buzz Flashcards
imaging findings of CSF leak
pachymeningeal enhancement, “sagging brain” can look like Chiari I with crowded posterior fossa, big pituitary, small vents, engorged venous sinuses, can see subdural hematomas/hygromas too
most common location of spontaneous CSF leak
thoracic spine
causes of low pressure CSF headache
trauma, LP, neurosurgery, dural tear from spondylosis, meningeal diverticula
symptoms associated with CSF leak
low pressure headache (positional), neck pain, tinnitus/hearing changes, nausea, photophobia
SUNCT
short unilateral neuralgiform HA with conjuctival injection + tearing
20+ attacks, mod-severe pain, lasting 1-600 seconds, occuring 1x+ daily
MRI w/wo contrast is warranted to exclude secondary cause like pituitary or posterior fossa tumors/abnormalities
headache red flags
NEW HEADACHE > 50 years old
systemic sx, hx cancer/immunocomp, focal neuro sx, thunderclap HA
name the TACs (trigeminal autonomic cephalalgias)
cluster headache
hemicrania continua
paroxysmal hemicrania
SUNCT/SUNA
difference between paroxysmal hemicrania versus SUNCT/SUNA
paroxysmal hemicrania = 20 attacks lasting 2 - 30 MINUTES, >5 x per day
vs
SUNCT/SUNA = 20 attacks lasting 1-600 SECONDS, >1 x per day
how long does cluster headache last
15 minutes - 3 hours in duration
temporal arteritis management
check ESR, but don’t wait for biopsy to start prednisone, to prevent vision loss
hemicrania continua management
indomethacin 150 mg daily, up to 225 mg x 1 week (MUST RESPOND TO DIAGNOSE)
MRI/MRA w/wo to look at trigeminal nerve
hemicrania continua management
indomethacin 150 mg daily, up to 225 mg x 1 week (MUST RESPOND TO DIAGNOSE)
MRI/MRA w/wo to look at trigeminal nerve
MOA of triptans
agonists at 5HT1B (vasoconstricts) and 5HT1D (inhibits trigeminal inflammatory peptide release, treats N/V)
pathophy of autonomic sx in TACs
parasympathetic outflow from superior salivatory nucleus of facial nerve –> activates lacrimal and nasal mucosal glands.
noxious stim to trigeminal distribution –> trigeminal-autonomic reflex via brainstem connection between TNC and SSN
pathophys of migraine
- activation of super sensitive central generator
- cortical spreading depression
- blood vessel dilation + activation of trigeminovascular system
- release of vasoactive neuropepties (CGRP!!) –> inflammation
- worsening vasodilation, more neuropeptides, more pain
- pain signals to trigeminal nucleus caudalis –> thalamus –> cortex
- more pain signals –> N/V/photo/phono
- more TNC firing –> central sensitization and allodynia - triptans useless at this stage