HA Flashcards
Trigeminal autonomic cephalgias
- SUNHA short unilateral neuralgiform HA attacks = SUNCT (+conjunctival injection + tearing) and
SUNA (+autonomic symptoms-fullness ear, miosis/ptosis)
- lasts sec-min, up to hundreds a time per day
-V1 distribution (vs trigeminal neuralgia - V2/3 distribution)
Tx: lamotrigine, topiramate, gabapentin - paroxysmal hemicrania - shorter-lasting cluster headache attacks that affect women more
- many short episodes a day (not hundreds) lasting<30 min, V1 distribution, autonomic Sx
-circadian periodicity,
-trigger: neck turning
Tx: indomethacin - has to respond 100% - cluster - once daily, 15 min-3 hrs
-side-locked, (contrasts with migraine, which, despite the etymology of the term, is bilateral in about 40%)
-agitation
trigger: alcohol
-acute Tx - oxygen, sumatriptan; intranasal lidocaine; NOT frovatriptan (long acting)
prevent: VERAPAMIL PLUS: valproic acid, melatonin (decreased during cluster period) steroids, lithium - hemicrania continua - constant unilateral baseline pain with superimposed attacks of more intense pain accompanied by autonomic features
-migraine features
-Tx: indomethacin
lacrimation, rhinorrhea, nasal congestion: parasympathetic outflow from CNVII superior salivatory nucleus running along greater superficial petrosal nerve->sphenopalatine ganglion->synapse on CN V to lacrimal glands
-all need MRI +/-
Migraine diagnosis
Dx: 5 total HA >4 hours-72 hours
+ 2 of 4: *unilateral,
*throbbing,
*moderate/severe intensity,
*aggravation by routine physical activity
+ N +/- V OR photophobia AND phonophobia
-if kids - can be 2 hrs
(status migrainosis = >72 hours)
+aura=classic migraine-sensory/speech/language
no aura = common migraine
-if migraine_aura +non smokers-can use OCP (progestin only better)
-CN V cross activation of PNS via superior salivatory nuc of the CN VII->rhinorrhea, lacrimation,sinus pressure, congestion, conjunctival injection
chronic migraine: >15 HA days per month for 3 months
-least likely to be associated with chronic migraine: brain tumor
-OnabotulinumtoxinA- cleave SNAP25 (SNARE protein)-
heavy chain binds cell membrane, endocytosis->light chain activated->cleaves SNAP25->no vesicle fusion, no ACh release into NMJ->muscle contraction blocked and blocks CGRP
episodic tension type HA
Most common primary HA disorder in general population (migraine most common for HA you see a doctor for)
10 HA 30 min-7 days
*bilateral
*NON pulsating -pressure/tight
*mild-mod pain
*not aggravated by routine activity
-no N, V;
-either photophobia or phonophobia, not both
pathophysiology of migraine
- cortical spreading depression - disrupted ion homeostasis
- meningeal blood vessel dilation, activate trigeminovascular system (triptans inhibit dilation)
- CGRP release from CN V sensory nerves, substance P
- worsening vasodilation
- CN V nociceptive afferents-> trigeminal nuc caudalis ->thalamus, cortex
- Trig. nuc claudalis firing -> central sensitization
migraine treatment
preventative if 4 HA days/month
CGRP monoclonal Ab: eptinezumab, erenumab, fremanezumab, and galcanezumab
gepants: atogepant and rimegepant
non migraine specific:
strongest evidence: topiramate, divalproex, sodium valproate, metoprolol, propranolol, timolol
2nd line-amitryptyline, venlafaxine, atenolol, nadolol
verapamil-causes constipation (lowest level of evidence)
triptan: agonist at 5HT-1B + 5HT-1D R
-1B- vasoconstricts in meninges
-1D- inhibits trigeminal peptide release presynaptically;
-decrease trig nuc caudalis processing
-decreases nucleus tractus solitarius - inhibit N/V
status migrainosis
> 72 hours
-cutaneous allodynia - central sensitization
-DHE only if triptan>24 hours
new daily persistent HA
-recall exact date it started
-starts suddenly
-3 months
-migraine or tension-type like
trigeminal neuralgia
can be 2/2 MS esp if bilateral; also DDx lyme, sarcoid
1st line carbamazepine; 2nd line lamotrigine, topiramate, gabapentin
CSF leak
-low pressure HA after trauma /dural tear from spondylosis, meningeal diverticula
-+/- stiff neck, tinnitus, nausea
-most common in thoracic spine
MRI: pachymeningeal enhancement, sagging, pituitary enlargement, engorgement venous sinuses
LP: low pressure
-MRI meylography with fat suppression (CSF leak protocol)
Tx: conservative, then blood patch
CADASIL
cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy
[migraine specific to CADASIL]
-migraine+aura + deep white matter strokes extending to anterior temporal lobes + dementia
-AD, NOTCH3, chromosome 19 (a Cad old enough to have notches in your bedpost and 9 divided by 3)
familial hemiplegic migraine
all AD, linked to Calcium, sodium/potassium ATPase, pre and post-synaptic VG sodium channel mutations
-only migraine with weakness
-FHM1-CACNA1A - P/Q calcium channel - cerebellar - nystagmus, ataxia, coma, prolonged hemiplegia
FHM2-ATP1A2- A1A2 - no cerebellar -seizures+intellectual disability,
FHM3-SCN1A-pre and post syn VG sodium channels
Dx: at least 2 attacks + aura, 1 aura has to be unilateral
idiopathic cranial pachymeningitis
HA + hemiparesis/ataxia/aphasia/confusion
-diffuse leptomeningeal enhancement
CSF: mild leukocyte predominance
biopsy: perivascular inflmmation
migraine with brainstem aura
NO motor weakness
-2 attacks, one type of aura has to be unilateral
Hypnic headache
headache only during sleep, causes patient to wake up
-10 or more days/month for 3 months
15 min-4 hours
-no restlessness/autonomic Sx
-in >50 years, bilateral,
Tx: lithium, indomethacin, caffeine, melatonin
retinal migraine
-vs migraine with aura: visual disturbance is monocular, draw what pt sees or examine during attack
-positive phenomenon usually
-can get rhinorrhea, lacrimation, sinus pressure, nasal congestion
-exclude amarosis fugax
