Headache Flashcards
migraine
syndrome characterized by intermittent pounding or throbbing headache, potentially preceded by an aura
frequent association with nausea, photophobia, phonophobia and exertional worsening
subarachnoid hemmorhage
bleeding into the CSF fluid, usually due to leakage of an aneurysm or vascular malformation
tension-type headache
recurrent headache with a bilateral squeezing and pressing senation that usually does not prevent normal activity and does not significantly worsen with exertion
cluster headache
recurrent, severe headache which is unilateral and periorbital and often asociated with autonomic symptoms of tearing and nasal congestion
temporal arteritis
condition of inflammation of major cranial blood vessels–>can result in blindness or stroke depending onvessels involved
paresthesia
abnormal sensation that is not due to an external stimulus
aura
warning, prior to onset of a symptom
increased intracranial pressures do NOT
cause headaches
drainage of spinal hluid
causes low pressure headache secondary to fluid traction on venous sinuses when brain sinks towards tentorium as it loses CSF
inflammation in subarachnoid space
results in headache
lesions above tentorium produce
pain referred to trigem distributions (forehead, behind eyes) because dura in this region is supplied by trigem nerve
lesions in posterior fossa produce
pain ine ar, back of head (cn 9,10, and upper 3 cervical roots)
meningeal irritation headache
subarachnoid hemorrhage and meningitis
subarachnoid hemorrhage
sevre, sudden onset, persists, remainder of neuro exam normal
what do you do if you suspect subarachnoid hemorrhage?
do CT
if CT negative, do lumbar uncture
neoplasms
mild, nonspecific, worse in morning
focal symptoms
abscess
focal signs of mental changes often present
evidence of increased ICP
infection?
acute hydrocephalus
caused by obstructing CSF pathways (inflammation, blood, tumor)
brain dysfunction
fundi–>increased ICP
predisposing factors to intracranial hypertension
polycystic ovarian disease
high estrogen
exogengeous estrogen, vitamin a, outdated tetracycline
what helps intracranial hypertension
carbonic anhydrase inhibitors
shunting
protoypical patient for intracranial hypertension
overweight young woman
three types of vascular headaches
giant cell (temporal) arteritis
hypertensive encephalopathy
vascular malformation
giant cell temporal arteritis
systemic vasculitis
hypertensive encephalopathy
vascular malformation
giant cell temporal arteritis
systemic vasculitis that likes cranial nerves; usually in people over 50
clinical picture giant cell arteritis
1- polymyalgia rheumatic- malaise, loss of energy, proximal jt pains
2- nonspecific headaches; associated with tenderness and swelling over temporal or occipital arteries
3- evidence of arterial insufficiency in distribution of branches of cranial vessels (jaw cluadication, infarction of tongue or scalp)
external carotid insuffiency
jaw claudication or infarction of the tongue or scalp
internal carotid insuffiency
produces retina ischemia, blindness, even stroke
sed rate giant cell arteritis
very high
treatment giant cell arteritis
steroids
ddx lupus
lupus inflames systemic
to confirm after high sed rate
biopsy (bilaterally)
hypertensive encephalopathy
cerebral vasoconstriction occurs in response to systemic HTN to preserve a constant cerebral blood flow–>autoregulation
–in this, autoreg fails at parts and arteries dilate despite severe HTN (–>edema and hemorrhage)
hypertensive encephalopathy should be considered
patients with severe HTN, or preveiously normotensive patients that develop less evere HTN
vascular malformations
may result in headaches with features of migraine
venous sinus thrombosis
headache probably results from stretching of pain sensitive veins that drain into sinuses (although increased ICP may play a role)
main predisposing factors of venous sinus thrombosis
hypercoagulability and increased osmolarity
high estrogen states, dehydration
cervical headache
pain from cervical region–usually felt over neck and occiput–>can be refferred around temples and even into frontal region
two types of cervical headaches
occipital neuralgia-irritation or entrapment of grater occipital nerve
aterial dissection-result in acute neck pain sometimes acompanied by ischemic symptoms-
metabolic headaches
often associated with hypoxemia, hypercapnia, anemia and possibly associated with cerebral vasodilation
glaucoma
pain localized in the eye or behind the head
most significant criteria of dangerous headache
duration
migraine aura assocaited wtih
intracranial vasoconstriction
BV dilation
does not directly cause pain; pain does appear to be from activation of nerves in BV that contribute to sterile inflame dilation
spreading depression
most prominant theroy of causation: slowly spreading wave of initial neuronal excitation, followed by depression that spreads over cortex
scintillating scotomata
enlarging blind spot with shimering edge
negative scotomata
blurring of visual field
photophasia
colored blind spots
fortification spectra
jagged lines
symptoms in migraine often____, but can also be____
homonymous (cortical involvment)
visual loss in one eye due to retinal ischemia
somatosensory march of migraine can be diffferentiated from sensory seizures by
- gradual onset
- slow march (several minutes between)
- NOT restricted to single BV as they are progressing on somatotrophic area
- usually clears first in area that was first involved
general progression of aphasia in aura
visual
- ->sensory
- ->speech
occulomotor, abducents nerve involvment in aura
less often, but may last for several weeks after onste at height of headache
mech–dilation of ICA compressed 3rd or 6th nerve in cavernosus sinus to cause paresis or paralysis
familial hemiplegic migraines
onset early in childhod, strong family history common (genetics)
Type 1 FHM
CACNA1A gene (P/Q channel)
Type 2
Na-K ATPase
Type 3
involves neuronal voltage gated Na channels
in FHM..
headache appears first and symptoms of weakness and sensory loss appear later
–neuro signs freq outlast headache by hours or days and occasionally may be permanent
treatment of migraine
avoidance of trigger factors
medications during headache
preventative (prophylactic) medications
medications DURING headache
- nonspecific analgesics/anti-inflam
- meds that activate 5HT R (ergotamine derivatives and triptans)
mechanism of ergotamine derivs and triptans
capable of affecting trigem nerve endings on BV–>decrease release of inflame neuropeptides (CGRP, Sub P) and constrict BV
two primary difficulties with short acting analgesics
becomes less effective when migraine is well established
frequent use of short acting meds results in gradual decrese in response to these meds (rebound headache)
preventative mds
betablockers
ca channel blockers
heterocyclic antidepressants
anticonvulsants
pacing the floor
cluster headache
horners syndrome
cluster headaches
gender and cluster headache
men more than women
migrane chemicals
increase in level of blood 5HT at the onset of headaches and later a depletion
cluster headaches (differentially)
no change in 5HT levels, but have an increase in blood histamine concentration coincident with headache
overactivity in caudal hypothalamus during attack
breathing in O2 aborts quickly
no aura
tension type headache
when under pressure, mild cervical or bifrontal headache
hyperactivity of frontalis and cervical musculature
tension type headaches are more likely to be
chronic, and threfore more likely to result in frequent analgesic intake
analgesic rebound headache may be a problem
indomethacin responsive headache symptoms
group of headache symptoms that share characteristics of being highly responsive to indomethacin (as opposed to other NSAIDs)
IRHs fall into several categories
trigeminal-autonomic cephalgias (unilateral headache accompanied by a variety of autonomic symptoms in head)
headaches induced by valsalva
headaches taht have primary stabbing quality
trigeminal autonomic cephalgias
Short lasting Unilateral Neuralgiform headache Conjunctival injfection Tearing
-middle aged men; reocur but only last a few minutes
trigem autonomic cephalgias vs paroxysmal hemicranias
similar but pain is longer and genreally in women
indomethacin responsive headache symptoms
sharp and localized, short duration
neuralgias
sharp, severe, brief
“trigger point”-areas of skin or mucosa that prvoke pain when touched
no sensory nerve included
Tic douloreaux
trigeminal neuralgia; usually occurs in elderly and involves second and tird trigem division
no sensory loss
treatment with carbamezapine- if dont treat you will need a procedure
glossopharyngeal neuralgia
less common; pain felt in throat, ear, neck
may be triggered by swallowing
definitive test for identifying aneurysm
angiogram
only way to rule out subarachnoid hemorrhage
lumbar puncture
sudden onset headache with focal neurologic deficit
intracerebral hemorrhage
treatment of giant temporal arteritis can prevent
blindness
stroke
headache that awakens from sound sleep
increased intracranial pressure?
mass lesion, sagittal sinus thrombosis, pseudotumor cerebri
behavior or personality change
encephalitis, mass
migraine unilateral or bilateral
unilateral
