncreased firing frequency (decreased recruitment)EarlyNormal
Table 21.1 EMG/NCS Reporting
21 How to Write a Report 193
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The
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rig
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e w
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s as
a h
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ph
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Phys
ical
Exa
min
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Up
on
ph
ysic
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xam
inat
ion
th
e p
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nt
app
eare
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an
d o
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to
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son
, pla
ce a
nd
tim
e an
d w
as in
no
acu
te d
istr
ess.
Th
ere
was
no
atr
op
hy
no
ted
in b
ilate
ral t
hen
ar a
nd
hyp
oth
enar
reg
ion
s. T
her
e w
as f
ull
ran
ge
of
mo
tio
n o
f b
oth
up
per
ext
rem
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s. M
oto
r ex
am o
fb
ilate
ral u
pp
er e
xtre
mit
ies
reve
aled
5/5
str
eng
th t
o a
ll u
pp
er e
xtre
mit
y m
usc
les
exce
pt
rig
ht
gri
p w
as 4
/5. T
her
e w
as a
po
siti
ve T
inel
’ssi
gn
elic
ited
at
the
rig
ht
wri
st. P
hal
en’s
tes
t w
as p
osi
tive
on
th
e ri
gh
t. U
po
n c
ervi
cal e
xam
inat
ion
th
ere
was
ver
y m
ild p
arav
erte
bra
lm
usc
le s
pas
m b
ilate
rally
. Sp
url
ing
’s t
est
was
neg
ativ
e b
ilate
rally
.
Fig
ure
21.
1Sa
mp
le R
epo
rt
Easy EMG194
SAM
PLE
REP
OR
T (c
on
t’d
)
ELEC
TRO
DIA
GN
OST
IC R
ESU
LTS:
Site
N
R
On
set
No
rm
O-P
N
orm
Se
gm
ent
Dis
t V
el
No
rm
(ms)
O
nse
t A
mp
A
mp
N
ame
(cm
) (m
/s)
Vel
(m
s)
(mV
)(m
V)
(m/s
)
Left
Med
ian
(A
bd
Po
ll B
rev)
W
rist
3.
36
<4.
2 10
.43
>4.
0 El
bo
w-W
rist
18
.5
52.5
6 >
50.0
El
bo
w
6.88
11
.00
>4.
0
Rig
ht
Med
ian
(A
bd
Po
ll B
rev)
W
rist
4.
61
<4.
2 12
.00
>4.
0 El
bo
w-W
rist
16
46
.51
>50
.0
Elb
ow
8.
05
12.3
4 >
4.0
Left
Uln
ar (
Ab
d D
ig M
in)
Wri
st
2.81
<
3.4
9.19
>
4.0
B E
lbo
w-W
rist
15
64
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>50
.0
B E
lbo
w
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6.
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>4.
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Elb
ow
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lbo
w
12
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>
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Fig
ure
21.
1(c
on
t’d
)
21 How to Write a Report 195
SAM
PLE
REP
OR
T (c
on
t’d
)
Sen
sory
Ner
ves
Site
N
R
On
set
No
rm O
nse
t O
-P A
mp
N
orm
Am
p
Seg
men
t N
ame
Dis
t (c
m)
Vel
(m
/s)
No
rm V
el
(ms)
(m
s)
(μV
) (μ
V)
(m/s
)
Left
Med
ian
Sen
D2
(2n
d D
igit
) M
id P
alm
0.
91
50.2
1 >
20.0
M
id P
alm
-2n
d D
igit
6
65.9
3 >
45.0
W
rist
2.
28
38.2
0 >
20.0
W
rist
-2n
d D
igit
12
52
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>44
.0
Rig
ht
Med
ian
Sen
D2
(2n
d D
igit
) M
id P
alm
0.
88
43.0
1 >
20.0
M
id P
alm
-2n
d D
igit
6
68.1
8 >
45.0
W
rist
3.
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18.3
4 >
20.0
W
rist
-2n
d D
igit
12
38
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>44
.0
Left
Uln
ar S
en (
5th
Dig
it)
Wri
st
2.34
23
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>18
.0
Wri
st-5
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igit
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.0
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Rig
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en (
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Wri
st
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>18
.0
Wri
st-5
th D
igit
14
.0
56.6
8
EMG
Sid
e M
usc
le
Ner
ve
Ro
ot
Ins
Act
PS
W
Fib
s A
mp
Po
ly
Fasc
ic
Rec
rt
Pt C
oo
p
Co
mm
ent
Rig
ht
Ab
d P
oll
Bre
v M
edia
n
C8-
T1
Nm
l 0
0 N
ml
0 0
Nm
l N
ml
Rig
ht
1st
Do
r In
t U
lnar
C
8-T1
N
ml
0 0
Nm
l 0
0 N
ml
Nm
l R
igh
t C
erv
Para
C6
Ram
i C
6 N
ml
0 0
Nm
l 0
0 N
ml
Nm
l R
igh
t C
erv
Para
C7
Ram
i C
7 N
ml
0 0
Nm
l 0
0 N
ml
Nm
l
Elec
tro
dia
gn
ost
ic E
valu
atio
n:
Ner
ve c
on
du
ctio
n s
tud
y o
f th
e m
oto
r an
d s
enso
ry d
ivis
ion
s o
f b
ilate
ral m
edia
n a
nd
uln
ar n
erve
s w
as d
on
e. R
igh
t m
edia
n c
om
po
un
dm
oto
r ac
tio
n p
ote
nti
al (
CM
AP)
sh
ow
ed in
crea
sed
dis
tal l
aten
cy w
ith
no
rmal
am
plit
ud
e an
d c
on
du
ctio
n v
elo
city
. Th
e le
ft m
edia
n a
nd
bila
tera
l uln
ar n
erve
CM
APs
sh
ow
ed n
orm
al d
ista
l lat
ency
, am
plit
ud
e an
d c
on
du
ctio
n v
elo
city
.
Fig
ure
21.
1(c
on
t’d
)
Easy EMG196
SAM
PLE
REP
OR
T (c
on
t’d
)
Rig
ht
med
ian
sen
sory
ner
ve a
ctio
n p
ote
nti
al (
SNA
P) s
ho
wed
dec
reas
ed a
mp
litu
de
and
slo
wed
co
nd
uct
ion
vel
oci
ty a
cro
ss t
he
wri
st. T
he
left
med
ian
an
d b
ilate
ral u
lnar
SN
APs
sh
ow
ed n
orm
al a
mp
litu
de
and
co
nd
uct
ion
vel
oci
ty.
Mo
no
po
lar
nee
dle
EM
G o
f th
e ri
gh
t ce
rvic
al p
aras
pin
al m
usc
les
and
rig
ht
abd
uct
or
po
llici
s b
revi
s an
d fi
rst
do
rsal
inte
ross
eou
s m
usc
les
was
per
form
ed. E
MG
of
the
mu
scle
s sh
ow
ed n
orm
al in
sert
ion
al a
ctiv
ity
wit
h n
o s
po
nta
neo
us
acti
vity
at
rest
, no
rmal
mo
tor
un
it a
ctio
np
ote
nti
al m
orp
ho
log
y an
d n
orm
al r
ecru
itm
ent
pat
tern
.
Imp
ress
ion
:Th
is s
tud
y sh
ow
ed e
lect
rod
iag
no
stic
evi
den
ce o
f ri
gh
t m
edia
n n
erve
dem
yelin
atin
g n
euro
pat
hy
acro
ss t
he
carp
al t
un
nel
invo
lvin
g b
oth
mo
tor
and
sen
sory
fib
ers.
Th
ere
are
no
sig
ns
of
den
erva
tio
n in
th
e ri
gh
t ab
du
cto
r p
olli
cis
bre
vis
mu
scle
. Th
is is
co
nsi
sten
t w
ith
rig
ht
mild
-to
-mo
der
ate
carp
al t
un
nel
syn
dro
me.
Than
k yo
u f
or
the
cou
rtes
y o
f th
is r
efer
ral.
––––
––––
––––
––––
––––
––––
––A
. Res
iden
t, M
DR
esid
ent
Phys
icia
n
I hav
e p
erfo
rmed
th
is t
est
wit
h t
he
resi
den
t an
d a
gre
e w
ith
th
e ab
ove
inte
rpre
tati
on
an
d c
on
clu
sio
n.
––––
––––
––––
––––
––––
––––
––A
. Att
end
ing
, M.D
.A
tten
din
g P
hys
icia
n
Fig
ure
21.
1(c
on
t’d
)
21 How to Write a Report 197
R
T
P
O
R
T
P
O
RR
R
T
T
T
P
P
P
O
O
O
R
R
T
T
P
O
RT
P
P
O
O
Left Median Mot
5000 (uV
Left Ulnar Mot
Elbow
Wrist Wrist
Wrist
Wrist
5 (ms 5 (ms
Right Ulnar Sen Sens
2 (ms 2 (ms20 (uV 20 (uV)
Mid Palm
Left Median Sen D2 Sens
A Elbow
B Elbow
Left Median Motor
5000 (μV)
Left Ulnar Motor
Elbow
Wrist Wrist
Wrist
Wrist
5 (ms) 5 (ms)
Right Ulnar Sen Sensory
2 (ms) 2 (ms)20 (μV) 20 (μV)
Mid Palm
Left Median Sen D2 Sensory
A Elbow
B Elbow
5000 (uV
5000 (uV
Elbow
Wrist
Wrist
Wrist
Wrist
5 (ms)
5 (ms)2 (ms)
2 (ms)
20 (uV
20 (uV
Mid Palm
A Elbow
B Elbow
Left Ulnar Sen Senso Right Median Mot
Right Median Sen D2 SensRight Ulnar Mot
5000 (μV)
5000 (μV)
R
R
T
T
P
O
O
RT
P
P
O
R
R
R
T
T
T
P
P
P
O
O
O
R
P
O
R
T
T
P
O
Elbow
Wrist
Wrist
Wrist
Wrist
5 (ms)
5 (ms)2 (ms)
2 (ms)
20 (μV)
20 (μV)
Mid Palm
A Elbow
B Elbow
Left Ulnar Sen Sensory Right Median Motor
Right Median Sen D2 SensoryRight Ulnar Motor
A
B
Figure 21.1(cont’d)
Motor Unit Action Potentials
Motor unit action potentials (MUAPs) should be classified as normal or abnormal basedon their morphology (appearance). If abnormal, the reason for the abnormality shouldbe indicated. Abnormalities could include duration, phases and/or amplitude.
Motor Unit Recruitment
Recruitment abnormalities should be noted. For example, if there are few functioningmotor units the remaining functioning units will fire at a higher frequency without otherunits being recruited. This abnormal (delayed) recruitment should be noted.
Table 21.1 summarizes the findings to be reported on in an NCS/EMG report.
Conclusion
Assuming you have completed a thorough electrodiagnostic examination, you want thepertinent information relayed to the referring physician. The conclusion should summarizeyour findings. Negative findings are sometimes also important. For example, a referringphysician is requesting an EMG to rule out carpal tunnel syndrome. You find no evidenceof carpal tunnel syndrome but you do find a C6 radiculopathy. It would be important tonote that there is no electrodiagnostic evidence of carpal tunnel syndrome. (The term‘electrodiagnostic evidence’ is important because although there may be clinical signsof nerve disorder, your conclusion should only report what the electrodiagnostic testreveals.)
Suggestions for possible treatments or interventions can be included in the report, butit is up to the referring physician to implement those suggestions. If further electro-diagnostic testing is indicated at a later time to help prognosticate, this should also bedocumented in the conclusion.
The sample report1 (Fig. 21.1) is an example of how electrodiagnostic reports can bewritten.
REFERENCE
1. Dumitru D. Electrodiagnostic Medicine. Philadelphia: Hanley & Belfus, 1995, p. 240.
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22Tables of Normals
Lyn Weiss, David Khanan, Chaim Shtock
It should be noted that each electrodiagnostic laboratory should develop its ownstandardized normal values. These tables should be used as a reference.
REFERENCES
1. Kimura J. Electrodiagnosis in Diseases of Nerve and Muscle, 2nd edn. New York:Oxford University Press, 1989.
2. Randall L, Braddom M. Physical Medicine and Rehabilitation. New York: WBSaunders, 1996.
3. DeLisa JA, Lee HJ, Baran EM, Lai K. Manual of Nerve Conduction Velocity andClinical Neurophysiology, 3rd edn. New York: Raven Press, 1994.
4. Geiringer SR. Anatomic Localization for Needle Electromyography, 2nd edn.Philadelphia: Hanley & Belfus, 1999.
5. Tan JC. Practical Manual of Physical Medicine and Rehabilitation. New York: Mosby,1998.
6. O’Young B. PM&R Secrets. Philadelphia: Hanley & Belfus, 1996. 7. DeLisa JA. Rehabilitation Medicine, 2nd edn. New York: Williams & Wilkins, 1988.8. Dumitru D. Electrodiagnostic Medicine, 2nd edn. Philadelphia: Hanley & Belfus,
2002.
199
Easy EMG200
Ner
veA
ctiv
e el
ectr
od
eSt
imu
lati
on
sit
eD
ista
nce
(cm
)O
nse
t la
ten
cy (
ms)
Am
plit
ud
e (m
V)*
*Se
gm
ent
nam
eV
elo
city
m/s
fro
m a
ctiv
e to
(met
ers/
sec)
1s
t st
imu
lati
on
sit
e
Med
ian
Ab
du
cto
r p
olli
cis
bre
vis
Wri
st8
<4.
2>
4.0
Elb
ow
-wri
st>
50.0
Elb
ow
>4.
0
Uln
arA
bd
uct
or
dig
iti m
inim
iW
rist
8<
3.4
>4.
0B
elo
w e
lbo
w (
BE)
>
4.0
BE-
wri
st>
50.0
Ab
ove
elb
ow
(A
E)>
4.0
AE-
BE
>50
.0
Rad
ial
Exte
nso
r in
dic
is p
rop
riu
s Fo
rear
m4
2.4
±0.
514
±8.
8A
E-EI
P61
.6 ±
5.9
Erb
’s p
oin
tEr
b’s
po
int-
AE
72 ±
6.3
Mu
scu
lo-
Dis
tal t
o m
idp
oin
t Er
b’s
po
int
23.5
–41.
54.
5 ±
0.6
Erb
’s p
oin
t-cu
tan
eou
sB
icep
s b
rach
iiB
icep
s b
rach
ii
Axi
llary
Mid
dle
del
toid
Erb
’s p
oin
t14
.8–2
6.5
3.9
±0.
5Er
b’s
po
int-
del
toid
*Ski
n t
emp
erat
ure
sh
ou
ld b
e m
ain
tain
ed a
t 32
ºC.
**Si
de
to s
ide
amp
litu
de
dif
fere
nce
of
>50
% is
sig
nif
ican
t, o
r >
20%
am
plit
ud
e d
rop
dis
tal t
o p
roxi
mal
is s
ign
ific
ant.
Tab
le 2
2.1
Up
per
ext
rem
ity
– m
oto
r*
Ner
veA
ctiv
e el
ectr
od
eSt
imu
lati
on
sit
eD
ista
nce
(cm
)O
nse
tA
mp
litu
de
μV
Seg
men
t n
ame
Vel
oci
tyla
ten
cy (
ms)
(m
icro
volt
s)(m
/s)
Med
ian
2nd
dig
it
Mid
pal
m7
<1.
9>
20.0
Mid
pal
m–2
nd
dig
it
>45
.0W
rist
7<
3.5
>20
.0W
rist
–mid
pal
m>
45.0
Uln
ar5t
h d
igit
Wri
st14
<3.
1>
18.0
Wri
st–5
th d
igit
>44
.0B
elo
w e
lbo
w>
15.0
Bel
ow
elb
ow
–wri
st>
53.0
Ab
ove
elb
ow
>14
.0A
bo
ve e
lbo
w–b
elo
w e
lbo
w>
54.0
Sup
erfi
cial
1st
do
rsal
1.8
±0.
331
+ 2
0 (1
3–60
)ra
dia
lw
eb s
pac
e14
2.1
±0.
331
+ 2
0 (1
3–60
)1s
t W
eb s
pac
e–Fo
rear
m2.
4 ±
0.3
31 +
20
(13–
60)
fore
arm
Late
ral
Fore
arm
Elb
ow
121.
8 ±
0.1
24.0
±7.
2 (1
2–50
)Fo
rear
m–e
lbo
w65
±3.
6an
teb
rach
ial
(1.6
–2.1
)
*Ski
n t
emp
erat
ure
sh
ou
ld b
e m
ain
tain
ed a
t 32
ºC.
Tab
le 2
2.2
Up
per
ext
rem
ity
– se
nso
ry*
22 Tables of Normals 201
Ner
veA
ctiv
e el
ectr
od
eSt
imu
lati
on
sit
eD
ista
nce
(cm
)O
nse
t la
ten
cy (
ms)
Am
plit
ud
e (μ
V)
Seg
men
t n
ame
Vel
oci
ty (
m/s
)(m
icro
volt
s)
Pero
nea
lEx
ten
sor
dig
ito
rum
bre
vis
An
kle
Fib
hea
d?8
?<5.
5?>
2.5
Fib
ula
r h
ead
–an
kle
>40
.0Po
plit
eal
Pop
litea
l–fi
bu
lar
hea
d>
40.0
Post
tib
ial
Ab
du
cto
r h
allu
cis
An
kle
10<
6.0
>3.
0K
nee
–an
kle
>40
.0K
nee
*Ski
n t
emp
erat
ure
sh
ou
ld b
e m
ain
tain
ed a
t 30
ºC.
Tab
le 2
2.3
Low
er e
xtre
mit
y –
mo
tor*
Ner
veA
ctiv
e el
ectr
od
eSt
imu
lati
on
sit
eD
ista
nce
(cm
)O
nse
t la
ten
cy (
ms)
Am
plit
ud
e (μ
V)
Seg
men
t n
ame
Vel
oci
ty (
m/s
)(m
icro
volt
s)
Sura
lLa
tera
l mal
leo
lus
Cal
f14
<3.
8>
10.0
Cal
f–la
tera
l mal
leo
lus
>36
.0
Late
ral
1cm
med
ial t
oA
nte
rio
r th
igh
12–1
62.
6 ±
0.2
10–2
5A
SIS–
ante
rio
r th
igh
47.9
±3.
7fe
mo
ral
ante
rio
r su
per
ior
cuta
neo
us
iliac
sp
ine
(ASI
S)
Sup
erfi
cial
An
teri
or
to la
tera
lA
nte
rola
tera
l cal
f14
3.4
±0.
418
.3 ±
8.0
Late
ral m
alle
olu
s to
cal
f51
.2 ±
5.7
per
on
eal
mal
leo
lus
*Ski
n t
emp
erat
ure
sh
ou
ld b
e m
ain
tain
ed a
t 30
ºC.
Tab
le 2
2.4
Low
er e
xtre
mit
y –
sen
sory
*
Easy EMG202
Site Active Latency (ms) Stimulation site
Medial Halfway from mid 28.0–35.0 Popliteal fossa (cathode gastrocnemius popliteal crease – proximal)soleus muscle proximal flare use submaximal
medial malleolus stimulation
*Skin temperature should be maintained at 30ºC.
Table 22.5 H-reflex* (see nomogram for normal values – Table 4.1)
Motor nerve Pick-up site F-latency (ms) F-ratio*
Median Abductor pollicis brevis Wrist 29.1 ± 2.3 0.7 < F < 1.3Elbow 24.8 ± 2.0Axilla 21.7 ± 2.8
Ulnar Abductor digiti minimi Wrist 30.5 ± 3.0 0.7 < F < 1.3BE 26.0 ± 2.0AE 23.5 ± 2.0Axilla 11.2 ± 1.0
Peroneal Extensor digitorum brevis Ankle 51.3 ± 4.7 0.7 < F < 1.3Knee 42.7 ± 4.0
Tibial Abductor hallucis Ankle 52.3 ± 4.3 0.7 < F < 1.3
Knee 43.5 ± 3.4
* F-ratio = (as measured at elbow or knee)
where F = F-wave latency, M = wave latency.
F – M – 12M
Table 22.6 F-waves and F-ratio upper extremities
23Reimbursement
Jay Weiss
This chapter is written to provide guidelines for electrodiagnostic reimbursement issues.It is difficult, in a few pages, to adequately cover all aspects of this topic. Two terms mustbe defined when discussing reimbursement – coding and billing. There are books andjournals that deal exclusively with these issues. Coding is the process of transformingdiagnoses and procedures into numeric codes, while billing is the process of transmittingthe correct diagnosis and procedure codes to the payer. This chapter will cover the mostcommonly used electrodiagnostic procedures. Every effort has been made to use codesthat are current as of the date of publication, however the codes used can and do changeover time. Therefore, it is incumbent upon the physician to remain up to date on currentacceptable coding and billing practices.
The electrodiagnostic evaluation is a complex, time-consuming examination requiringreal-time interpretation of data and continual reassessment and modification of whichnerves and muscles are to be tested. It also requires highly specialized computerizedequipment, and complete familiarity with the technology. As such, it should be appro-priately reimbursed for a test requiring this level of skill, training, knowledge, time andequipment.
The electrodiagnostic consultation is an extension of the neurologic portion of thephysical examination. It is essential for the electromyographer to perform a history andphysical examination as part of the study. If such an examination is performed anddocumented, it would be entirely appropriate to bill for the examination under theMedical Evaluation and Management Codes. These are the same codes used to describeoffice visits and consultations. Usually, Codes 99242–4 would be used.
Before we discuss billing we must tackle the issue of coding. Most insurancecompanies and Medicare carriers require all listed procedures and diagnoses to beprovided in the form of numeric codes, because computers can more easily processthese codes (rather than narrative descriptions). The importance of proper codingcannot be overstated. Insurance carriers will deny or reimburse electrodiagnosticprocedures based on the diagnostic code used. Often there are several diagnosis codesthat may fit a clinical picture. There are generalized codes for pain or numbness in a limband more specific codes for peripheral entrapments or radiculopathies. In instanceswhere there is neck pain and clinical evidence of radiculopathy, it is more important touse the radiculopathy code than the neck pain code because generic neck pain may ormay not merit electrodiagnostic studies but radiculopathies most often will. Therecan be (and frequently is) more than one diagnostic code that is used.
203
Where Do These Codes Come From?
There are two books that are necessary for proper coding. For diagnosis codes, the bookis called ICD-9 CM (International Classification of Diseases, 9th Edition1). ICD-9 codesgenerally do not change from year to year. The second book is the Current ProceduralTerminology2 (CPT) book that is published annually by the American MedicalAssociation (AMA) and attempts to most accurately describe procedures. For the mostcommonly used electrodiagnostic codes, see Table 23.1. The AMA’s CPT Manualfrequently eliminates, revises and/or creates new codes. As a practical matter, someinsurance carriers or systems may not recognize all current CPT codes; some may useeliminated codes. In specific instances it may be necessary to discuss individual codingquestions with the carrier to find their closest acceptable code.
Using the Procedure Codes
When billing for nerve studies it should be remembered that 95900 and 95904 are usedfor each nerve and therefore each code can be used more than once. Multiple stimulationsites on the same nerve are all part of one nerve study and should only be coded once. Inother words, a median motor nerve study with electrodes over the abductor pollicisbrevis and stimulations at the wrist, elbow, axilla and Erb’s point counts as one nervestudy. Median motor and sensory studies of both upper extremities and ulnar motor andsensory studies of both upper extremities would correctly be coded as 95900 four timesand 95904 four times. If there were F-wave studies performed on both ulnar nerves (inaddition to the median and ulnar motor and sensory nerves) then the proper billingwould be:
95900 × 2 for the right and left median motor studies95903 × 2 for the right and left ulnar motor nerve studies with F-waves95904 × 4 for the right and left median and right and left ulnar sensory
studies.
The 95860, 95861, 95863, 95864 codes include all muscles examined in an extremityalong with related paraspinal areas. The CPT manual is not specific as to whatconstitutes an extremity however; if only one or two muscles are examined it isprobably most appropriate to code this as 95870 – limited study of muscles in oneextremity. Medicare requires that five muscles be examined to bill for an extremity.
Most carriers permit (and encourage) electronic submission. In these instances yourdiagnosis and procedure codes are the only information the carrier will receive fromyou. Some carriers may request additional documentation. In other instances the carriermay not realize that a Code (95900 – as an example) can be billed four times and they mayonly reimburse one study. A review of the explanation of benefits portion of the claim mayshow that a code was denied three times as ‘repeat study’ or ‘previously billed’. Ininstances such as these it would be helpful to send your report along with a copy of theCPT page noting that the code is ‘per nerve’. You may have to educate the carrier or theclaims representative as to the definitions of codes.
While it is the physician’s decision to determine his or her own fees for procedures,in many instances (including Medicare and managed care plans), a physician agrees toaccept a predetermined fee schedule. In cases of Workers’ Compensation and motorvehicle accidents most states have fixed fee schedules. The practitioner should be awareof the current testing fees in use in his or her geographic area.
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Who Can Perform Testing?
The details of electrodiagnostic studies are discussed elsewhere in this text. In terms ofreimbursement, it is important to note that a needle EMG test is a dynamic test that isindividualized to the clinical circumstance. The EMG portion of the test must beperformed by a physician, as opposed to a technician, and is interpreted in real-time as itis being performed. During the study, different muscles may or may not be examineddepending on the results of the study to that point. The working diagnosis is continuallymodified and re-examined based on the findings. Therefore the examination may bealtered to confirm or refute different diagnoses.
As opposed to needle EMG, a technician, with physician supervision, can performnerve conduction studies. It is important however, to note that it is the physician whomust dictate the design of the study (choice of nerves) to fit the clinical circumstancesand is ultimately responsible for the analysis of the study. A physician should beavailable to confirm or refute any abnormal or unexpected electromyographic findings.Both the electromyographer and the technician should be aware of the numeroustechnical factors that can give false results.
In general, the EMG data cannot be recorded in order to be independently reviewedand separately interpreted as can, for instance, an MRI of the spine. In this way it isdifferent from many other diagnostic tests. It is most similar to a physical examinationwhere the only recording of the data is by the physician’s independent record of theencounter. Thus, it can be seen that the validity of any electrodiagnostic study is totallydependent on the knowledge, experience and integrity of the electromyographer reportingthe data.
23 Reimbursement 205
!
95860 Needle electromyography, one extremity with or without relatedparaspinal areas
95861 Needle electromyography, two extremities with or without relatedparaspinal areas
95863 Needle electromyography, three extremities with or without relatedparaspinal areas
95864 Needle electromyography, four extremities with or without relatedparaspinal areas
95867 Needle electromyography, cranial nerve supplied muscles, unilateral95868 Needle electromyography, cranial nerve supplied muscles, bilateral95869 Needle electromyography; thoracic paraspinal muscles95870 Limited study of muscles in one extremity or non-limb (axial) muscles
(unilateral or bilateral), other than thoracic paraspinal, cranial nervesupplied muscles, or sphincters
Nerve conduction studies95900 Nerve conduction, amplitude and latency/velocity study, each nerve;
motor, without F-wave study95903 Nerve conduction, amplitude and latency/velocity study, each nerve;
motor with F-wave study95904 Nerve conduction, amplitude and latency/velocity study, each nerve;
motor with F-wave study, each nerve; sensory95934 H-reflex, amplitude and latency study; record gastrocnemius/soleus muscle95936 Record muscle other than gastrocnemius/soleus muscle
Table 23.1 Current procedural terminology (CPT™) codes in electrodiagnosticmedicine2
Overuse of Studies
An electrodiagnostic consultation can be an expensive battery of tests and unfortunatelythere have been problems with overuse and inappropriate use of electrodiagnosticstudies. The cost of these studies, along with instances of inappropriate use and overuse,make these studies likely to come under close scrutiny. Ultimately, this can lead toinsurance denials or partial denials of payment for appropriate studies. Thus, it isimportant to be sure that the electrodiagnostic study fits the clinical picture.
An ‘adequate’ number of nerve studies and needle insertions insure the greatestdegree of accuracy without undue discomfort or inappropriate expense. EMG testing ofthe extremity should be sufficient to refute or confirm a diagnosis. In most instancesEMG should include the most symptomatic muscle or muscles (generally the weakest).If a symptomatic extremity is normal on EMG, examination of the asymptomaticextremity is not likely to be needed.
Nerve studies should be performed to provide specific information. Generally oneor two motor and sensory nerves are adequate in ruling out a generalized peripheralneuropathy. Beyond that, specific nerves can be helpful in evaluating a peripheralentrapment versus a more proximal lesion. In instances where a diagnosis of rootavulsion is being considered, sensory nerve studies can be crucial. In all cases thereshould be reasons based on the clinical circumstances for the nerve studies performed(Table 23.2).
Peer Review Process
If there are questions as to the appropriateness of electrodiagnostic studies, the AmericanBoard of Electrodiagnostic Medicine (ABEM) recommends the use of a peer reviewprocess. A physician with training in electrodiagnostic medicine should perform thepeer review process for electrodiagnostic studies. Such a physician is almost alwayseither a neurologist or a physiatrist. It is most appropriate for this specialist to be apracticing electromyographer who would therefore utilize the same criteria employed inhis or her clinical practice. The ABEM has guidelines which suggest the number ofnerve studies that should be adequate in greater than 90% of studies for a particulardiagnosis. Studies that exceed these numbers could trigger peer review or other scrutiny(see Table 23.3).
While the actual electrodiagnostic study cannot be reviewed for purposes of confirmingor refuting the findings, a review of electrodiagnostic reports can, in some circumstances,be helpful. A review can address whether there were indications for the testing and it canalso note instances where the study was poorly designed. This can include a study that wastoo limited to fit the clinical circumstances or inadequate in its muscle selection. A reviewcan address whether the conclusions were or were not supported by the data.
Summary
It is not enough merely to be a good electromyographer. The appropriate diagnosesand procedure codes are necessary for obtaining proper reimbursement. Theprocedures performed should fit the clinical circumstances and should be adequatewithout being excessive. The procedures and indications should be adequatelydocumented. By satisfying these criteria, the likelihood of proper reimbursement ismaximized.
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23 Reimbursement 207
Nee
dle
ele
ctro
myo
gra
ph
y N
erve
co
nd
uct
ion
Oth
er e
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rom
yog
rap
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CPT
™ 9
5860
-958
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nd
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ud
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CPT
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, st
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CPT
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, 95
867-
9587
0 95
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959
0495
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36In
dic
atio
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tor
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-ref
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rom
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ith
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ctio
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esti
ng
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ave
(rep
etit
ive
stim
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tio
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Car
pal
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nn
el (
un
ilate
ral)
13
4
Car
pal
tu
nn
el (
bila
tera
l)2
46
Rad
icu
lop
ath
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2
Mo
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ath
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33
2
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ath
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44
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on
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ltip
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Myo
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22
22
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tor
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ron
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.g.,
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42
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2
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rom
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nct
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22
23
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al t
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1
44
syn
dro
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(u
nila
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l)
Tars
al t
un
nel
2
56
syn
dro
me
(bila
tera
l)
Wea
knes
s, f
atig
ue,
cra
mp
s,
23
42
or
twit
chin
g (
foca
l)
Wea
knes
s, f
atig
ue,
cra
mp
s,
44
42
or
twit
chin
g (
gen
eral
)
Pain
, nu
mb
nes
s, o
r 1
34
2ti
ng
ling
(u
nila
tera
l)
Pain
, nu
mb
nes
s, o
r 2
46
2ti
ng
ling
(b
ilate
ral)
Use
d w
ith
per
mis
sio
n ©
200
2 A
AEM
Tab
le 2
3.2
AA
EM r
eco
mm
end
ed p
olic
y fo
r el
ectr
od
iag
no
stic
med
icin
e3 ; dia
gn
osi
s/u
nit
usa
ge
tab
le o
f th
e re
com
men
ded
po
licy
(see
Tab
le 2
3.1)
REFERENCES
1. International Classification of Diseases, 9th Revision, Clinical Modification.Physician ICD-9-CM.2002. AMA Press Chicago; 2001, Ingenix, Inc.
2. Current Procedural Terminology, CPT 2003. AMA Press, Chicago.3. AAEM Recommended Policy for Electrodiagnostic Medicine, Revised 2002.
www.aaem.net/position_statements.htm.
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Glossary of EMG Terms
Action potentialan electrical potential that moves along an axon or muscle fibermembrane.
Action potential morphologythe electrical representation of the nerve stimulation – seen as asmall hill on the screen – commonly called a waveform.
Amplitudethe maximal height of the action potential (can be measuredbaseline to peak or peak to trough); expressed in millivolts (mV) ormicrovolts (μV).
Antidromicwhen the electrical impulse travels in the opposite direction ofnormal physiologic conduction (e.g., conduction of a motor nerveelectrical impulse away from the muscle and toward the spine).
Axonotmesisinjury to the axon of a nerve but not the supporting connectivetissue. Results in Wallerian degeneration distal to the injury.
Compound motor action potential (CMAP)summation of action potentials recorded over a muscle followingstimulation of a motor nerve.
Conduction block failure of an action potential to propagate past an area of injury,generally due to focal demyelination.
Conduction velocity a measure of how fast the fastest part of the impulse travels (canalso be referred to as a motor conduction velocity or a sensoryconduction velocity).
Electrodiagnostic studies includes many tests, e.g., nerve conduction studies (NCS) andelectromyography (EMG) – is a physiological assessment of theelectrical functioning of nerves and/or muscles.
F-wavea compound muscle action potential evoked from antidromicallystimulated motor nerve fibers using a supramaximal electricalstimulus. Generally represents only a small percentage of fibersand therefore much smaller than M-wave. 209
Fasciculation potentialspontaneous electrical potential originating in the nerve and whichcan have the morphology of a motor unit action potential.
Fibrillation potential spontaneous potential found on EMG at rest; biphasic, initiallypositive deflection, originating in the muscle.
Frequencycycles per second (frequently abbreviated Hertz or Hz).
H-reflexa compound muscle action potential evoked through orthodromicstimulation of sensory fibers and orthodromic activation of motorfibers. This is evoked with a submaximal stimulation and disappearswith supramaximal stimulation. It is found in normal adults only inthe gastrocnemius-soleus and flexor carpi radialis muscles. Theresponse is thought to be due to a mono- or oligosynaptic spinalreflex (Hoffmann reflex).
Insertional activity the electrical activity generated as a result of disruption of themuscle membrane by a needle.
Late responsean evoked potential with a latency longer than an M-wave; includesH-reflexes and F-waves.
Latencytime interval between the onset of a stimulus and the onset of aresponse.
M-wavemuscle action potential evoked by stimulating a motor nerve.
Miniature endplate potentialpotential produced spontaneously by the release of one quanta ofacetylcholine from the presynaptic axon terminal.
Motor point where the nerve enters the muscle (endplate zone).
Motor unitincludes the anterior horn cell, its axon, neuromuscular junctionand all the muscle fibers innervated by that axon.
Myokymic dischargemotor unit action potentials that fire repetitively (often referred toas sounding like marching soldiers).
Easy EMG210
Myopathic recruitmentincreased number and early recruitment of motor unit actionpotentials for the strength of contraction; motor units are generallyof small amplitude. Frequently seen in myopathies.
Myotonic dischargehigh frequency discharges whose amplitude and frequency waxand wane (sometimes referred to as ‘dive bombers’).
Nerve conduction studies (NCS)assessment of functioning of nerves via electrical stimulation.
Neurapraxiaa lesion where conduction block is present. The axon remains intact.
Neurotmesisa complete injury of a nerve (such as a transection) involving themyelin, axon and all the supporting structures.
Orthodromicwhen the electrical impulse travels in the same direction as normalphysiologic conduction (e.g., when a motor nerve electrical impulseis transmitted toward the muscle and away from the spine).
Positive sharp waveprimarily monophasic spontaneous potential found on EMG at rest,initially positive deflection with a characteristic ‘V’ formation.
Recruitmentthe orderly addition of motor units with increasing voluntary musclecontraction.
Sensory nerve action potential (SNAP)summation of action potentials recorded from the nerve followingstimulation of a sensory nerve.
Stimulusan electrical depolarization of a nerve initiating an action potential. Astimulus can be supramaximal or submaximal.
Submaximal stimulusan electrical stimulus that results in the initiation of an actionpotential in some (but not all) of the nerve fibers. Increasing theintensity of a submaximal stimulus will change the appearance ofthe CMAP or SNAP.
Supramaximal stimulusan electrical stimulus that results in the initiation of an actionpotential in all of the fibers of the targeted nerve. Increasing the
Glossary of EMG Terms 211
intensity of a supramaximal stimulus will not change the appearanceof the CMAP or SNAP (but may shorten the latency).
Temporal dispersionlong duration, low amplitude potential due to extreme variations inthe conduction velocities of individual nerve fibers contributing tothe action potential.
Easy EMG212
Appendix 1Figures for Table 4.3 Nerveconduction studies setup
213
Reference
Active
Midwriststimulation
Axillastimulation
Elbowstimulation
GroundG d(on dorsum)
Figure A1.1Median nerve –motor.
Figure A1.2Median nerve –sensory(orthodromic).
Ground
Reference 2
Reference 1
Activeelectrode
2
Activeelectrode
1
Ringanode
Ringcathode
Easy EMG214
Ground
Wriststimulation
Handstimulation
Activeelectrode
Referenceelectrode
Figure A1.3Median nerve –sensory(antidromic).
Figure A1.4 Ulnarnerve – motor.
Ground
Activeelectrode
Wrist
Refeerence
AxillaBelow elbow(locate justdistal to theulnar groovewith elbow90º flexed)
Aboveelboww
Appendix 1 Figures for Table 4.3 Nerve conduction studies setup 215
ReferenceActive
electrode
GroundRing
cathodeRing
anode
Figure A1.6 Ulnarnerve – sensory(orthodromic).
Figure A1.5Dorsal ulnarcutaneous nerve –sensory(orthodromic).
Stimulation
Activeelectrode
Referenceelectrode
Ground
Easy EMG216
Stimulation
GroundActive
electrodeReferenceelectrode
Figure A1.7 Ulnarnerve – sensory(antidromic).
Figure A1.8Radial nerve –sensory(antidromic).
Figure A1.9Radial nerve –motor.
Stimulation
Stimulation
Ground
Ground
ferenceRef
Reference
Alternative approachutilizing
ring electrodes
tiveActtrodedelect
Activeelectrode
Elbowstimulation
Activeelectrode
ReferenceReferenceGround
Forearmstimulation
Axillastimulation
Appendix 1 Figures for Table 4.3 Nerve conduction studies setup 217
Reference
Activeelectrode
Ground
Stimulation
Figure A1.10Musculocutaneousnerve – sensory(antidromic)(lateralantebrachialcutaneous nerve).
Figure A1.11Musculocutaneousnerve – motor.
Figure A1.12Axillary nerve –motor.
Cathode
Anode
Ground
Activeelectrode
Reference
AnodeCathode
GroundActive
Reference
Easy EMG218
Ground
Poplitealstimulation
Fibulastimulation
Anklestimulation
Reference
Active
Figure A1.13Peroneal nerve –motor.
Figure A1.14Sural nerve –sensory.
Reference
Ground
Stimulation
Activeelectrode
Appendix 1 Figures for Table 4.3 Nerve conduction studies setup 219
Figure A1.15Tibial nerve –motor toabductor hallucis.
Figure A1.16Superficialperoneal nerve –sensory(antidromic).
Poplitealstimulation
Malleolusstimulation
Ground
ReferenceActive
Stimulation
Ground
Active
Reference
Easy EMG220
Stimulation can beintroduced to sciatic nerve(in gluteal fold between
ischial tuberosity and greatertrochanter)
Active overabductorhallucismuscle(tibial
component)
Ground
Reference
Active over extensordigitorum brevis (forperoneal component)
Figure A1.19Sciatic nerve –motor.
Figure A1.20Lateral femoralcutaneous nerve –sensory(antidromic).
Stimulation
Ground
Active
Reference
Appendix 1 Figures for Table 4.3 Nerve conduction studies setup 221
Active
Reference
Ground
Poplitealstimulation
Figure A1.19H-reflex.
Appendix 2Figures to Table 5.4 Commonmuscles – innervation,location and needleplacement
223
Figure A2.1 Sternocleidomastoid.
Easy EMG224
Figure A2.2Trapezius.
Figure A2.3Rhomboid major(RMa), rhomboidminor (RMi).
RMiRMa
Appendix 2 Figures to Table 5.4 Common muscles 225
Figure A2.4Levator scapula.
Figure A2.5Supraspinatus.
Easy EMG226
Figure A2.6Infraspinatus.
Figure A2.7 Teresmajor.
Appendix 2 Figures to Table 5.4 Common muscles 227
Figure A2.8Deltoid.
Figure A2.9 Teresminor.
Easy EMG228
Figure A2.10Coracobrachialis.
Figure A2.11Biceps brachii.
Appendix 2 Figures to Table 5.4 Common muscles 229
Figure A2.12Brachialis.
Figure A2.13Latissimus dorsi.
Easy EMG230
Figure A2.14Serratus anterior.
Figure A2.15Triceps.
Appendix 2 Figures to Table 5.4 Common muscles 231
Figure A2.16Anconeus.
Figure A2.17Brachioradialis.
Easy EMG232
Figure A2.18Extensor carpiradialis.
Figure A2.19Supinator.
Appendix 2 Figures to Table 5.4 Common muscles 233
Figure A2.20Extensor carpiulnaris.
Figure A2.21Extensordigitorum.
Easy EMG234
Figure A2.22Extensordigitorum minimi.
Figure A2.23Abductor pollicislongus.
Appendix 2 Figures to Table 5.4 Common muscles 235
Figure A2.24Extensor pollicislongus.
Figure A2.25Extensor pollicisbrevis.
Easy EMG236
Figure A2.26Extensor indicis.
Figure A2.27Pronator teres(PT), pronatorquadratus (PQ).
PT
PQ
Appendix 2 Figures to Table 5.4 Common muscles 237
Figure A2.28Flexor carpiradialis.
Figure A2.29Palmaris longus.
Easy EMG238
Figure A2.30Flexor digitorumsuperficialis.
Figure A2.31Flexor digitorumprofundus.
Appendix 2 Figures to Table 5.4 Common muscles 239
Figure A2.32Flexor pollicislongus.
Figure A2.33Abductor pollicisbrevis.
Easy EMG240
Figure A2.34Opponens pollicis.
Figure A2.35Flexor pollicisbrevis.
Appendix 2 Figures to Table 5.4 Common muscles 241
Figure A2.36Flexor carpiulnaris.
Figure A2.37Abductor digitiminimi.
Easy EMG242
Figure A2.38Opponens digitiminimi.
Figure A2.39Flexor digitiminimi.
Appendix 2 Figures to Table 5.4 Common muscles 243
Figure A2.40Palmar interossei.
Figure A2.41Dorsal interossei.
Easy EMG244
Figure A2.42Adductor pollicis.
Figure A2.43Lumbricals.
Appendix 2 Figures to Table 5.4 Common muscles 245
PMiPMa
Figure A2.44Pectoralis major(PMa), pectoralisminor (PMi).
Figure A2.45Iliopsoas.
Easy EMG246
Adductor magnusAdductor brevis
Adductor longus
Rectus femoris
Vastus intermedius
Vastus lateralis
Vastus medialis
Gracilis
Sartorius
Figure A2.46Muscles of theanterior thigh.
Figure A2.47Sartorius.
Appendix 2 Figures to Table 5.4 Common muscles 247
Figure A2.48Rectus femoris.
Figure A2.49Vastus lateralis.
Easy EMG248
Figure A2.50Vastusintermedius.
Figure A2.51Vastus medialis.
Appendix 2 Figures to Table 5.4 Common muscles 249
Figure A2.52Pectineus.
Figure A2.53Adductor brevis.
Easy EMG250
Figure A2.54Adductor longus.
Figure A2.55Gracilis.
Appendix 2 Figures to Table 5.4 Common muscles 251
Figure A2.56Adductormagnus.
Figure A2.57Gluteus medius.
Easy EMG252
Figure A2.58Gluteus minimus.
Figure A2.59Tensor fascialatae.
Appendix 2 Figures to Table 5.4 Common muscles 253
Figure A2.60Gluteus maximus.
Figure A2.61Semitendinosus.
Easy EMG254
Long head
Short head
Figure A2.62Semimembranosus.
Figure A2.63Biceps femoris.
Appendix 2 Figures to Table 5.4 Common muscles 255
Figure A2.64Extensordigitorum longus.
Figure A2.65Tibialis anterior.
Easy EMG256
Figure A2.66Extensor hallucislongus.
Figure A2.67Peroneus tertius.
Appendix 2 Figures to Table 5.4 Common muscles 257
Figure A2.68Extensordigitorum brevis.
Figure A2.69Peroneus longus.
Easy EMG258
Medialgastrocnemius
Lateralgastrocnemius
Figure A2.70Peroneus brevis.
Figure A2.71Medial lateralgastrocnemius.
Appendix 2 Figures to Table 5.4 Common muscles 259
Figure A2.72Popliteus.
Figure A2.73Soleus.
Easy EMG260
Figure A2.74Muscles of thecalf.
Figure A2.75Flexor hallucislongus.
Meddialgastrocnnemius
Lateralgastrocnemius
s posteriorTibialisTibialis posteriior
Soleus
Appendix 2 Figures to Table 5.4 Common muscles 261
Figure A2.76Abductor digitiminimi.
Figure A2.77Flexor digitiminimi (plantarsurface).
Easy EMG262
Figure A2.78Dorsal interossei.
Figure A2.79Plantar interossei(plantar surface).
Appendix 2 Figures to Table 5.4 Common muscles 263
Figure A2.80Adductor hallucis(plantar surface).
Figure A2.81Abductor hallucis(plantar surface).
Easy EMG264
Figure A2.82Flexor digitorumbrevis (plantarsurface).
Figure A2.83Flexor hallucisbrevis (plantarsurface).
Appendix 2 Figures to Table 5.4 Common muscles 265
Figure A2.84Cervicalparaspinal.
Figure A2.85Thoracicparaspinal.
C7
C7
T12
Easy EMG266
L4-L5interspace
L1
L2
L3
L4
L5
Figure A2.86Lumbosacralparaspinal.
Aaction potential 4, 19–30, 209
amplitude 21–2conduction velocity 20–1duration 22latency 20see also individual types
active electrode 23, 42adipose tissue, stimulation over 116–17age of patient 118amplifiers 12–13amplitude 4, 21, 191, 209amyotrophic lateral sclerosis 2, 189anatomy error 117anomalous innervation 115–16
accessory peroneal nerve 116Martin-Gruber anastomosis 115–16Riche-Cannieu anastomosis 116
antidromic impulses 4, 17, 209arcade of Frohse 135axonal injuries 82–4
nerve conduction studies 84–6axonal neuropathy 83axonotmesis 81, 209
BBell’s palsy 49billing 203–8bipolar needle electrodes 44bleeding disorders 7blood precautions 8brachial plexopathies 171–80
anatomy 172–7clinical presentation 171–2electrodiagnostic assessment 177–80
Ccarpal tunnel syndrome 6, 121–6
anatomy 121–2clinical presentation 121electrodiagnostic assessment 122–5written report 125
cathode ray tube 13cervical or lumbar radiculopathy 2coding 203–8
common mode rejection 12complex repetitive discharges 47, 49, 169compound motor action potentials 17, 18, 31,209
amplitude changes 21, 116brachial plexopathies 178carpal tunnel syndrome 123lumbosacral plexopathies 186–7motor neuron disease 190myopathy 169peripheral neuropathy 165–6peroneal neuropathy 153positive deflection 115radial neuropathy 139radiculopathy 143–4spinal stenosis 150tarsal tunnel syndrome 158ulnar neuropathy 131–2
compound nerve action potentials 17concentric needle electrodes 42–4conduction block 15, 19, 81–2, 83, 209
nerve conduction studies 84conduction velocity 4, 20–1, 191, 209
increased 115–16negative 115–16
congenital myopathy 168contracture 169cramps 47cubital tunnel syndrome 130
DDe Quervain’s syndrome 135demyelinating injuries 81–2
nerve conduction studies 84demyelination 19display system 13–14
Eearly recruitment 54electrodes 42–4
bipolar needle 44monopolar needle 42recording see recording electrodessingle-fiber needle 44standard or concentric needle 42–4 267
Index
electrodiagnostic assessment 1, 2, 3, 209carpal tunnel syndrome 122–5complications 8contraindications 8controversies 8peripheral neuropathy 162–4, 165–6peroneal neuropathy 153–5radial neuropathy 137–9radiculopathy 143–7reasons for performing 5–8tarsal tunnel syndrome 158–60ulnar neuropathy 130–3
electromyography 4, 41–80brachial plexopathies 178–80carpal tunnel syndrome 123–5electrodes 42–4examination of muscle at rest 46–50insertional activity 45–6lumbosacral plexopathies 187motor neuron disease 190motor units 41, 50–3muscle physiology 41myopathy 169–70needle placement 56–80peripheral neuropathy 162–4, 166peroneal neuropathy 153–5radial neuropathy 138, 139radiculopathy 145–7recruitment 53–4spinal stenosis 150
EMG see electromyographyendplate region 50endplate spikes 50equipment 9–18
amplifiers 12–13artifacts and technical factors 14–15display system 13–14machine 9–10measurements 16recording electrodes 10–11stimulation 15–16sweep speed and sensitivity 16
Erb’s point 178evoked response 111examination 87–109
EMG evaluation 108–9lower extremities 101–7pitfalls 111–19
anatomy error 117anomalous innervation 115–16measurement errors 112–14non-physiologic factors 119physiologic factors 118stimulation over subcutaneous/adipose
tissue 116–17technical factors 111–12temperature 112, 113, 114
upper extremities 89–100
FF-wave 4, 23–9, 30, 39, 209
brachial plexopathies 178carpal tunnel syndrome 123lumbosacral plexopathies 187motor neuron disease 190normal values 202peripheral neuropathy 166peroneal neuropathy 153radial neuropathy 139radiculopathy 145spinal stenosis 150tarsal tunnel syndrome 158ulnar neuropathy 132
F-wave ratio 29, 31fasciculation potential 210fasciculations 47fibrillation potential 47, 48, 86, 210filters 12–13, 15flexor retinaculum 122focal conduction block 139focal nerve slowing 81, 82, 84frequency 210Froment’s sign 127, 129
Ggain 13ground electrode 23Guillain-Barré syndrome 2Guyon’s canal 127, 130
HH-reflex 4, 23–9, 30, 39, 210, 221
carpal tunnel syndrome 123lumbosacral plexopathies 187motor neuron disease 190normal values 202peripheral neuropathy 166peroneal neuropathy 153radial neuropathy 139radiculopathy 145spinal stenosis 150tarsal tunnel syndrome 158ulnar neuropathy 132
height of patient 118high frequency filters 13high pass filters 12Hoffmann reflex 4honeymooner’s palsy 135humeroulnar arcade 130
Iinching 131–2increased recruitment 54inflammatory myopathy 168insertional activity 45–6, 192, 210
Easy EMG268
Llate responses 17, 23–9, 210
brachial plexopathies 178carpal tunnel syndrome 123lumbosacral plexopathies 187motor neuron disease 190myopathy 169peripheral neuropathy 166peroneal neuropathy 153spinal stenosis 150tarsal tunnel syndrome 158ulnar neuropathy 132see also F-wave; H-reflex
latency 4, 20–1, 210limb-girdle dystrophy 49low frequency filters 12low pass filters 13lower extremities 101–7
normal values 201lumbar plexus 181, 182lumbosacral plexopathies 181–7
anatomy 181–5clinical presentation 181electrodiagnostic assessment 185–7
MM-response 24, 145M-wave 210Martin-Gruber anastomosis 115–16measurement errors 112–14metabolic myopathy 168miniature endplate potentials 50, 210monopolar needle electrodes 42morbid obesity 7motor nerves 21motor neuron disease 49, 189–90motor point 210motor unit 41, 50–3, 210
amplitude 52analysis of 50–2duration 52phase 53rise time 52
motor unit action potentials 52–4, 118, 198motor neuron disease 190myopathy 169peripheral nerve injury 86peroneal neuropathy 155
motor unit architecture 41motor unit recruitment 198multiples 47muscle physiology 41muscles
abductor digiti minimi 66–7, 78–9, 132,172, 241, 261
abductor hallucis 263abductor pollicis brevis 64–5, 115, 172, 239abductor pollicis longus 62–3, 234
adductor brevis 72–3, 249adductor hallucis 78–9, 263adductor longus 72–3, 250adductor magnus 74–5, 251adductor pollicis 68–9, 172, 244anconeus 60–1, 231biceps brachii 58–9, 228biceps femoris 74–5, 254brachialis 58–9, 229brachioradialis 60–1, 231cervical paraspinal 265coracobrachialis 58–9, 228deltoid 58–9, 227dorsal interossei 78–9, 262extensor carpi radialis 60–1, 232extensor carpi ulnaris 60–1, 233extensor digiti minimi 62–3extensor digitorum 62–3, 233extensor digitorum brevis 76–7, 257extensor digitorum longus 74–5, 255extensor digitorum minimi 234extensor hallucis longus 76–7, 256extensor indicis 62–3, 236extensor pollicis brevis 62–3, 235extensor pollicis longus 62–3, 235first dorsal interosseous 68–9flexor carpi radialis 62–3, 237flexor carpi ulnaris 66–7, 172, 241flexor digiti minimi 68–9, 78–9, 242, 261flexor digitorum brevis 78–9, 264flexor digitorum indicis 172flexor digitorum profundus 64–5, 238flexor digitorum superficialis 64–5, 238flexor hallucis brevis 264flexor hallucis longus 78–9, 260flexor pollicis brevis 66–7, 78–9, 240flexor pollicis longus 64–5, 239gastrocnemius
lateral 76–7medial 76–7
gluteus maximus 74–5, 253gluteus medius 74–5, 251gluteus minimus 74–5, 252gracilis 72–3, 250iliopsoas 72–3, 245infraspinatus 58–9, 226interossei
dorsal 243palmar 243
lateral gastrocnemius 260latissimus dorsi 58–9, 229levator scapula 56–7, 225lumbosacral paraspinal 266lumbricals 68–9, 244medial gastrocnemius 260medial lateral gastrocnemius 258opponens digiti minimi 66–7, 242opponens pollicis 66–7, 172, 240
Index 269
muscles (cont’d)palmar interosseous 68–9palmaris longus 64–5, 237pectineus 249pectoralis major 70–1, 245pectoralis minor 70–1, 245peroneus brevis 76–7, 258peroneus longus 76–7, 257peroneus tertius 76–7, 256plantar interossei 78–9, 262popliteus 76–7, 259pronator quadratus 64–5, 236pronator teres 62–3, 236rectus femoris 72–3, 247rhomboids 56–7, 224sartorius 72–3, 246semimembranosus 74–5, 254semitendinosus 74–5, 253serratus anterior 60–1, 230soleus 76–7, 259, 260sternocleidomastoid 56–7, 223subscapularis 58–9supinator 60–1, 232supraspinatus 56–7, 225tensor fasciae latae 74–5, 252teres major 58–9, 226teres minor 58–9, 227thoracic paraspinal 265tibialis anterior 255tibialis posterior 76–7, 260trapezius 56–7, 224triceps 60–1, 230vastus intermedius 72–3, 248vastus lateralis 72–3, 247vastus medialis 72–3, 248see also lower extremities; upper extremities
muscular dystrophy 2, 168myasthenia gravis 2myelin 18myokymic discharges 47, 49–50, 210myopathic recruitment 211myopathy 167–70
anatomy 168clinical presentation 167–8electrodiagnostic assessment 168–70
myotomal distribution 141myotonic discharges 47, 49, 169, 211myxedema 49
Nneedle placement 56–80nerve conduction studies 1, 2–4, 17–39
action potential 4, 19–30physiology 17–19set-up 35–9
nervesaxillary 36, 58–9, 217dorsal scapular 56–7, 176femoral 72–3, 182, 183genitofemoral 182, 183
glutealinferior 74–5, 184, 185superior 74–5, 184, 185
iliohypogastric 182, 183ilioinguinal 182interosseous
anterior 64–5posterior 60–1, 62–3
lateral antebrachial cutaneous 36lateral cutaneous of forearm 171lateral femoral cutaneous 38, 182, 183, 220long thoracic 60–1medial antebrachial cutaneous 127, 171median 32–3, 64–5, 66–7, 68–9, 176, 213,
214carpal tunnel syndrome 6, 121–6injury to 123
musculocutaneous 36, 58–9, 176, 217obturator 72–3, 74–5, 182, 183pectoral 70–1peroneal 37, 218
accessory 116, 152deep 74–5neuropathy 151–5superficial 38, 76–7, 219
plantarlateral 78–9medial 78–9
posterior femoral cutaneous 184, 185pudendal 184radial 35–6, 60–1, 216
neuropathy 135–41saphenous 182sciatic 38, 74–5, 184, 185, 220spinal accessory 56–7subscapular 58–9suprascapular 56–7, 58–9, 176sural 37, 218thoracodorsal 58–9tibial 74–5, 76–7, 78–9, 219
posterior 38tarsal tunnel syndrome 157–61
ulnar 33–5, 64–5, 66–7, 68–9, 214, 215, 216neuropathy 127–34
see also lower extremities; upper extremitiesneurapraxia 19, 81neurogenic claudication 149neurogenic recruitment 53–4neuromyotonic discharges 47neuropathic recruitment 53–4neuropraxia 211neurotmesis 81, 211nodes of Ranvier 19noise 119normal values 200–2
Oobese patients 7, 118onset latency 20orthodromic impulses 4, 17, 211
Easy EMG270
Ppatients
morbid obesity 7putting at ease 6–7thin individuals 7
peer review 206peripheral nerve injury 81–6
axonal injuries 82–4demyelinating injuries 81–2nerve conduction studies and EMG 84–6
peripheral neuropathy 161–6anatomy 161, 165clinical presentation 161electrodiagnostic assessment 162–4, 165–6
peroneal neuropathy 151–5anatomy 152–3clinical presentation 151–2electrodiagnostic assessment 153–5
Phalen’s test 121poliomyelitis 49, 189positive sharp waves 47, 48, 86, 211pulse width 29, 112
Rradial neuropathy 135–41
anatomy 135–7clinical presentation 135electrodiagnostic assessment 137–9
radiculopathy 141–8anatomy 142–3clinical presentation 141–2electrodiagnostic assessment 143–7
recording electrodes 10–11, 23active 23ground 23needle electrodes 10–11placement 15reference 23surface electrodes 10
recruitment 53–4, 211reference electrode 23reimbursement 203–8report writing 191–8
sample report 193–7Riche-Cannieu anastomosis 116
Ssacral plexus 183–5saltatory conduction 18, 19Saturday night palsy 135, 137Schwann cells 18Schwartz/Jampel syndrome 49Seddon Classification of Nerve Injuries 81segmental demyelination 81, 82, 84sensitivity 13, 16sensory nerve action potentials 17, 18, 211
brachial plexopathies 177–8
carpal tunnel syndrome 122–3lumbosacral plexopathies 186motor neuron disease 189myopathy 169peripheral neuropathy 165peroneal neuropathy 153radial neuropathy 137radiculopathy 143spinal stenosis 149tarsal tunnel syndrome 158ulnar neuropathy 130–1
single-fiber needle electrodes 44SNAPs see sensory nerve action potentialsspinal muscular atrophy 49spinal stenosis 149–50spiral groove 135spontaneous activity 46–50, 192stimulation 15–16
sites of 22stimulators 22stimulus artifact 14–15subcutaneous tissue, stimulation over 116–17submaximal stimulus 211supramaximal stimulus 15, 22, 211–12sweep speed 13, 16
Ttardy ulnar palsy 129tarsal tunnel syndrome 157–60
anatomy 157–8clinical findings 157electrodiagnostic assessment 158–60
technical factors 111–12temperature 112, 113, 114temporal dispersion 212tenosynovitis 135thin patients 7tibialis anterior 74–5Tinel’s sign 157Tinel’s test 121toxic neuropathy 2tremors 47
Uulnar neuropathy 127–34
anatomy 129–30clinical presentation 127–9electrodiagnostic assessment 130–3
uniform demyelination 81upper extremities 89–100
normal values 200
WWallerian degeneration 86Wartenberg’s sign 127weight of patient 118
Index 271