The sensory system and pain syndromes

Vth year, dentistry, 30.09.2008Department of Neurology

Semmelweis University

Sensory system

Receptors:

- specialised (smell, vision, hearing, taste

- visceral (viscera, smooth muscle - unconscious or autonomic)

- somatic (skin, striated muscle, joints)

Cutaneous receptors

Muscle, tendon receptors

The sensory systemSpinothalamic system (tractus spinothalamicus)

exteroceptive sensation) :pain temperature light touch

Dorsal column pathway ( lemniscus medialis) “conscious” proprioception: joint position

vibration deep pressure two point discrimination

graphaesthesia ! stereoaesthesia !

Dorsal and ventral spinocerebellar pathway

“unconscious” proprioception

Pain

Nociceptors:

-Unimodal: mechanoreceptors, thinly myelinated fiber

-Bimodal: cold + mechanoreceptors, thinly myelinated and unmyelinated fibers

warm+mechanoreceptors

-Polymodal:warm-mechano-chemical receptors, unmyelinated fibers

Spinothalamic system

Pain perceptionC fibers: thin, unmyelinatedA delta: thinly myelinated

TemperatureA delta: thinly myelinated

Peripheral:• Postherpetic neuralgia• Trigeminal neuralgia• Polyneuropathy in diabetes mell.• Posttraumatic neuropathyCentral:• Poststroke pain

Description:2

• Burning• Tickling, itching,pins and needles• Hypersensitivity to touch/cold

• inflammation• fractures• osteoarthritis.• Postoperativ visceral pain Description:2

• smarting• Sharp• Pulsating, throbbing

• Low back pain with

radiculopathy• Cervical pain with

radiculopathy• Cancer pain• Carpal tunnel

syndrome

MixedNeuropathic pain

primary lesion or dysfunction of CNS (peripheral or central)1

Nociceptiv paincaused by tissue damage

(bones,joints, tendons, muscles, skin, viscera)2

origin of pain - manifestations

1. International Association for the Study of Pain. IASP Pain Terminology.2. Raja et al. in Wall PD, Melzack R (Eds). Textbook of pain. 4th Ed. 1999.;11-57

Dorsal column pathway/lemniscus medialis

Proprioceptiv modalities: pressure, vibration,joint positiontwo points discrimination,

graphaesthesia ! stereoaesthesia !

Type of fibers: thick, myelinated fibers (Aα, I, II)

Somatotopia in the cortex

Segmental innervation (dermatomes)Peripheral innervation

Sensory disturbancesPositive symptoms:• Pain• Hyperaesthesia:increased sensitivity to any stimulus• Hyperalgesia: increased sensitivity to a painful

stimulus• Hyperpathia: increased sensitivity with increasing

pain threshold to repetitive stimulation

• Paraesthesia:“pins and needles sensation”, “burning feeling”

• Dysaesthesia: inappropriate sensation to a stimulus• Allodynia: pain provoked by a non-painful stimulus

Sensory disturbances

Negative symptoms:

• Hypoalgesia: reduced sensitivity to a painful

stimulus• Hypoesthesia: reduced sensitivity to any

stimulus• Analgesia: absent sensitivity to a painful

stimulus• Anaesthesia: absent sensitivity to any stimulus

Examination of the sensory system 1.

Special standpoints:• “Subjective “ examination• Requires good cooperation on the patient`s side.• Allows accurate localisation of the pathology.• Preliminary diagnosis is needed. Examine according to the

expected damage !• Most often we compare different parts of the body.• Do not tell the patient what should be felt !• The patient should not see the examined part of the body !• “Subjective” sensory disturbance ( pain, paraesthesia ) is not

necessarily accompanied by “objective” sensory disturbance (hypaesthesia, anaesthesia )

Examination of the sensory system 2.

Pain: pin prick, tooth picksLight touch: use a wisp of cotton wool !Temperature:use cold (5-10 0C)/or hot (40-45 0C) test tubes !

-Instruct the patient to reply: “Tell me if you feel the stimulus ! Name the area stimulated !” “Is it equal on both sides?

-Map out the extent of abnormality by moving from the abnormal to the normal area (“Tell me if sensation changes!”)Joint position / motion: -Hold the sides of the patient’s finger ! Move it up and down at random ! Ask to specify the direction of movement !Vibration: -Place a vibrating tuning fork on a bony prominence ( ankle, knee, processus spinosus, processus styloideus radii et ulnae, elbow, clavicula)

Examination of the sensory system 3.• Two point discrimination:

-The ability to discriminate two blunt points when applied simultaneously. (3-5 mm on the finger, 4-7 cm on the trunk)

• Sensory inattention (perceptual rivalry) -The ability to detect sensory stimuli applied simultaneously

on both limbs. -Subdominant parietal lobe, associative areas

• Stereoaesthesia- An object is placed in the patient’s hand.- Ask patient to describe its size, shape, surface, material !- Stereoanaesthesia:disturbance of the sensory afferent tracts.

Examination of the sensory system 4.• Astereognosis.

-Inability to identify an object by palpation

-The primary sense data being intact

-Lesion of the opposite hemisphere, postcentral gyrus • Tactile agnosia :

-The patient is unable to recognize an object by touch in both

hands

-Disorder of perception of symbols.

-Lesion of the dominant parietal lobe, associative areas • Graphaesthesia

- The ability to recognize numbers or letters traced out

on the palm.

Examination of the sensory system

• Nerve conduction studies:

sensory antidrom neurography

median nerve, ulnar nerve

• Somatosensory evoked potentials (SEP)

median nerve, tibial nerve

Peripheral nerve, Polyneuropathies

Peripheral nerve: according to thedistribution area of the affected nerve

Polyneuropathies: symmetricalsensory disturbance in stocking/glovelike distribution, more pronounced distallySensory disturbance usually starts onthe toes, gradually spreads higher,rarely above the knee; later on the hands

Spinal ganglion

segmental, localised to dermatomes

Root damage

• Sensory disturbance and pain according to the dermatome (variability!)

• Anaesthesia does not develop because of overlapping dermatomes

C7

S1

Syringomyelia

• spinothalamic fibers crossing at cervical level are affected first• dissociated sensory loss: temperature, pain disturbance on both hands

Cranial structures - pain

• skull• cervical spine• eyes• ears• nose, sinuses• teeth• temporomandibular joint

HeadachePathways

PAG:periaqueductal gray matter

LC: locus ceruleus

TG:trigeminal ganglion

DRG:dorsal root ganglion

Taking a headache history

• Age of onset ?• Duration of complaint ?• Time pattern

Continuous or transient ? Frequency and duration of each headache ?

• Site ?• Intensity, quality ?• Associated phenomena ?• Aggravating and relieving factors ?

Headache - duration - frequency

Headache - „danger signals” „Danger signals”:• sudden onset of new, severe headache• onset of headache after exertion, straining, coughing or sexual activity• progressively worsening headache• any abnormality on neurological examination• systemic features: fever, arthralgia • onset of first headache after the age of 50 years

Refer to specialist:• Cooperating patient – ineffective treatment• Chronic daily headache – drug abuse, dependency• Severe anxiety , depression• Severe comorbid diseases

International classification of headache disorders

Primary headaches:

1. Migraine

2. Tension-type headache

3. Cluster headache and other

trigeminal autonomic headaches

4. Other primary headaches

Secondary headaches:

5. Posttraumatic (head/neck trauma)

6. Vascular disorder (cranial/cervical)

7. Non vascular intracranial disorder

8. Substance abuse/ withdrawal

9. Infection

10 Disorder of homeostasis

11.Disorder of facial/cranial structures

12.psychiatric disorderCranial neuralgias, central and primary facial pain :

13.Cranial neuralgias and central causes of facial pain

14.Other headacheInternational Headache Society. ICHD-II. Cephalalgia 2004; vol 24: suppl 1.

A) n 5

B) 4 - 72 h

C) 1.

2.

3. ++ / +++

4.

D) 1. +

2.

E) normal

Migraine without aura

2/4

1/2

//

Phases of migraine

Blau, Lancet, 1992

Woods et al. 1994

Migraine and „spreading depression”

Lancet Neurology 2002;1:251-257.

Trigemino - vascular system

migraine - treatment

•Acute:- Non specific: analgesics, NSAID, antiemetics- Specific: ergotamine, dihydroergotamine, triptans

•Preventive (prophylactic):- Episodic: if there is a trigger for a limited time ( menses)

- Chronic: decrease the frequency independently of triggers

Migrén gyógyszeres kezelésének protokollja,Magyar Fejfájás Társaság, 2003

Tension type headache: criteriaA. n > 10

B. 30 min < duration of pain< 7 nap

C.

2/4

+ / ++

D.

2/2

E. normal

/ /

Trigeminus nucleuscaudalis

art. temp.

Brainstem and spinal cord

Convergence and sensitisation in the trigeminal nuclei

masticatory masticatory musclemuscle

ThalamusDRN, LC

pia / duravessels

Tension type headache - treatment

Acute treatment: analgesics

NSAID

+ antiemetics, coffein

Preventive treatment: tricyclic AD

SSRI

valproat (?)

Complex treatment: pharmacological treatment

psychotherapy

relaxation

physiotherapiy (Not massage!)

A)A) n n 5 5

B)B) +++ +++

30-180 min30-180 min

D)D) Frequency = 1/2 ->50Frequency = 1/2 ->50

E)E) normalnormal

Cluster headache: criteria

1/4C)

Cluster headache: treatmentAcute treatment: oxygen (7 l/min, 10 perc)

sumatriptan sc. inj.

ergotamine

indomethacin supp.

Preventive treatment: verapamil (360 mg/day)

valproate (600-1500 mg /day)

infiltration of occipital nerve ?

methysergide, pizotifen ?

lithium (chronic cluster!)

corticosteroids/dihydroergotamine

Surgical ?

International classification of headache disorders

Primary headaches:

1. Migraine

2. Tension-type headache

3. Cluster headache and other

trigeminal autonomic headaches

4. Other primary headaches

Secondary headaches:

5. Posttraumatic (head/neck trauma)

6. Vascular disorder (cranial/cervical)

7. Non vascular intracranial disorder

8. Substance abuse/ withdrawal

9. Infection

10 Disorder of homeostasis

11.Disorder of facial/cranial structures

12.psychiatric disorder

Cranial neuralgias, central and primary facial pain :

13.Cranial neuralgias and central causes of facial pain

14.Other headacheInternational Headache Society. ICHD-II. Cephalalgia 2004; vol 24: suppl 1.

Trigeminal neuralgiaV/1

V/3

C2/3

V/3

V/2

V/1

V/1

Trigeminal neuralgia• Prevalence: 10-20 / 100 000 population• female/male : 1.6• age of onset: > 50 years (90%)• site: most frequently V/2,3

< 5 % V/1 division ~ 10 % all the three division

~ 5 % bilateralFeatures:• placebo effect 0 -1 % !• trigger zone 90 %• refracter phase• spontanous remission ~ 50 %, < 6 months • „pretrigeminal neuralgia”

Trigeminal neuralgiaClassical/Idiopathic• duration < 2 minutes• affecting one/more divisions• sudden onset• severe, sharp,stabbing pain• precipitated from trigger areas• patiens is pain free between

paroxysm • no neurological deficit

• no causative lesion

Symptomatic• pain as described before

•persistence of aching between paroxysm

• sensory impairment or other neurological deficit

•causative lesion , other than vascular compression

Trigeminal neuralgia

mouth -ear zone, 60% nose - orbit zone, 30 %

Peripheral aetiology -central pathogenesis

chronic irritation of trigeminal nerve division

focal demyelinisation

ectopic action potentials decrease of segmental inhibition

paroxysmal discharge of LTM interneurons of nucleus oralis n.V

paroxysmal discharge of WDR neurons of nucleus caudalis n.V

attack of trigeminal neuralgia

sites of trigeminal nerve damage

Trigeminal neuralgia

• differential diagnosis• examinations: anamnesis

physical examinationRtgotology dental surgeryophthalmologybrain MRtrigeminal SEPpsychology„diagnostic blockade”

Trigeminal neuralgia• If it is possible determine causative lesion, treat it

• Pharmacological treatment

- antiepileptics

- muscle relaxants

- tranquillants

• TENS?

• surgery

Trigeminal neuralgia-pharmacological treatment

• Carbamazepine 400-1200 mg/day• Phenytoin 300-600 mg/day• Valproate 500-2000 mg/day• L baclofen 40-80 mg/day• Clonazepam 2-8 mg/day• Pimozide 4-12 mg/day• Tiapridal 300-600 mg/day• Gabapentin up to 3600 mg/day• Pregabalin ?

Trigeminal neuralgia - phamacological treatment

• start with small dose, increase gradually• prefer combination• blood counts, hepatic, renal function tests are needed• monitoring of complaints is important• timing of discontinuation (after pain free for 8 weeks)• gradual tapering is necessary• 30 % of patients fail to respont to medical therapy

Trigeminal neuralgia – surgical management• Peripheral nerve blockade• Percutanous radiofrequency trigeminal thermocoagulation

(Sweet, Wespic, 1974)

• Retrogasserian Glycerol injection

(Hakansson, 1981)

• Radiosurgery - gamma knife• Microvascular decompression

(Gardner 1966, Janetta 1967, MéreiFT 1973)Janetta: 85 % vascular compression a. cerebelli superior V/2,3a. cerebelli inferior anterior V/1pain free : 80%,

mortality: 0.5 %

neuralgias Glossopharyngeal neuralgia: classical/symptomatic

- pain in the tonque, tonsillar fossa, angle of the jaw, ear- peritonsillar abscess, oropharyngeal carcinoma !

Nervus intermedius neuralgia- posterior wall of the auditory canal- herpes zoster oticus !

Superior laryngeal neuralgiaNasociliary neuralgiaSupraorbital neuralgiaOccipital neuralgia

- greater or lesser occipital nerves- cervical spine !

Central causes of facial pain

• Anaesthesia dolorosa:- lesion of the relevant nerve/ after trauma (surgical?)

- diminished sensation to pin prick over the affected area(hypalgesia)

- spontaneous, persistent pain and dysaesthesia (allodynia)

• Central post stroke pain

• Persistent idiopathic (atypical) facial pain- persisting pain without features of neuralgia

- on a limited area of the face, poorly localised

- no sensory deficit, investigations exclude relevant abnormality

Chronic postherpetic neuralgia• herpes zoster: trigeminal ggl. 15 % (V/1 80%)

ggl. Geniculi (VII, Ramsay-Hunt)• pain > 3 months• indicence: <40years:5 %, >60years:50 %, >70years:75 %• lymphoma patients with lymphoma: 10-25 %• treatment: capsaicin cream, vincristin iontoforesis

amitryptilincarbamazepine,

valproat neurolepticsamantadingabapentin

• prognosis: 56 % remission > 3 years

Symptomatic headaches

• Giant cell arteritis- incidence 3-9 / 100 000, 133 / 100 000(>50 years), 843 / 100 000 (>80 years)

- headache (70-90 %): permanent or transient, unilateral or bilateral

- swollen tender scalp artery, decreased pulsation (60 %)

- blindness (50 % -13 %): amaurosis fugax, AION transient / permanent

- diplopia (15 %)

- jaw claudication (25- 40 %)

- polymyalgia rheumatica (25 %)

- neurological signs: stroke, hearing loss, myelopathy, neuropathy

- elevated ESR and/or CRP (41 % > 100 mm/h, 89 % > 31 mm/h) biopsy

- treatment: 60- 80 mg methylprednisolon ( gradually decrease in every third day,

to 30 mg, then decrease weekly with 5 mg to 10 mg) 3 months, We ?

- headache relief within 3 days after the start of steroid treatment

• Costen syndroma