Headache Disorders Flashcards
what are the main causes of secondary headaches?
- meningitis
- encephalitis
- normal pressure hydrocephalus
- subarachnoid hemorrrhage
- intracerebral hemorrhage
- enoplasm
- temporal arteritis
meningitis (secondary HA) - sx
HA + fever
encephalitis (secondary HA) - general sx
HA + fever + stupor
subarachnoid hemorrhage (secondary HA) - general sx
- sudden SEVERE HA (“worst HA of life”)
- nuchal rigidity (neck pain)
intracerebral hemorrhage (secondary HA) - general sx
- sudden HA
- localized neurologic finding
- hypertension
neoplasm (secondary HA) - general sx
- chronic progressive worsening headache
- focal neurological finding
temporal arteritis (secondary HA) - general sx
- HA
- patient over 50
- tender temporal arteries
which type of cranial bleed classically presents with hypertension?
intracerebral
temporal arteritis
- cause
- demographics
- presentation
- diagnosis
- treatment
- sequelae
giant cell arteritis
- cause: thickened temporal artery -> radiating pain
- demographics: pt > 50
- presentation:
- tender, non-pulsatile temporal artery
- pain that radiates to:
- jaw (jaw claudication)
- occiput
- +/- polymyalgia rheumatica
- diagnosis:
- granulomatous (giant cell) inflammation
- elevation of ESR > 50
- treatment: high dose corticosteroids ASAP
- sequelae: irreversible blindness w/out immediate tx
what are the “rule of 50s” regarding temporal arteritis?
aka giant cell arteritis
- pts > 50
- 50% present w/ polymyalgia rheumatica
- elevation of ESR > 50
thunderclap headache
- cause
- presentation
- diagnosis
- cause: secondary HA d/t a vascular injury (ex- SHA)
- presentation: abrupt, severe HA that reaches max intensity in under 1 min
- diagnosis (for SHA):
- CT scan - most sensitive for SAH 6 hrs post event (wont show past 12 hrs)
- lumbar puncture (if neg CT) - xanthochromia shows from 2 hrs - 2 wks post event
what vascular injuries may be responsible for thunderclap headache?
- subarachnoid hemorrhage (SHA)
- cerebral vasoconstriction syndrome
- cerebral venous thrombosis
- disection: carotid > vertebral artery
- spontaneous intracranial hypotension
identify & explain
CT scan showing subarachnoid hemorrhage (SHA)
hyperintense blood product around the cisterns of the brain - common cause of thunderclap headache.
dx of thunderclap HA
- if the CT scan has negative findings for SAH, which test should be done next to officially r/o SAH as a cause?
- how is this test done?
- what consistutes a positive result?
-
lumbar puncture
- how to: take multiple blood samples (~4 tubes)
- positive result:
- xanthocromia - detectible 2 hrs - 2 weeks after event
- similarly appearing blood in each tube (progressively dilute blood = probably sampled a vessel)
reversile cerebral vasoconstriction syndrome
- definition
- cause
- triggers
- diagnosis
- treatment:
- definition: recurrent thunderclap headaches over 1-2 weeks
- triggers: urinating, sexual activity, valsalva
- cause: multli-vessel, multi-focal erebral vasoconstriction (but NOT SAH aneurysm)
- findings:
- CSF - normal
- MRI / CT - normal
- angiography - shows vasoconstriction
- treatment: CCBs
identify
RCVS angiography
multi-vessel, multi-focal, segmental cerebral vasoconstriction that reserves within 12 weeks
what is the treatment for reversible cerebral vasoconstriction syndrome?
CCBs
contrast RCVS and primary CNS angitis based on
- gender prevalence
- CSF findings
- angiogram findings
- treatment
intracranial hypotension headaches
- cause
- presentation
- diagnosis
- treatment
- cause: usually, a CSF due to a
- lumbar puncture
- CSF fistula - trauma, surgery
- presentations: holocephalic HA that are better lying down and worsen when standing
- diagnosis:
- lumbar tap: CSF opening pressure < 6 cm
- MRI: diffuse meningeal enhancement
- radioisotope cisternography; abnormal
- beta-2 transferring test: shows CSF
- treatment: blood patch to stop CSF leak
outline the treatment of intracranial hypotension headaches
- initial: best rest + hydration / caffeine
- key: blood patch to stop CSF leak
- bad dural tear: surgery
explain the proper technique of a lumbar puncuture.
why is this important?
- bevel must be oriented parallel to the long axis of the patient
- this lowers the risk of a CSF leak & thus a post-dural intracranial hypotension HA
identify
diffuse meningeal enhancement - d/t irriated dura
dx of intracranial hypotension HA
identify, explain significance
radioisotope cisternography - radioisotopes injected to label CSF; its flow rate is measured, confirming extracrnial CSF extravasation
dx of intracranial hypotension headache
rhinorrhea is a possible manifestation of which HA?
explain
- intracranial hypotension HA (CSF leak)
- do a beta-2-transferrin test to confirm if CSF
Chiari type I malformation HA
- cause
- presentation
- diagnosis
- cause: often synringomelia; leads to cerebellar herniation
- presentation: occipital / sub-occipital HA triggered by
- COUGH
- VALSALVA
- diagnosis: MRI shows cerebellar tonsillar ectopia of ~ 5m
which pathologies can lead to intracranial hypertension headaches?
- charli I malformation (hypo or hyper)
- psuedotumor cerebri
idiopathic intracranial hypertension
- cause
- presentation
- diagnosis
- treatment
aka psueodtumor cerebri
- cause: unkown
- presentation: loss of peripheral visual fields
- diagnosis:
- lumbar tap: CSF opening pressure > 25 cm
- MRI: compressed features d/t HTN
- slit like ventricles
- orbital flattening
- tortuous optic nerves
- empty sella
- treatment: diuretics - lasix, acetozolamine
identify, explain significance
MRI - orbital flattening, tortuous optic nerves
dx of intracranial hypertension (psuedotumor cerebri)
identfiy, explain significance
MRI - slit like ventricles
dx of incranial hypertension (psuedotumor cerebri)
what is the tx for idiopathic intracranial hypertension?
diruetics
- lasix
- acetozolamide
- topiramate
contrast intracranial hypotension and intracranial hypertension based on
- CSF opening pressure
- MRI findings
- treatment
- intracranial hypotension (lumbar puncture, CSF fistula):
- CSF pressure: < 6 cm H20 cm
- MRI: enhancement of meninges
- tx: hydration / caffeine + patch
- intracranial hypertension / pseudotrumor cerebri
- CSF pressure: > 25 H20 cm
- MRI: slit-like ventricles, orbital flattening, turtuous optic nerves
- tx: diuretics
what is the general pathogenesis of migraines?
= disorder of brain hyperexitability
people are unable to habituate to repetitive electrical stimulation
what are the 5 general phases of migraine with aura ?
- prodrome
- aura
- pain phases
- resolution
- postdrom
each symptomatic phase of migraine with aura is mediated by what CNS changes?
- prodrome: activation of menigneal nociopreceptors
- aura: spreading cortical depression
- pain: activation of trigeminal complex
ourine the prominitory phase of migraine with aura
= activation of meingeal nociopreceptors
- noxious brain stimuli activate thalamic nocioreceptors heading to the SSN
- from the SSN, parasympathetic pre-ganglions travel to the sphenopalatine ganlgion
- parasympathetic post-ganglionics exiting the ganlgion head to the menginges
- the meninges become irritated, which triggers:
- inflammatory molecule release (CGRP)
- meningeal vasodilation
outline the aura phase of migraine with headache
= spreading cortical depression
- the occipital cortex is high pre-disposed to meningeal depolarization
- repeated slow depolarizations eventually lead to K+ efflux
- this inhibitirs cortical activation for up to 30 min (cortical depression)
- cortical depression = reverislbe visual, sensory and speech sx
explain the timing of the aura phase of migraine with aura
- onset: within 5 miutes
- duration: less than 1 hour
- followed by HA: within 1 hour
what specific symptoms characterize aura in an episode of migrain with aura
-
fully reversible sensory symptoms:
-
visual sx:
-
positive scotoma: perception of addition structures
- flickering lights
- spots / lines
- fortilfication (zizags)
- negative scotoma: loss of awareness of local structures (one sided)
-
positive scotoma: perception of addition structures
- sensory sx
- dysphasic speech distrurbance
-
visual sx:
does aura in migraine with aura present with motor effects?
no! sensory only
migraine with aura
indicate the reversible visual change shown in each picture
migraine with aura - is associated with what health risk?
in what populations?
- ischemic stroke
- especially in women who
- smoke
- are taking estrogens
women with migraine with aura should take which health percautions? why?
they should not
- take estrogens
- smoke cigarettes
= exacerbates risk for ischemic stroke
list the features of the migraine headache
lasts up to 72 hrs
- unilateral
- pulsating
- aggavated by physical activity
- associated with
- nausea and/or vomitting
- photophotobia + phonophobia
list the features of a tension-type headache
- bilateral
- non-pulsating (pressing, tightening)
- NOT aggravated by physical activity
- NOT associated with
- nausea
- vomitting
- photophobia + phonotophobic (just one)
aura with which characteristics would make you suscpicious of TIA?
an aura that
- occurs for the first time after 40
- is rapid onset (< 5 minutes)
- is not followed by a migraine
- consists only of negative visual sx (loss)
- is associated with weakness
if you suspect a pt’s aura is d/t a TIA, you should…?
- refer them to neurology
- avoid treatment with any vasoconstrictors - i.e., most migraine drugs: triptans, dhidroergotamine, ubrogepant / rimagepant
acute headache (migraine) is mostly treated with which drugs?
- analgesics - NSAIDS, acetaminophen
- vasoconstrictors / vasoactive-suppressants:
- triptans
- dihydroerogtamine (DHE)
- ubrogepant, rimagepant
which acute headache (migraine) drug is C/I in pts with cardiovascular risk factors?
why?
triptans
are potent peripheral vasoconstrictors, and increase risk for MI, arrythmias, HTN
which acute headache (migraine) drug does NOT cause vasoconstriction?
lamsitidan
what is a status migrainosus?
how is it treated?
- migraine HA, but lasts > 72 hours
- is treated with IV fruids + CNS depressants:
- MgSO4
- diphenhydramine
- solumedrol
- metoclopramide
