Headache Disorders Flashcards
(50 cards)
1
Q
what are the main causes of secondary headaches?
A
- meningitis
- encephalitis
- normal pressure hydrocephalus
- subarachnoid hemorrrhage
- intracerebral hemorrhage
- enoplasm
- temporal arteritis
2
Q
meningitis (secondary HA) - sx
A
HA + fever
3
Q
encephalitis (secondary HA) - general sx
A
HA + fever + stupor
4
Q
subarachnoid hemorrhage (secondary HA) - general sx
A
- sudden SEVERE HA (“worst HA of life”)
- nuchal rigidity (neck pain)
5
Q
intracerebral hemorrhage (secondary HA) - general sx
A
- sudden HA
- localized neurologic finding
- hypertension
6
Q
neoplasm (secondary HA) - general sx
A
- chronic progressive worsening headache
- focal neurological finding
7
Q
temporal arteritis (secondary HA) - general sx
A
- HA
- patient over 50
- tender temporal arteries
8
Q
which type of cranial bleed classically presents with hypertension?
A
intracerebral
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
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
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):
- 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
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
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.
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)
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
16
Q
identify
A
RCVS angiography
multi-vessel, multi-focal, segmental cerebral vasoconstriction that reserves within 12 weeks
17
Q
what is the treatment for reversible cerebral vasoconstriction syndrome?
A
CCBs
18
Q
contrast RCVS and primary CNS angitis based on
- gender prevalence
- CSF findings
- angiogram findings
- treatment
A
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
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
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
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**
26
which pathologies can lead to intracranial hypertension headaches?
* charli I malformation (hypo or hyper)
* psuedotumor cerebri
27
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**
28
identify, explain significance
MRI - **orbital flattening, tortuous optic nerves**
dx of intracranial hypertension (psuedotumor cerebri)
29
identfiy, explain significance
MRI - **slit like ventricles**
dx of incranial hypertension (psuedotumor cerebri)
30
what is the tx for idiopathic intracranial hypertension?
diruetics
* lasix
* acetozolamide
* topiramate
31
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: e**nhancement 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
what is the general pathogenesis of migraines?
= disorder of brain hyperexitability
people are _unable to habituate_ to repetitive electrical stimulation
33
what are the 5 general phases of _migraine with aura_ ?
1. prodrome
2. aura
3. pain phases
4. resolution
5. postdrom
34
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
35
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:
1. inflammatory molecule release (CGRP)
2. meningeal vasodilation
36
outline the _aura phase_ of migraine with headache
= spreading cortical depression
* the **occipital cortex** is high pre-disposed to meningeal depolarization
* **repeated slow depolarization**s 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
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
38
what _specific symptoms_ characterize _aura_ in an episode of migrain with aura
* **fully reversible sensory symptoms:**
* **visua**l **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
does aura in migraine with aura present with motor effects?
no! sensory only
40
migraine with aura
indicate the reversible visual change shown in each picture
41
migraine with aura - is associated with _what health risk?_
in what populations?
* **ischemic stroke**
* especially in women who
* smoke
* are taking estrogens
42
women with _migraine with aura_ should take which health percautions? why?
they should not
* take estrogens
* smoke cigarettes
= exacerbates risk for ischemic stroke
43
list the features of the **migraine headache**
lasts up to 72 hrs
1. **unilateral**
2. **pulsating**
3. aggavated by physical activity
4. associated with
* nausea and/or vomitting
* photophotobia + phonophobia
44
list the features of a **tension-type headache**
1. **bilateral**
2. **non-pulsating** (pressing, tightening)
3. NOT aggravated by physical activity
4. NOT associated with
* nausea
* vomitting
* photophobia + phonotophobic (just one)
45
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**
46
if you suspect a pt's aura is d/t a TIA, you should...?
1. refer them to neurology
2. avoid treatment _with any vasoconstrictors_ - i.e., most migraine drugs: triptans, dhidroergotamine, ubrogepant / rimagepant
47
acute headache (migraine) is mostly treated with which drugs?
* analgesics - NSAIDS, acetaminophen
* vasoconstrictors / vasoactive-suppressants:
* **triptans**
* **dihydroerogtamine (DHE)**
* **ubrogepant, rimagepant**
48
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
49
which acute headache (migraine) drug does NOT cause vasoconstriction?
lamsitidan
50
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
