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RB Y3 1.2 Neurology > Headaches > Flashcards

Headaches Flashcards

1
Q

name 4 red flags

A
  • new onset >55
  • known or previous malignancy
  • early morning headache
  • exacerbation by valsalva
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2
Q

are migraines more common in male or females

A

female

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3
Q

how long can migraines last

A

4-72 hours

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4
Q

outline the IHS criteria for migraine with/out aura

A
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5
Q

outline the pathophysiology of migraines

A

Primarily neural influences, the old theory was based around vascular but this is less used now

  • defects in the neurons (possibly inherited) means they are hyper excitable - they depolarise more easily and there is increased activity
  • CNV1 is particularly effected - are activated and release neurotransmitters - neurogenic inflammation
    • CGRP stimulate mast cells which release histamine, this produces an inflammatory reaction and formation of NO, which in turn leads to vasodilation.
  • neurogenic inflam causes pain and swelling over brain covering, and sensitize nerve fibres so that previously innocious stimuli is found to be painful/uncomfortable (eg light, sound, pulsating vessels (throbbing character)
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6
Q

what is responsible for the increased sensitivity to light and sound etc in migraines

A

senstization of trigeminal neurons and brainstem pain pathways makes otherwise innocuous sensory stimuli (eg CSF pulsation and head movement) painful and light and sound are perceived as uncomfortable

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7
Q

when do migraines usually develop

A

around puberty, with increasing prevalence into teh 4th decade

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8
Q

describe the character of migraines, and what makes the better/worse

A

pulsating and unilateral. moderate to severe pain

made worse by routine physical activity eg walking

typically relieved by lying down in a darkened room

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9
Q

what featurs are migraines assoicated with

A

Nausea and vomiting

Photophobia, phonophobia

There may be allodynia (eg cant brush hair, wear glasses, earrings)

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10
Q

preferred patient setting during migraine

A

quiet, darkened room

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11
Q

what 3 forms does a migraine aura usually take

A

visual, sensory or speech disturbance

are all fully reversible

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12
Q

migraine prodrome

A
  • Precedes headaches by hours/days
  • Yawning, cravings, mood/sleep change
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13
Q

migraine triggers

A
  • Chocolate
  • hangovers
  • orgasms
  • cheese
  • OCP
    • hormonal factors for women, eg menstrual migraine just before menses
  • lie ins
    • too much/little sleep
  • alcohol
  • tumult
  • exercise
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14
Q

migraine with aura

A
  • focal neurological symptoms immediately preceding headache in some/all attacks
  • Visual aura is the most common type: shimmering, teichopsia (zig-zag lines), fragmentation of image, patches of loss of vision.
  • Positive sensory symptoms (mainly tingling), dysphasia and rarely loss of motor function may also occur following visual symptoms
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15
Q

acephalic migraine

A

migraine aura without headache

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16
Q

what is acephalic migraine often misidagnosed as

A

TIA - can get senory and motor problems as wel as visual

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17
Q

first line acute medication for migraine

A

NSAID ± anti emetic

  • only 25% achieve complete pain relief
  • less chance of medication misuse headache
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18
Q

2nd line acute treatment of migraines

A
  • triptans - 5HT agonists
  • several methods of administration
  • subcutaenous sumatriptan is good if patient eg vomiting
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19
Q

acute management of migraines: when to take NSAIDs adn triptans

A

take NSAIDs ASAP, take triptans at start of headache (not aura)

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20
Q

what triptan is good if the patient is vomiting

A

sumatriptan canbe given subcutaneously

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21
Q

which triptan is good for sustained relief

A

fovatriptan

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22
Q

when would you consider migraine prophylaxis

A

patient having >3 attacks/month or if they are very severe

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23
Q

how long must each migraine prophylaxis drug be trialed for

A

minimum of 4 months

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24
Q

first line migraine prophylaxis drugs

A
  1. beta blockers
  2. topiramate
  3. amitriptyline
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25
Q

topiramate AE

A
  • weight loss, paraesthesia, impaired concentration, enzyme inducer, short term memory decrease
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26
Q

topiramate and contraception

A

topiramate is an AED that induces hepatic enzymes (in epilepsy higher doses are used)

    • OCP needs a higher dose as its efficacy is decreased
    • progesterone only methods cant be used
  • can use copper IUD - normal or emergency
  • can use Leveonelle within 72 hours of UPSI
  • cant use ellaOne
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27
Q

is topiramate teratogenic?

A

yes, higher risk of congenital abnormalities eg cleft lip and palate

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28
Q

basilar migraine

A
  • usually presents with symptoms of vertebrobasilar insufficiency (dizziness, vertigo) then headache
  • may also have ataxia, tinnitus, decreased hearing , n and v
29
Q

retinal migraine

A

transient unilateral visual disturbance withb minimal or no headache

30
Q

ophthalmoplegic migraine

A
  • transient migraine
  • followed by periorbital pain and diplopia secondary to cranial neuropathies a few days later (and pupillary abnormalities and ptosis if CNIII involved)
31
Q

hemiplegic migraine

A
  • recurrent headaches assoicated with temporary unlateral hemiparesis/hemiplegia
  • may have accompanying ipsilateral numbness or tingling
  • speech distrubance
32
Q

which gene defect is the familial form of hemiplegic migraine due to

A

SCN1A

33
Q

are migraines uni or bi lateral?

A

unilateral

34
Q

tension type headache

A

bilateral, non-pulsatile (tight band sensation) headache, pressure behind eyes

35
Q

severity of TTH pain

A

mild to moderate

36
Q

what other features does TTH have

A
  • non-pulsatile - tight band
  • relatively featureless - no nause and vomiting, no phono or photo phobia
37
Q

what psychiatric disorders are TTH strongly associated with

A

anxiety and depression

38
Q

management of TTH

A
  • simple analgesics
  • physical treatments and stress relief: massage, ice packs
  • tricyclics: amitryptyline, dothiepin
39
Q

what are the trigeminal autonomic cephalgias

A
  • unilateral headaches in the distribution of CNV1, that are associated with ipsilateral autonomic features (eg ptosis, miosis, nasal stuffiness etc)
40
Q

epidemiology of cluster headaches

A

common in young people, men>women

more common in smokers

41
Q

features of cluster headaches

A
  • excruciating unilateral retro-orbita pain
  • redness and tearing of eye
  • nasal congestion
  • facial flushing
  • lid swelling
  • transient Horner’s syndrome
42
Q

how does patient act during cluster headaches

A

terribel pain, patient prefers to rock or move about

43
Q

timing and duration of cluster headaches attacks

A
  • attacks are shorter than migraines (30-90 minutes)
  • may occur several times per day
  • often at night or v early in the morning
  • cluster bout can last for weeks to months, and can recur after a year or so
44
Q

acute treatment of cluster headaches

A
  • analgesics are unhelpful
  • high flow oxygen for 20 min and subcut sumatriptan
45
Q

prophylactic treatment of cluster headaches

A

verapamil, lithium and/or short course of steriods

46
Q

which age group are paroxysmal hemicranias seen in

A

elderly females

47
Q

features of paroxysmal hemicranias

A
  • severe unilateral throbbing headache
  • pain goes in, around or behind eye. occasionally can reach towards back of neck
48
Q

paroxysmal hemicranias attacks

A
  • briefer (10-30 min) and more frequent than cluster headaches
  • do not occur in clusters
49
Q

management of paroxysmal hemicranias

A

rapid and complete response to indomethacin - diagnostic

50
Q

sunct

A

short lived (20 seconds), unilateral, neuralgia form headache, conjunctival injection (red eye), tearing

51
Q

treatment of SUNCT

A

lamotrigine (anti convulsant) and gabapentin

52
Q

what is sunct often misidagnosed as, and how would you differentiate it

A

trigeminal neuralgia - sunct has autonomic features such as red eye and tearing

TN will have inceased sensitivity and pain in CNV1 distribution

53
Q

primary cough headache

A

sudden sharp head pain on coughing

54
Q

what must be ruled out with primary cough headache

A

intracranial pathology

55
Q

management of primary cough headache

A

indomethacin, lumbar puncture removal of CSF

56
Q

new onset unilateral cranial autonomic features require imaging: MRI brain and MR angiogram.

A
57
Q

who is trigeminal neuralgia usually seen in

A

elderly women

58
Q

which CNV branch does trigeminal neuralgia usually invovle

A

2/3, tends to start in 3 and can spread

59
Q

decribe trigeminal neuralgia pain

A

sharp, severe, stabbing, unilateral

60
Q

duration and frequency of trigeminal neuralgia

A

1-90sec, 10-100/day

often spontaneous remission

61
Q

what can trigger trigeminal neuralgia

A

swallowing, chewing, touching, talking

62
Q

what is the main risk factor for trigeminal neuralgia

A

hypertension - compresion of CNV near the pons by an ectatic loop (dilated)

63
Q

secondary causes of trigeminal neuralgia

A

tumour compressing nerve root, MS, zoster, skull base malformation

64
Q

young patient with bilateral trigeminal neuralgia?

A

think MS

65
Q

management of trigeminal neuralgia

A
  • carbamazepine reduces the severity of attacks int the majority of cases
  • gabapentin, phenytoin, baclogen
  • surgery: ablation or decompression - high risk
66
Q

what investigation must be performed for trigeminal neuralgia

A

MRI to exclude secondary causes

67
Q

medication misuse headache - which are the top 3 causes

A

A common reason for an episodic headache becoming a chronic headache is medication misuse. The culprits are mixed analgesics (paracetamol + codeine/opiates), ergotamine and triptans. Limit OTC analgesia (no more than 6 days/month).

This is why NSAIDs are first line over triptans

68
Q

what is the timeframe for the definiton of a medication misuse headache

A

has to last 15 days, and have started/wrosened when pt on regular medication

must improve within 2month sof stopping medication

69
Q
A

RB Y3 1.2 Neurology (23 decks)

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