Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

are migraines more common in male or females

A

female

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

how long can migraines last

A

4-72 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

outline the IHS criteria for migraine with/out aura

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

when do migraines usually develop

A

around puberty, with increasing prevalence into teh 4th decade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

preferred patient setting during migraine

A

quiet, darkened room

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what 3 forms does a migraine aura usually take

A

visual, sensory or speech disturbance

are all fully reversible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

migraine prodrome

A
  • Precedes headaches by hours/days
  • Yawning, cravings, mood/sleep change
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

acephalic migraine

A

migraine aura without headache

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is acephalic migraine often misidagnosed as

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

first line acute medication for migraine

A

NSAID ± anti emetic

  • only 25% achieve complete pain relief
  • less chance of medication misuse headache
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

2nd line acute treatment of migraines

A
  • triptans - 5HT agonists
  • several methods of administration
  • subcutaenous sumatriptan is good if patient eg vomiting
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

acute management of migraines: when to take NSAIDs adn triptans

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what triptan is good if the patient is vomiting

A

sumatriptan canbe given subcutaneously

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

which triptan is good for sustained relief

A

fovatriptan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

when would you consider migraine prophylaxis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

how long must each migraine prophylaxis drug be trialed for

A

minimum of 4 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

first line migraine prophylaxis drugs

A
  1. beta blockers
  2. topiramate
  3. amitriptyline
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

topiramate AE

A
  • weight loss, paraesthesia, impaired concentration, enzyme inducer, short term memory decrease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

is topiramate teratogenic?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

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.

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?

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

RB Y3 1.2 Neurology (23 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions