reflex testing

Neurologic examinationREFLEX TESTING

Reflex testing incorporates an assessment of the function and interplay of both sensory and motor pathways. It is simple yet informative and can give important insights into the integrity of the nervous system at many different levels.

Assessment of reflexes is based on a clear understanding of the following principles and relationships:

• Tendons connect muscles to bones, usually crossing a joint. When the muscle contracts, the tendon pulls on the bone, causing the attached structure to move.

• When the tendon is struck by the reflex hammer, stretch receptors contained within it generate an impulse that is carried via sensory nerves to the spinal cord. At this juncture, the message is transmitted across a synapse to an appropriate lower motor neuron. An upper motor neuron, whose cell body resides in the brain, also provides input to this synapse.

• The signal then travels down the LMN to the target muscle.

REFLEX TESTING

• The sensory and motor signals that comprise a reflex arc travel over anatomically well characterized pathways. Pathologic processes affecting discrete roots or named peripheral nerves will cause the reflex to be diminished or absent. The Achilles Reflex is dependent on the S1 and S2 nerve roots. Herniated disc material can put pressure on the S1 nerve root, causing pain along its entire distribution (i.e. the lateral aspect of the lower leg). If enough pressure if placed on the nerve, it may no longer function, causing a loss of the Achilles reflex.

• In extreme cases, the patient may develop weakness or even complete loss of function of the muscles innervated by the nerve root, a medical emergency mandating surgical decompression.

• A normal response generates an easily observed shortening of the muscle. This, in turn, causes the attached structure to move.

REFLEX TESTING

Grade Description0 Absent; No evidence of contraction1+ Decreased, but still present (hypo-reflexic)2+ Normal or physiologic3+ Increased and maybe normal or pathologic4+ Markedy hyperactive with transient clonus5+ Markedy hyperactive with sustained clonus

(Repetitive shortening of the muscle after a single stimulation)

The vigor of contraction is graded on the following scale:

Technique:• You will need to use a reflex hammer when performing

this aspect of the exam. Regardless of the hammer type, proper technique is critical.

• The larger hammers have weighted heads, such that if you raise them approximately 10 cm from the target and then release, they will swing into the tendon with adequate force.

• The smaller hammers should be swung loosely between thumb and forefinger.

The Reflex Hammer

Small Hammers

Large Hammers

Technique:• The muscle group to be tested must be in a neutral position (i.e.

neither stretched nor contracted). • The tendon attached to the muscle(s) which is/are to be tested

must be clearly identified. The extremity should be positioned such that the tendon can be easily struck with the reflex hammer.

• If you are having trouble locating the tendon, ask the patient to contract the muscle to which it is attached. When the muscle shortens, you should be able to both see and feel the cord like tendon, confirming its precise location. You may, for example, have some difficulty identifying the Biceps tendon within the Antecubital Fossa. Ask the patient to flex their forearm (i.e. contract their Biceps muscle) while you simultaneously palpate the fossa. The Biceps tendon should become taut and thus readily apparent.

• Strike the tendon with a single, brisk stroke. While this is done firmly, it should not elicit pain. Occasionally, due to other medical problems (e.g. severe arthritis), you will not be able to position the patient’s arm in such a way that you are able to strike the tendon. If this occurs, do not cause the patient discomfort. Simply move on to another aspect of the exam.

REFLEX TESTING

Technique:• This is most easily done with the patient seated, feet dangling

over the edge of the exam table. Other positions: supine, crossing one leg over the other in a figure 4 or a frog-type position.

• Identify the Achilles tendon, a taut, discrete, cord-like structure running from the heel to the muscles of the calf. If you are unsure, ask the patient to plantar flex (i.e. “step on the gas”).

• Strike the tendon directly with your reflex hammer.• Be sure that the calf if exposed so that you can see the muscle

contract.• NORMAL RESPONSE: plantar flexion (contraction of the

Gastrocnemius).

ACHILLES REFLEX (S1, S2 – Sciatic Nerve):

ACHILLES TENDON

Technique:• This is most easily done with the patient seated, feet dangling

over the edge the exam table. • Identify the patellar tendon, a thick, broad band of tissue

extending down from the lower aspect of the patella (knee cap). If you are not certain where it’s located, ask the patient to extend their knee. This causes the quadriceps (thigh muscles) to contract and makes the attached tendon more apparent.

• Strike the tendon directly with your reflex hammer. If you are having trouble identifying the exact location of the tendon (e.g. if there is a lot of subcutaneous fat), place your index finger firmly on top of it. Strike your finger, which should then transmit the impulse.

• For the supine patient, support the back of their thigh with your hands such that the knee is flexed and the quadriceps muscles relaxed.

• NORMAL RESPONSE: The lower leg will extend at the knee. (contraction of the Quadriceps)

PATELLAR REFLEX (L3, L4 – Femoral Nerve):

Patellar Tendon

PATELLAR REFLEX TESTING

Technique:• Identify the location of the biceps tendon in the antecubital fossa.

The tendon will look and feel like a thick cord. • The patient’s arm can be positioned in one of two ways:

A. Allow the arm to rest in the patient’s lap, forming an angle of slightly more then 90 degrees at the elbow.

B. Support the arm in yours, such that your thumb is resting directly over the biceps tendon (hold the right arm with your right)

• It may be difficult to direct your hammer strike such that the force is transmitted directly on to the biceps tendon, and not dissipated amongst the rest of the soft tissue in the area. If you are supporting the patient’s arm, place your thumb on the tendon and strike this digit. If the arm is unsupported, place your index or middle fingers firmly against the tendon and strike them with the hammer.

• NORMAL RESPONSE: elbow flexion

BICEP REFLEX (C5, C6 – Musculocutaneous Nerve):

BICEP TENDON

BICEP REFLEX TESTING

Technique:• This is most easily done with the patient seated. The lower arm

should be resting loosely on the patient’s lap. • The tendon of the Brachioradialis muscle cannot be seen or well

palpated, which makes this reflex a bit tricky to elicit. The tendon crosses the radius (thumb side of the lower arm) approximately 10 cm proximal to the wrist.

• Strike this area with your reflex hammer. Usually, hitting anywhere in the right vicinity will generate the reflex.

• NORMAL RESPONSE: elbow flexion and supination of the forearm (turn palm upward).

BRACHIORADIALIS REFLEX (C5, C6 – Radial Nerve):

BRACHIORADIALIS REFLEX

Technique:• Identify the triceps tendon, a discrete, broad structure that can be

palpated as it extends across the elbow to the body of the muscle, located on the back of the upper arm. Ask the patient to extend their lower arm at the elbow while you observe and palpate in the appropriate region

• The arm can be placed in either of 2 positions: A. Gently pull the arm out from the patient’s body, such that it roughly forms a right angle at the shoulder. The lower arm should dangle directly downward at the elbow. B. Have the patient place their hands on their hips.

• NORMAL RESPONSE: the lower arm to extend at the elbow and swing away from the body. If the patient’s hands are on their hips, the arm will not move but the muscle should shorten vigorously .

TRICEP REFLEX (C7, C8 – Radial Nerve):

TRICEP BRACHII TENDON

TRICEP REFLEX (C7, C8 – Radial Nerve):

DEEP TENDON REFLEXES

Pectoralis Reflex C5 – T1• have patient elevate arm; place fingers of your left hand upon the pt’s shoulders with your thumb extended downwards. Strike your thumb directed slightly upwerd toward the pt’s axilla. • NORMAL RESPONSE: muscle contraction can be seen or felt

Pronator Reflex C6 – C7• grasp pt’s hand and hold it vertically so the wrist is suspended• from the medial side, strike the distal end of the radius directlywith horizontal blow• NORMAL RESPONSE: pronation of the forearm

Upper Abdominal Muscle Reflex T8 – T9• tap the muscles directly near their insertions on the costal margins and xiphoid process

Mid Abdominal Muscle Reflex T9 – T10• tapping an overlaid finger

Lower Abdominal Muscle Reflex T11 – T12• tap the muscle insertion directly near the symphysis pubis

DEEP TENDON REFLEXES

Adductor Reflex L2 – L4• patient supine, arrange the lower limb in slight abduction. Tap directly on the Adductor magnus, just proximal to its insertion on the medial epicondyle of the femur • NORMAL RESPONSE: the thigh adducts

Hamstring Reflex L4 – S2• Patient supine with hips and knees flexed at 90 degrees, and thigh rotated slightly outward. • place your left hand under the popliteal fossa to compress the medial hamstring• NORMAL RESPONSE: flexion of the knee and contraction of the medial mass of hamstring

Normal reflexes require that every aspect of the system function normally. Breakdowns cause specific patterns of dysfunction.

These are interpreted as follows:• Disorders in the sensory limb will prevent or delay the

transmission of the impulse to the spinal cord. This causes the resulting reflex to be diminished or completely absent. Diabetes induced peripheral neuropathy, for example, is a relatively common reason for loss of reflexes.

• Abnormal LMN function will result in decreased or absent reflexes. If, for example, a peripheral motor neuron is transected as a result of trauma, the reflex dependent on this nerve will be absent.

• If the UMN is completely transected, as might occur in traumatic spinal cord injury, the arc receiving input from this nerve becomes disinhibited, resulting in hyperactive reflexes. Of note, immediately following such an injury, the reflexes are actually diminished, with hyper-reflexia developing several weeks later. A similar pattern is seen with the death of the cell body of the UMN (located in the brain), as occurs with a stroke affecting the motor cortex of the brain.

Making Clinical Sense of Reflexes:

• Primary disease of the neuro-muscular junction or the muscle itself will result in a loss of reflexes, as disease at the target organ (i.e. the muscle) precludes movement.

• A number of systemic disease states can affect reflexes. Some have their impact through direct toxicity to a specific limb of the system. Poorly controlled diabetes, as described above, can result in a peripheral sensory neuropathy. Extremes of thyroid disorder can also affect reflexes, though the precise mechanisms through which this occurs are not clear. Hyperthyroidisim is associated with hyperreflexia, and hypothyroidism with hyporeflexia.

• Detection of abnormal reflexes (either increased or decreased) does not necessarily tell you which limb of the system is broken, nor what might be causing the dysfunction. Decreased reflexes could be due to impaired sensory input or abnormal motor nerve function. Only by considering all of the findings, together with their rate of progression, pattern of distribution (bilateral v unilateral, etc.) and other medical conditions can the clinician make educated diagnostic inferences about the results generated during reflex testing.

Making Clinical Sense of Reflexes:

If you are unable to elicit a reflex, stop and consider the following:

– Are you striking in the correct place? Confirm the location of the tendon by observing and palpating the appropriate region while asking the patient to perform an activity that causes the muscle to shorten, making the attached tendon more apparent.

– Make sure that your hammer strike is falling directly on the appropriate tendon. If there is a lot of surrounding soft tissue that could dampen the force of the strike, place a finger firmly on the correct tendon and use that as your target.

– Make sure that the muscle is uncovered so that you can see any contraction (occasionally the force of the reflex will not be sufficient to cause the limb to move).

– Sometimes the patient is unable to relax, which can inhibit the reflex even when all is neurologically intact. If this occurs during your assessment of lower extremity reflexes, ask the patient to interlock their hands and direct them to pull, while you simultaneously strike the tendon. This sometimes provides enough distraction so that the reflex arc is no longer inhibited.

Trouble Shooting

Occasionally, it will not be possible to elicit reflexes, even when no neurological disease exists. This is most commonly due to a patient's inability to relax. In these settings, the absence of reflexes are of no clinical consequence. This assumes that you were otherwise thorough in your history taking, used appropriate examination techniques, and otherwise identified no evidence of disease.

Trouble Shooting

BRAINSTEM REFLEXES

• Direct Pupillary Reaction to Light - the iris constricts when bright light is shone upon the retina

• Consensual Pupillary Reaction to Light - stimulation of one retina causes contralateral constriction of the pupil

• Ciliospinal Reflex - pinching the skin of the back of neck causes pupillary dilatation

• Corneal Reflex - touching the cornea causes blinking of the eyelids• Orbicularis Oculi Reflex - the eyelids close when the retina is exposed to bright light• Auditocephalogyric Reflex - the head and eyes turn toward the

source of a loud sound• Jaw Reflex - when the mouth is partially opened and the muscles

relaxed, tapping the chin causes the jaw to close. The reflex center is in the midpons

• Gag Reflex - gagging occurs when the parhynx is stroked. The reflex center is is the medulla

SUPERFICIAL REFLEXES

• have reflex arcs whose receptor organs are in the skin rather than in muscle fibers

• adequate stimulus is stroking, scratching or touching• these reflexes are lost in disease of the pyramidal tract

SUPERFICIAL REFLEXES

Upper Abdominal Skin Reflex T5 – T8• with patient supine, stroke the skin with blunt handle towards the midline• watch for ipsilateral contraction of muscles or umbilical deviation towards the stimulated side

Mid Abdominal Skin Reflex T9 – T11Lower Abdominal Skin Reflex T11 – T12Cremasteric Reflex L1 – L2

• stroke the inner aspect of the thigh from the pubis distad• prompt elevation of the testis on the ipsilateral side

Plantar Reflex L4 – S2• stroke the sole near its lateral aspect from the heel towards toes• produces plantar flexion of the toes

Superficial Anal Reflex L1 – L2• stroke the skin of the perianal region• the external and anal sphincter contracts

Glabellar Reflex (Corticopontine)- lightly tapping the forehead between the eyebrows with the fingersAbnormal response: persistent blepharospasm and closing of the eyes

Snout Reflex (Corticopontine)- tapping the noseAbnormal response: excessive grimace of the face

Sucking Reflex (Frontal cortex)- stroking the lip with the finger or a tongue depressor- present in infants but disappears after weaning; reappears in diffuse lesions of the frontal lobe and commonly noted in dementiasAbnormal response: lips pout and make sucking movements

Chewing Reflex (Frontotemporal cortex)- placing a tongue depressor in the mouth- seen in dementia, general paresis and anoxic encepalopathyAbnormal response: chewing movement of the teeth and jaw

ABNORMAL REFLEXES IN PYRAMIDAL TRACT DISEASE

Babinski Sign (Hallucal Dorsiflexion Reflex)• The Babinski response is a test used to assess upper motor

neuron dysfunction and is performed as follows:• The patient may either sit or lie supine. • Start at the lateral aspect of the foot, near the heel. Apply steady

pressure with the end of the hammer as you move up towards the ball (area of the metatarsal heads) of the foot.

• When you reach the ball of the foot, move medially, stroking across this area.

• Then test the other foot. • Some patients find this test to be particularly noxious

/uncomfortable. Tell them what you are going to do and why. If it’s unlikely to contribute important information (e.g. screening exam of the normal patient) and they are quite averse, simply skip it.

Babinski Response Present

Babinski Sign (Hallucal Dorsiflexion Reflex)• Interpretation: In the normal patient, the first movement of the great

toe should be downwards (i.e. plantar flexion). If there is an upper motor neuron injury (e.g. spinal cord injury, stroke), then the great toe will dorsiflex and the remainder of the other toes will fan out. A few additional things to remember:

• Newborns normally have a positive Babinksi. It usually goes away after about 6 months.

• Sometimes you will be unable to generate any response, even in the absence of disease. Responses must therefore be interpreted in the context of the rest of the exam.

• If the great toe flexes and the other toes flair, the Babinski Response is said to be present. If not (i.e. normal), it is recorded as absent. For reasons of semantics, the Babinski is not recorded as ‘+’ or ‘-‘.

• Withdrawal of the entire foot (due to unpleasant stimulation), is not interpreted as a positive response

ABNORMAL REFLEXES IN PYRAMIDAL TRACT DISEASE

Grasp ReflexStroke the pt’s palm so he grasps your index finger. If present, he cannot release the fingers; lesions of the premotor cortex

Hoffmann’s SignHave pt present pronated hand with fingers extended and relaxed. With your thumb, press his fingernails to flex the terminal digit and stretch his flexorAbnormal response: flexion and adduction of thumb

Mayer’s ReflexHave pt present his supinated hand with thumb relaxed and

abducted. Grasp his ring finger and firmly flex the metacarpophalengeal joint

Normal response: adduction and apposition of the thumb

Palm-Chin Reflex (Radovici’s sign)Vigorous scratching or pricking of the thenar eminence causes

ipsilateral contraction of the muscles of the chin

SIGNS OF MENINGEAL IRRITATION

Nuchal Rigidity- pt cannot place the chin upon the chest- passive flexion of the neck is limited by involuntary muscle spasm

Spinal Rigidity- movements of the spine are limited by spasms of the Erector spinae

Kernig’s Sign- with pt supine, passively flex the hip to 90 deg while the knee is flexed at about 90 deg- attempts to extend the knee produce pain iun the hamstring and resistance

Brudzinski’s Sign- with pt supine and the limbs extended, passively flex the neck- produces involuntary flexion of the hips

Making Sense of Neurological Findings

• While compiling information generated from the motor and sensory examinations, the clinician tries to identify patterns of dysfunction that will allow him/her to determine the location of the lesion(s). What follows is one way of making clinical sense of neurological findings.

• Is there evidence of motor dysfunction (e.g. weakness, spasticity, tremor)?

• If so, does the pattern follow an upper motor neuron or lower motor neuron pattern? – If it’s consistent with a UMN process (e.g. weakness with spasticity),

does this appear to occur at the level of the spinal cord or the brain? Complete cord lesions will affect both sides of the body. Brain level problems tend to affect one side or the other. It is, of course, possible for a lesion to affect only part of the cord, leading to findings that lateralize to one side (see below, under description of Brown Sequard lesion).

– Is it consistent with an LMN process (e.g. weakness with flaccidity)? Does the weakness follow a specific distribution (e.g. following a spinal nerve root or peripheral nerve distribution)? Bilateral? Distal?

Making Sense of Neurological Findings• Do the findings on reflex examination support a UMN or LMN

process (e.g. hyper-reflexic in UMN disorders; hyporeflexic in LMN disorders)?

• Do the findings on Babinski testing (assuming the symptoms involve the lower extremities) support the presence of a UMN lesion?

• Is there impaired sensation? Some disorders, for example, affect only the Upper or Lower motor pathways, sparing sensation.

• Which aspects of sensation are impaired? Are all of the ascending pathways (e.g. spinothalamic and dorsal columns) affected equally, as might occur with diffuse/systemic disease?

• Does the loss in sensation follow a pattern suggestive of dysfunction at a specific anatomic level? For example, is it at the level of a Spinal nerve root? Or more distally, as would occur with a peripheral nerve problem?

• Does the distribution of the sensory deficit correlate with the “correct” motor deficit, assuming one is present? Radial nerve compression, for example, would lead to characteristic motor and sensory findings.

THE END

reflex testing

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