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Adrian Pratama 405100018 Blok Neuropsikiatri
LO 1
Menjelaskan nyeri kepala (primer & sekunder)
Headache & other craniofacial pains
-General considerations-
Headache encompass all aches & pains located in the
head but in practice its application is restricted to
discomfort in the region of the cranial vault

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

Migraine with aura ~ Classic / neurologic migraine


Disturbance of nervous function (most often visual), followed in
few minutes to hours by hemicranial headache, nausea, vomitting
Last for hours / as long as a day or more
Migraine without aura ~ Common migraine
Unheralded onset over minutes/longer of increasing hemicranial
headache with or without vomitting
Epidemiology
Women >
1/3 more than 3 attacks monthly & require bedrest
May have its onset in childhood, but usually adolescence &
young adulthood >
Onset is < 30 yo
15% catamenial migraine
Some patients link their attacks to certain dietary items
(chocolate, cheese, fatty foods, oranges, tomatoes, onions,
excessive caffeine/withdrawal of caffeine)
Other clinical features (with/without aura)
Sensitivity to light, noise, often smells
Intensification with movement of the head
Severe pain lie down in a quiet, darkened room, tries to
sleep
Hemicranial & throbbing aspects most characteristic
features
Temporal scalp vessels may be tender (allodynia)
Headache is worsened by strain/jarring of the body/head
Tend to occur during the let down period
Other clinical features (with aura)
Onset soon after awakening
Mild changes in mood
hunger/anorexia, drowsiness, frequent yawning
Disturbance of vision
Unformed flashes of white, silver / multicolored light (photopsia)
Enlarging blind spot with a shimmering edge (scintillating
scotoma)
Dazzling zigzag lines (fortification spectra/teichopsia)
Blurred/shimmering/cloudy vision
Other focal neurologic symptoms
Numbness & tingling of lips, face, hand, slight confusion,
weakness of arm & leg, mild aphasia/dysarthria, dizziness,
uncertainty of gait/drowsiness
Migraine variants
Basilar migraine
Ophtalmoplegic & retinal migraine
Migraine following head injury
Migraine in young children
Reccurent attacks
Headache, limp & pale, abdominal pain, vomit, slight fever
Staggering, vertigo headache
Familial hemiplegic migraine
Mostly of infants & children, episodes of unilateral paralysis that may
long outlast the headache result of a mutation in an ion channel
Stroke & TIA with migraine
Status migrainosus
Migraine with CSF pleocytosis
Basilar migraine
Prominent brainstem symptoms
Young women/children/adolescence with a family history
of migraine, first develop visual phenomena

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)

In adults serious causes


Stroke & TIA with migraine
Have onset later in life
Transient aphasic, hemianesthetic, hemiplegic attacks of later
life may be migrainous origin (Fisher)
Leave a prolonged or even permanent deficit, indicative of an
ischemic stroke
Platelet aggregation, edema of the arterial wall, coagulability
>, dehydration from vomitting, intense prolonged spasm of the
vessels
Children with MELAS (mitochondrial myopathy, encepalopathy,
lactic acidosis, stroke like episodes); adult with rare CADASIL
(cerebral autosomal dominant, arteriopathy with subcortical
infarcts & leukoencepalopathy) migraine may be prominent
features
Status migranisous
Condition of daily/virtually severe contionuous headache
Clinical features
Initially unilateral, later more generalized; more or less
throbbing
Constant superimposed ache & is disabling
Vomitting/nausea
Sometimes follows a head injury/viral infection
DD tension+migraine, analgesia rebound headache,
ergotamine/serotonin agonist dependency headache
Treatment
Admit to the hospital, discontinue all ergot & narcotic medication
Administer IV hydration, corticosteroids, one of the serotonin
agonist medications/dihydroergotamine & lidocaine IV infusion
Cause & pathogenesis of migraine
Underlying genetic factors

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

Severely ill patients failed to obtain relief from a prolonged


headache with above medications
metoclopramide 10 mg IV, followed by DHE 0.5 to 1 mg IV every 8 h
for 2 days
Preventive treatment
Beta adrenergic blocker
Propranolol beginning with 10 to 20 mg two to three times daily and
increasing the dosage gradually to as much as 240 mg daily
atenolol (40 to 160 mg/d), timolol (20 to 40 mg/d), or metoprolol (100
to 200 mg/d)
Antiepileptic drugs (4-6weeks failed of beta blocker)
valproic acid 250 mg taken three to four times daily
Tricycilic antidepressants
amitriptyline, 25 to 125 mg nightly
CCB verapamil, 320 to 480 mg/d; nifedipine, 90 to 360 mg/d
Methysergide 2 to 6 mg daily for several weeks or months
Isometheptene; indomethacin, 150 to 200 mg/d; and cyproheptadine
4 to 16 mg/nightly
injection of botulinum toxin (Botox) into sensitive temporalis and other
cranial muscles
Limitting precipitating foods
Cluster headache
Occurs predominantly in adult male; 20-50 yo
Consistent unilateral orbital localization
Pain is felt deep in & around the eye, very intense,
nonthrobbing, often radiates into the forehead, temple, & cheek
Nightly reccurence (1-2 hr after the onset of sleep /
several times during the night, less ofteh during the day)
Unattended by aura/vomitting
alarm clock headache (recurs with remarkable regularity
each night for periods extending over 6-12 weeks,
followed by complete freedom for many months/years
Associated vasomotor phenomena
Blocked nostril, rhinorrhea, injected conjunctivum, lacrimation,
miosis, flush & edema of the cheek (lasting 45 min)
Slight ptosis on the side of orbital pain
Homolateral temporal artery become prominent & tender
during an attack
Skin over the scalp & face may be hyperalgesic
Most patient arise from bed during an attack & sit in a
chair holding a hand to the side of the side
Variants of cluster headache
(trigeminal autonomic cephalgias)
Sphenopalatine, petrosal, vidian & ciliary neuralgia
Paroxysmal pain behind the eye/nose/in the upper jaw or temple
Associated with blocking of the nostril/lacrimation
Lower cluster headache
Syndrome with infraorbital radiation of the pain
Ipsilateral partial Horner syndrome
Chronic paroxysmal hemicrania
Shorter duration (2-45 min); affect temporoorbital region of one side
Accompanied by conjunctival hyperemia, rhinorrhea, partial Horner
syndrome, periorbital ecchymosis
Occur many times each day, recur daily (16 attacks daily for more
than 40 years)
Th/ respond dramatically to the adminstration of indomethacin, 2-
50mg tid
Treatment
Inhalation of 100 percent oxygen via mask for 10 to 15
min at the onset
Verapamil 80 mg qid and increasing the dose over days
ECG monitoring
single anticipatory dose of ergotamine at bedtime (2 mg
orally)
Intranasal lidocaine or sumatriptan
If ergotamine & sumatriptan are ineffective verapamil,
up to 480 mg per day
Lithium 600 mg, up to 900 mg daily
prednisone, beginning with 75 mg daily for 3 days and
then reducing the dose at 3-day intervals
Tension headache
most common variety of headache, women >, middle age >,
coincide with anxiety, had readily recognized symptoms of
depression

Usually bilateral with occipitonuchal, temporal, or frontal


predominance or diffuse extension over the top of the cranium
Pain description dull & aching; fullness, tightness, pressure,
feeling that the head is swollen & may burst
Onset is more gradual
Persist only mild fluctuation for days, weeks, months or even
years
Undisturbed sleep
Headache develops soon after awakening
Pathogenesis
Result of excessive contraction of craniocervical muscles & an
associated contriction of the scalp arteries
NO creating a central sensitization to sensory stimulation
from cranial structures (recently)
The craniocervical muscles are quite relaxed by palpation,
show no evidence of persistent contraction when measured
by surface EMG
Pericranial & trapezius muscles are hardened in patients
with tension headache
Treatment
Simple analgesics (aspirin, acetaminophen, NSAIDs)
Stronger analgesic medication should be AVOIDED
Anxiety & depression relieve amytriptiline
CCB, phenelzine, cyproheptadine
Massage, meditation, biofeedback tech
Trigeminal neuralgia (tic douloureux)
Common disorder of middle & later life
Paroxysms of intense, stabbing pain in the distribution of
mandibular & maxillary divisions
Pain seldom lasts more than a few seconds or a minute (tic)
Recur frequently both day & night for several weeks at a time
Continous discomfort, itching, sensitivity
Induced by touch & possibly tickle rather than painful/thermal
stimuli
Another characteristic
Initiation of a jab/series of jabs of pain by stimulation of certain
areas of face, lips, gums (ex. Shaving, brushing teeth, movement of
these parts in chewing, talking, yawning) trigger factors
Diagnosis
Rest on strict clinical features
Specify the type
idiopathic
Symptomatic
Multiple sclerosis (bilateral)
Aneurysm of the basilar artery
Tumor in the cerebellopontine angle (meningioma, epidermoid)
Treatment
Antiepileptic drugs alone/in combination
phenytoin (300 to 400 mg/d),
valproic acid (800 to 1,200 mg/d),
clonazepam (2 to 6 mg/d),
gabapentin (300 to 900 mg/d or more),
pregabalin (150 to 300 mg/d),
carbamazepine (600 to 1,200 mg/d)
anesthetic (proparacaine 0.5 percent)
Surgery
repositioning a small branch of the basilar artery that was found to
compress the fifth nerve
controlled thermocoagulation of the trigeminal roots
microvascular decompression
Gamma Knife
LO 2
Menjelaskan vertigo
Anatomic & physiologic consideration
Dizziness & vertigo
Along with headache, back pain, & fatigue
Dizziness a number of different sensory experiences (a
feeling of rotation or whirling as well as nonrotatory
swaying, weakness, faintness, light headedness,
unsteadiness)
4 categories
Vertigo a physical sensation of motion of self or the
environment
Near syncope sensation of faintness
Disequilibrium disorder imbalance of stance or gait
Ill defined light headedness, accompanies anxiety
Etiology
Approach to the patient with vertigo
Spontaneous vertigo
Single prolonged episode
Vestibular neuronitis
Labyrinthine concussions
Lateral medullary / cerebellar infarction
Recurrent episodes
Meniere disease
Perilymph fistula
Migraine
Posterior circulation ischemia
Positional vertigo
Peripheral
BPPV
Central
Clinical characteristics of vertigo
Statement that objects in the environment have spun
around/moved rhythmically in one direction/that a sensation of
whirling of the had & body
Up & down movement of the body, usually the head
Patient may compare the feeling to that imparted by the pitch
& roll of a ship
Floor or wall may seem to tilt/to sink/rise up
In walking the patient may have had sensation of leaning/
being pulled to the ground/to one side or another (static tilt)
Being drawn by strong magnet
Oscillopsia illusionary movement of the environment
should be interpreted as vertigo (due to nystagmus)
An aggravation of symptoms by turning over in bed or
closing his eyes, a sense of imbalance when making a quick
turn on foot/in car
Abruptness & severity virtually throw the patient to the
ground
Mildest form vertigo+nausea, vomitting, palor,
perspiration, some difficulty with walking
Forced to lie down, realized that one position (one side
with the eyes closed) reduced vertigo
Meniere disease & other forms of labyrinthine vertigo
Meniere disease recurrent attacks of vertigo + fluctuating
tinnitus & deafness
Labyrinthine disease most common cause of true vertigo

Men & women equally; 5th decade of life; hereditary form


& sporadic

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

Vertigo started when lying down/rolling over in bed,


bending over, straightening up, tilting the head backward
Began in the middle of the night/early morning,
presumably while shifting position during sleep & rapidly
making one ear dependent/rolling over to get out of bed
Last for less than a minute, but these may recur periodically
for several days/for many months (rarely years)
As the rule examination discloses no abnormalities of
hearing/other identifiable lesions in the ear/elsewhere
Vertigo accompanied ny oscillopsia & nystagmus with the
rapid component away from the affected ear
Nystagmus is predominantly torsional & may have additional
vertical component in the eye opposite the affected ear
Etiology
Several days/weeks after cerebral trauma
Viral neurolabyrinthitis
Meniere disease, types with vertebrobasilar stroke, trauma,
posterior fossa tumors + positional change that induce vertigo &
nystagmus

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

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