The sensory system and
pain syndromes
Vth year, dentistry, 30.09.2008
Department 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 system
Spinothalamic 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 perception
C fibers: thin, unmyelinated
A delta: thinly myelinated
Temperature
A delta: thinly myelinated
origin of pain - manifestations
Neuropathic pain
Mixed
caused by tissue damage
(bones,joints, tendons, muscles,
skin, viscera)2
primary lesion or dysfunction
of CNS (peripheral or central)1
Peripheral:
• Postherpetic neuralgia
• Trigeminal neuralgia
• Polyneuropathy in diabetes mell.
• Posttraumatic neuropathy
Central:
• Poststroke pain
Description:2
• Burning
• Tickling, itching,pins and needles
• Hypersensitivity to touch/cold
Nociceptiv pain
• Low back pain with
radiculopathy
• Cervical pain with
radiculopathy
• Cancer pain
• Carpal tunnel
syndrome
•
•
•
•
inflammation
fractures
osteoarthritis.
Postoperativ visceral pain
Description:2
• smarting
• Sharp
• Pulsating, throbbing
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 position
two points discrimination,
graphaesthesia !
stereoaesthesia !
Type of fibers: thick, myelinated
fibers (Aα, I, II)
Somatotopia in the cortex
Segmental innervation (dermatomes)
Peripheral innervation
Sensory disturbances
Positive 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 picks
Light 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 the
distribution area of the affected nerve
Polyneuropathies: symmetrical
sensory disturbance in stocking/glove
like distribution, more pronounced
distally
Sensory disturbance usually starts on
the 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
Headache
Pathways
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 disorder
Cranial neuralgias, central and primary facial pain :
13.Cranial neuralgias and central causes of facial pain
14.Other headache
International Headache Society. ICHD-II. Cephalalgia 2004; vol 24: suppl 1.
Migraine without aura
n 5
A)
B)
4 - 72 h
C)
1.
2.
2/4
3. ++ / +++
4. 
D)
1.
1/2
E)
/
+ 
2.
normal
Phases of migraine
Blau, Lancet, 1992
Migraine and „spreading depression”
Woods et al. 1994
Trigemino - vascular system
Lancet Neurology 2002;1:251-257.
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: criteria
A.
B.
n > 10
30 min < duration of pain< 7 nap
C.
2/4
+ / ++
D.
2/2
E.
/
normal
Convergence and sensitisation in the trigeminal nuclei
DRN, LC
Thalamus
pia / dura
vessels
art.
temp.
masticatory
muscle
Trigeminus
nucleus
caudalis
Brainstem and
spinal cord
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!)
Cluster headache: criteria
A)
n 5
B)
+++
30-180 min
C)
1/4
D)
Frequency = 1/2 ->50
E)
normal
Cluster headache: treatment
Acute 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 headache
International Headache Society. ICHD-II. Cephalalgia 2004; vol 24: suppl 1.
Trigeminal neuralgia
V/1
V/2
V/1
V/1
V/3
V/3
C2/3
Trigeminal neuralgia
•
•
•
•
Prevalence:
female/male :
age of onset:
site:
10-20 / 100 000 population
1.6
> 50 years (90%)
most frequently V/2,3
< 5 % V/1 division
~ 10 % all the three division
~ 5 % bilateral
Features:
• placebo effect
0 -1 % !
• trigger zone
90 %
• refracter phase
• spontanous remission ~ 50 %, < 6 months
• „pretrigeminal neuralgia”
Trigeminal neuralgia
Classical/Idiopathic
Symptomatic
• pain as described before
duration < 2 minutes
affecting one/more divisions
sudden onset
severe, sharp,stabbing pain
precipitated from trigger areas
patiens is pain free between
•persistence of aching
paroxysm
between paroxysm
• no neurological deficit
• sensory impairment or other
neurological deficit
•causative lesion , other than
• no causative lesion
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 examination
Rtg
otology
dental surgery
ophthalmology
brain MR
trigeminal SEP
psychology
„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
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•
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•
•
•
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•
Carbamazepine
Phenytoin
Valproate
L baclofen
Clonazepam
Pimozide
Tiapridal
Gabapentin
Pregabalin ?
400-1200 mg/day
300-600 mg/day
500-2000 mg/day
40-80 mg/day
2-8 mg/day
4-12 mg/day
300-600 mg/day
up to 3600 mg/day
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/2,3
a. cerebelli inferior anterior V/1
pain 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 neuralgia
Nasociliary neuralgia
Supraorbital neuralgia
Occipital 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:
•
•
•
•
pain
indicence:
lymphoma
treatment:
• prognosis:
trigeminal ggl. 15 % (V/1 80%)
ggl. Geniculi (VII, Ramsay-Hunt)
> 3 months
<40years:5 %, >60years:50 %, >70years:75 %
patients with lymphoma: 10-25 %
capsaicin cream, vincristin iontoforesis
amitryptilin
carbamazepine, valproat
neuroleptics
amantadin
gabapentin
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