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Week 2 (Neuro 2) > Headache Disorders > Flashcards

Headache Disorders Flashcards

1
Q

what are the main causes of secondary headaches?

A
  • meningitis
  • encephalitis
  • normal pressure hydrocephalus
  • subarachnoid hemorrrhage
  • intracerebral hemorrhage
  • enoplasm
  • temporal arteritis
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2
Q

meningitis (secondary HA) - sx

A

HA + fever

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3
Q

encephalitis (secondary HA) - general sx

A

HA + fever + stupor

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4
Q

subarachnoid hemorrhage (secondary HA) - general sx

A
  • sudden SEVERE HA (“worst HA of life”)
  • nuchal rigidity (neck pain)
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5
Q

intracerebral hemorrhage (secondary HA) - general sx

A
  • sudden HA
  • localized neurologic finding
  • hypertension
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6
Q

neoplasm (secondary HA) - general sx

A
  • chronic progressive worsening headache
  • focal neurological finding
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7
Q

temporal arteritis (secondary HA) - general sx

A
  • HA
  • patient over 50
  • tender temporal arteries
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8
Q

which type of cranial bleed classically presents with hypertension?

A

intracerebral

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9
Q

temporal arteritis

  • cause
  • demographics
  • presentation
  • diagnosis
  • treatment
  • sequelae
A

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
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10
Q

what are the “rule of 50s” regarding temporal arteritis?

A

aka giant cell arteritis

  • pts > 50
  • 50% present w/ polymyalgia rheumatica
  • elevation of ESR > 50
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11
Q

thunderclap headache

  • cause
  • presentation
  • diagnosis
A
  • 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):
    1. CT scan - most sensitive for SAH 6 hrs post event (wont show past 12 hrs)
    2. lumbar puncture (if neg CT) - xanthochromia shows from 2 hrs - 2 wks post event
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12
Q

what vascular injuries may be responsible for thunderclap headache?

A
  • subarachnoid hemorrhage (SHA)
  • cerebral vasoconstriction syndrome
  • cerebral venous thrombosis
  • disection: carotid > vertebral artery
  • spontaneous intracranial hypotension
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13
Q

identify & explain

A

CT scan showing subarachnoid hemorrhage (SHA)

hyperintense blood product around the cisterns of the brain - common cause of thunderclap headache.

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14
Q

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?
A
  • 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)
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15
Q

reversile cerebral vasoconstriction syndrome

  • definition
  • cause
  • triggers
  • diagnosis
  • treatment:
A
  • 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
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16
Q

identify

A

RCVS angiography

multi-vessel, multi-focal, segmental cerebral vasoconstriction that reserves within 12 weeks

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17
Q

what is the treatment for reversible cerebral vasoconstriction syndrome?

A

CCBs

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18
Q

contrast RCVS and primary CNS angitis based on

  • gender prevalence
  • CSF findings
  • angiogram findings
  • treatment
A
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19
Q

intracranial hypotension headaches

  • cause
  • presentation
  • diagnosis
  • treatment
A
  • 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
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20
Q

outline the treatment of intracranial hypotension headaches

A
  • initial: best rest + hydration / caffeine
  • key: blood patch to stop CSF leak
  • bad dural tear: surgery
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21
Q

explain the proper technique of a lumbar puncuture.

why is this important?

A
  • 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
22
Q

identify

A

diffuse meningeal enhancement - d/t irriated dura

dx of intracranial hypotension HA

23
Q

identify, explain significance

A

radioisotope cisternography - radioisotopes injected to label CSF; its flow rate is measured, confirming extracrnial CSF extravasation

dx of intracranial hypotension headache

24
Q

rhinorrhea is a possible manifestation of which HA?

explain

A
  • intracranial hypotension HA (CSF leak)
  • do a beta-2-transferrin test to confirm if CSF
25
Q

Chiari type I malformation HA

  • cause
  • presentation
  • diagnosis
A
  • cause: often synringomelia; leads to cerebellar herniation
  • presentation: occipital / sub-occipital HA triggered by
    • COUGH
    • VALSALVA
  • diagnosis: MRI shows cerebellar tonsillar ectopia of ~ 5m
26
Q

which pathologies can lead to intracranial hypertension headaches?

A
  • charli I malformation (hypo or hyper)
  • psuedotumor cerebri
27
Q

idiopathic intracranial hypertension

  • cause
  • presentation
  • diagnosis
  • treatment
A

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
28
Q

identify, explain significance

A

MRI - orbital flattening, tortuous optic nerves

dx of intracranial hypertension (psuedotumor cerebri)

29
Q

identfiy, explain significance

A

MRI - slit like ventricles

dx of incranial hypertension (psuedotumor cerebri)

30
Q

what is the tx for idiopathic intracranial hypertension?

A

diruetics

  • lasix
  • acetozolamide
  • topiramate
31
Q

contrast intracranial hypotension and intracranial hypertension based on

  • CSF opening pressure
  • MRI findings
  • treatment
A
  • 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
32
Q

what is the general pathogenesis of migraines?

A

= disorder of brain hyperexitability

people are unable to habituate to repetitive electrical stimulation

33
Q

what are the 5 general phases of migraine with aura ?

A
  1. prodrome
  2. aura
  3. pain phases
  4. resolution
  5. postdrom
34
Q

each symptomatic phase of migraine with aura is mediated by what CNS changes?

A
  • prodrome: activation of menigneal nociopreceptors
  • aura: spreading cortical depression
  • pain: activation of trigeminal complex
35
Q

ourine the prominitory phase of migraine with aura

A

= 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:
    1. inflammatory molecule release (CGRP)
    2. meningeal vasodilation
36
Q

outline the aura phase of migraine with headache

A

= 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
37
Q

explain the timing of the aura phase of migraine with aura

A
  • onset: within 5 miutes
  • duration: less than 1 hour
  • followed by HA: within 1 hour
38
Q

what specific symptoms characterize aura in an episode of migrain with aura

A
  • 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)
    • sensory sx
    • dysphasic speech distrurbance
39
Q

does aura in migraine with aura present with motor effects?

A

no! sensory only

40
Q

migraine with aura

indicate the reversible visual change shown in each picture

A
41
Q

migraine with aura - is associated with what health risk?

in what populations?

A
  • ischemic stroke
  • especially in women who
    • smoke
    • are taking estrogens
42
Q

women with migraine with aura should take which health percautions? why?

A

they should not

  • take estrogens
  • smoke cigarettes

= exacerbates risk for ischemic stroke

43
Q

list the features of the migraine headache

A

lasts up to 72 hrs

  1. unilateral
  2. pulsating
  3. aggavated by physical activity
  4. associated with
    • nausea and/or vomitting
    • photophotobia + phonophobia
44
Q

list the features of a tension-type headache

A
  1. bilateral
  2. non-pulsating (pressing, tightening)
  3. NOT aggravated by physical activity
  4. NOT associated with
    • nausea
    • vomitting
    • photophobia + phonotophobic (just one)
45
Q

aura with which characteristics would make you suscpicious of TIA?

A

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
46
Q

if you suspect a pt’s aura is d/t a TIA, you should…?

A
  1. refer them to neurology
  2. avoid treatment with any vasoconstrictors - i.e., most migraine drugs: triptans, dhidroergotamine, ubrogepant / rimagepant
47
Q

acute headache (migraine) is mostly treated with which drugs?

A
  • analgesics - NSAIDS, acetaminophen
  • vasoconstrictors / vasoactive-suppressants:
    • triptans
    • dihydroerogtamine (DHE)
    • ubrogepant, rimagepant
48
Q

which acute headache (migraine) drug is C/I in pts with cardiovascular risk factors?

why?

A

triptans

are potent peripheral vasoconstrictors, and increase risk for MI, arrythmias, HTN

49
Q

which acute headache (migraine) drug does NOT cause vasoconstriction?

A

lamsitidan

50
Q

what is a status migrainosus?

how is it treated?

A
  • migraine HA, but lasts > 72 hours
  • is treated with IV fruids + CNS depressants:
    • MgSO4
    • diphenhydramine
    • solumedrol
    • metoclopramide

Week 2 (Neuro 2) (9 decks)

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