Primary HA
no obvious pathologic cause
migraine, cluster, tension type
secondary HA
pathological cause: tumor hemorrhage infection
warning signs and Sx of secondary HA
single HA sudden onset onset HA after age 50 recent onset HA <6 mo systemic disease change in HA pattern neuro Sx or abnormal neuro exam
PE for HA
general appearance
fever or abnormal vital signs, supple neck
mental status, speech, LOC
vision and retinal discs, pupils, EOMI, papilledema
asymmetry of strengths or reflexes
babinski
imaging for recurrent migraines
no CT or MRI unless recent change in HA pattern, focal neurologic signs or Sx
imaging for nonmigraine HA
CT MRI role unclear
imaging more likely to show cause for HA
MRI
imaging for HA in pregnancy
MRI w/o contrast
LP necessary for
Dx meningitis or encephalitis or possible carcinomatous meningitis
confirm subarachnoid hemorrhage but no blood on CT or MRI
increased opening pressure in LP
it can help Dx pseudotumor cerebri or idiopathic intracranial HTN
Dx primary headache syndrome
clinical features
characteristics of migraine features
sick HA with light and sound sensitivity worse with activity build up intensity 4-72 hours aura or sensory or motor deficits before pain
migrain criteria
>5 attacks >2 of following: -unilateral -pulsating -mod- severe intensity -aggravation routine physical activity >1 of following: -nausea and/or vomiting -photophobia, phonophobia No evidence of Hx or exam of disease that might cause HA
most common HA type that patients seek medical care
migraine
migraine demographics
W>africans>asians
genetics in migraines
possible 80% close family members with migraines too
transmission of migraine genetics
mother to daughter
mutations for familial hemiplegic migraine
Na and Ca Channels in neurons
causes of migraines
environmental factors “triggers”
psychiatric disorders
hormones: migraines can end with menopause
triggers for migraines
fasting, medication, circadian rhythms, environment, hormones, stress/overexertion
visual auras before migraines
blurred vision or blind spots
seeing flashing lights
seeing jagged lines
difficulty in focusing
sensory or motor changes before migraines
numbness or tingling of lips, face of hands on one side body
weakness in arms or legs, usually one side body
speech or language changes before migraines
inability to understand words
loss of speech or inability to speak normally
wolff concluded migraine pain from
reduction blood flow to occipital Cx in visual aura and the frontal or parietal cortices with other auras
actual pain from increase blood to brain
cortical spreading depression
sudden brief depolarization of cortical neurons, followed by reduction in neuronal depolarization and synaptic transmission
pain for migraine on PET
region of pons active up to 30 minutes before there is an increase in blood flow to brain
increased activity to CN V leads to what
secondary vasodilation and inflammation of dura mater
“trigeminovascular activation”
what NT are released from pons in migraine
serotonin
CGRP
substance P
NO
what is increased in urine from migraine attack
increased 5-hydroxyindoleacetic acid in urine from increased release serotonin 5-hydroxytyptamine
migraine ends with what
when neurons stop releasing more serotonin
sumatriptan
serotonin 1b 1d agonist
effective in stopping migraine attack by binding these inhibitory serotonin autoR
what is in migraine center
dorsal raphe nucleus
locus coeruleus
antagonists to what molecule help stop migraine
CGRP
help show not purely vascular process because CGRP has no role in vasoconstriction
most common type HA
tension type
clinical features tension type HA
dull, b/l, squeezing, tight
non pulsating
routine physical acitivty does not aggravate pain
no vomiting and more than one of : nausea, photophobia, phonophobia
MSK component, cervicogenic
medication seldom necessary
average length chronic tension type HA
> 15/mo
avg duration >4 hr/day if untreated and history >6 mo
chronic tension type HA should not take what
more than one analgesic a week
common findings with tension type HA
HTN depression anxiety insomnia DM/hypoglycemia
pain pills in people with frequent HA
cause increase frequency
cluster HA characteristics
brief 15 minutes-2 hours
one sided around eye
often 1 hr after falling asleep
occur daily or multiple times a day for weeks or mo at a time “season”
intense unilateral HA causing patient to bang head on wall
cluster HA
autonomic features of cluster HA
conjunctival injection lacrimation congestion rhinorrhea swelling miosis ptosis eyelid edema
weight gain abnormal vision and HA
secondary HA
pseudotumor cerebri
idiopathic intracranial HTN
signs pseudotumor cerebri
-progressive diffuse HA with intermittent loss of vision in 1+ eyes especially with eye movements
- obese young women!! E and P maybe or acutane
- increased intracranial P, from overproduction CSF
opening P >25
papilledema
what can occur in idiopathic intracranial HTN if not Dx early
irreversible loss of visual acuity
often extraocular palsy
CN VI III IV
Dx idiopathic intracranial HTN
spinal tap P and imaging
Tx idiopathic intracranial HTN
weight loss, corticosteroids, carbonic anhydrase inhibitors, topiramate
Trigeminal neuralgia
tic douloureux
brief shooting pain lasting only a sec
triggered by facial contact
one branch CN V
triggers for trigeminal neuralgia
touching face
eating
shaving
applying lipstick or makeup
causes trigeminal neuralgia
idiopathic
age of trigeminal neuralgia
uncommon under 50 y.o
unlesss brainstem lesion, MS tumors
Giant Cell Arteritis
temporal
example of vasculitis
non-infectious inflammation of aa leading to gradual occlusion
involves superficial temporal a (off external carotid a)
temporal arteritis can spread how leading to what complication
to adjacent internal carotid a
reaching ophthalmic a and cause complete visual loss via ischemia
other Sx temporal arteritis
fatigue
difficulty chewing
pain in neck and shoulders
giant cell arteritis component of
polymyalgia rheumatica
Dx temporal arteritis
ESR and CRP
confirmed by superficial temporary artery biopsy
cure for temporal arteritis
prednisone within 1st weeks of onset!!
typically 60 mg per day then gradually and slowly dec over mo