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How to approach?
Quality of pain
Intensity of the pain
Location of the pain
Mode of onset
Relationship of headache to certain biologic events & also to
certain precipitating / relieving factors
Quality
Tightness, aching, pressure, bursting, sharpness, stabbing
Pulsatile/throbbing waxing & waning of the headache
without any relation of the pulse
Authentic pulsatile throobing migraine
Intensity of pain
Severe migrain headahe seldom allows to perform the
days work
The most intense cranial pains associated with meningitis
& subarachnoid hemorrhage
Location
Migraine unilateral, associated with nausea, sensitivity to light,
sound, smells
Lesions of paranasal sinuses, teeth, eyes, upper cervical vert
less sharply localized pain, but still one that is referred to a
certain region
Lesions in the posterior fossa pain in the occipitonuchal region,
usually are homolateral if the lesion is one sided
Supreatentorial lesion frontotemporal pain
Glaucoma, sinusitis, thrombosis of vertebral/basilar artery,
pressure on the tentorium, ICP > frontal pain
Ear pain ear disease, throat, cervical muscles, spine, structure
on posterior fossa
Periorbital/supraorbital pain dissection cervical portion of int
carotid artery
Vertex/biparietal pain sphenoid/ethmoid sinus disease,
thrombosis of superior sagittal venous sinus
Mode of onset
Subarachnoid hemorrhage abrupt attack (second / min)
Meningitis gradual, over several hours/days
Migraine early in morning hours/daytime, peak
reached over 30 min (4-24 hours/ -72 hours)
Cluster headache unbearably severe unilateral
orbitotemporal pain, hour/two after falling
asleep/predictable time during the day, recurring
nightly/daily for a period of several weeks months
(30-45 min)
Posterior fossa masses worse in morning on awakening
Tension headache varying intensity for weeks months /
longer; associated depressive illness
Relationship of headache to certain biologic events &
certain precipitating/relieving factors
Premenstrual tension & catamenial migraine
Headache from cervical spine disease
Intense after period of inactivity
Face ache from infection of nasal sinus
Clock-like regularity, worsened by stooping/changes in atmospheric
pressure
Eyestrain headache
Follow prolonged use of the eyes
Alcohol, intense exercise, stooping, straining, coughing, sexual
intercourse bursting type of headache
Headache is made worse by coughing, sudden movement,
straining intracranial source
Migraine
Weekend headache, when the scalp is stroked in combing/fixing hair
Pain sensitive cranial structures
Skin, subcutaneus tissue, muscle, extracranial arteries,
periosteum
Delicate structures of the eye, ear, nasal cavities,
paranasal sinuses
Intracranial venous sinuses
Parts of the dura, arteries within the dura
Middle meningeal & superficial temporal arteries
Optic, occulomotor, trigeminal, glossopharyngeal, vagus,
first three cervical nerves
Mechanisms of cranial pain
Intracranial masses only if they deform, displace or exert
traction on vessels & dural structures; happen long before ICP >
Dilatation of intracranial/extracranial arteries
Infection/blockage of paranasal sinuses
Headache of ocular origins
Headaches that accompany diseases of ligaments, muscles,
apophysial joints in the upper part of cervical spine
Headache of meningeal irritation
LP / spontaneous low CSF pressure
Headache that are aggravated by lying down
Exertional headache
Types of headaches
Primary Secondary
Migraine Glaucoma
Tension type headache Purulent sinusitis
Cluster headache Subarachnoid hemorrhage
One of the trigeminal- Bacterial/viral meningitis
sympathetic migraine
variants of migraine /
cluster
Migraine
Highly prevalent & largely familial disorder
Periodic, commonly unilateral, pulsatile headache (childhood,
adolescence, early adult life), recur with diminishing frequency
during advancing years
Clinical features
Associated vertigo, staggering, incoordination of the limbs,
dysarthria, tingling in both hand & feet, both sides of mouth
(last 10-30 min) usually occipital headache
Symptoms = ischemia of the basilar-posterior cerebral arteries
Ophtalmoplegic & retinal migraine
Common in children
Recurrent unilateral headaches associated with weakness
of extraocular muscles
Transient 3rd nerve palsy with ptosis with/without
involvement of the pupil
Ocular paresis often outlasts the headache (days/weeks)
after many attacks slight mydriasis;
ophthalmoparesis may remain permanently (rare)
Uniocular visual disturbance with scotoma, retinal
hemorrhages (some patients)
Pathogenesis
Distention & excessive pulsation of branches of the external
carotid artery (Harold Wolff)
Regional reduction in cerebral circulation spreading forward
from the occipital region during the period when neurologic
symptoms appear (Olsen & colleagues)
Dilatation of the superior temporal artery on the side of the
migraine during the headache period; frequently a reduction in
posterior cortical blood flow during auras, similarly during aura
(Iversen)
The trigeminovascular complexs pathogenesis
(Moskowitz)
Innervation both extracranial & intracranial vessels by
small unmyelinated fibers of trigeminal nerve that subserve
both pain & autonomic function
Activation of these fibers
Releases substance P, calcitonin gene related peptide (CGRP),
other peptides to vessel wall
Sensitize the trigeminal system
pulsatility of cranial vessels
Permeability > inflammatory response
5-HT/serotonin humoral mediator in the neural &
vascular component of migraine headache
Treatment
Aspirin, acetaminophen, NSAID
Codeine / oxycodeine; usually combined with
aspirin/acetaminophen limited periods
Combination of aspirin/acetaminophen, caffeine &
butalbital
Severe attacks sumatriptan/other triptans or ergot
alkaloids, ergotamine & dihydroergotamine (DHE)
single 6-mg dose of sumatriptan
Sumatriptan can also be given orally in a 50- or 100-mg tablet,
zolmitriptan in a 2.5- or 5-mg tablet, and rizatriptan in a 10-
mg dose repeated, if needed, in 2 h
Ergotamine uncoated 1- to 2-mg tablet of ergotamine tartrate,
held under the tongue until dissolved (or swallowed) can +
caffeine
single oral dose of promethazine 50 mg, or of metoclopramide
20 mg, given with the ergotamine nausea & vomitting
because of ergotamine
serotonin agonists and ergots are generally avoided if there is an
ongoing and prolonged aura of any type
sympathomimetic drug isometheptene combined with a sedative,
and acetaminophen
prochlorperazine, chlorpromazine, ketorolac, and intranasal
lidocaine
IV corticosteroids refractory cases
Pathogenesis
Endolymph volume > distention of the endolymphatic system
(endolympathic hydrops)
Ruptures of the membranous labyrinth
Dumping of potassium containing endolymph into perilymph
paralyzing effect on vestibular nerve degeneration of cochlear
hair cells
Immune circulating antibodies
Clinical features
Abrupt & last for several minutes to an hour/longer
Unmistakably whirling/rotational
Cannot stand/walk (severe)
Nausea & vomitting, low pitched tinnitus, feeling fullness in
ear, diminution in hearing
Nystagmus is present during acute attack horizontal in
type
Patient prefers to lie with the faulty ear uppermost
Recur several times weekly for many weeks on end, may
be remissions of several years duration
Symptoms on anxiety
Sudden, violent falling attacks (otolithic catastrophe)
Little evidence deformation of the otolothic membrane of the
utricle & saccule
Sensation of being pushed/knocked to the ground without
warning
May be sudden movement/tilt of the environment before the fall
Hearing loss
May be the 1st attack of vertigo, but may appear later
Episodic deafness without vertigo (cochlear meniere syndrome)
Treatment
Rest in bed (most effective)
antihistaminic agents cyclizine (Marezine), meclizine
(Bonine, Antivert), or transdermal scopolamine are useful in
the more protracted cases
Promethazine (an effective vestibular suppressant),
trimethobenzamide 200-mg suppositories nausea &
vomitting
low-salt diet in combination with ammonium chloride or
potassium and diuretics
dehydrating agents such as oral glycerol
CCB
Mild sedative drugs
Surgical means
Destruction of the labyrinth
Only in patient with strictly UNILATERAL diseas
Endolympathic-subarachnoid shunt
Selective destruction of the vestibule by cryogenic probe
Decompression of the eight cranial nerve
Separating it from an adjacent vessel
Benign positional vertigo
Paroxysmal vertigo & nystagmus that occur only with the
assumption of certain positions of the head
More frequent than meniere
Cupulolithiasis (pathophysiology)
Otolithic crystal that detached attached themselves to the cupula
of the posterior semicircular canal
free-floating clot in the endolymph of the canal (canalolithiasis)
gravitates to the most dependant part of the canal during changes in
the position of the head
90% posterior semicircular canal
10% lateral canal
Diagnosis (Dix-Hallpike maneuver)
Dix-Hallpike maneuver to elicit benign positional vertigo
(originating in the right ear). The maneuver begins with the
patient seated and the head turned to one side at 45 degrees
(A),
which aligns the right posterior semicircular canal with the
sagittal plane of the head. The patient is then helped to recline
rapidly so that the head hangs over the edge of the table (B),
still turned 45 degrees from the midline.
Within several seconds, this elicits vertigo and nystagmus that is
right beating with a rotary (counterclockwise) component. An
important feature of this type of "peripheral" vertigo is a
change in the direction of nystagmus when the patient sits up
again with his head still rotated. If no nystagmus is elicited, the
maneuver is repeated after a pause of 30 s, with the head
turned to the left
Treatment (Dix-Hallpike maneuver)
Bedside maneuver for the treatment of a patient with benign
paroxysmal positional vertigo affecting the right ear. The presumed
position of the debris within the labyrinth during the maneuver is
shown on each panel. The maneuver is a four-step procedure. First, a
DixHallpike test is performed with the patient's head rotated 45
degrees toward the (affected) right ear and the neck slightly
extended with the chin pointed slightly upward. This position results in
the patient's head hanging to the right (A).
Once the vertigo and nystagmus provoked by this maneuver cease,
the patient's head is rotated about the rostralcaudal body axis until
the left ear is down (B).
Then the head and body are further rotated until the head is almost
face down (C).
The vertex of the head is kept tilted upward throughout the rotation.
The patient should be kept in the final, facedown position for about
10 to 15 s. With the head kept turned toward the left shoulder, the
patient is brought into the seated position (D).
References
Adams Principles of Neurology, 10th edition
Blueprints Neurology, 3rd edition