Migraine/headache Flashcards

1
Q

migrain is more a ___ disorder than a vascular

A

neurological

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

what is cortical spreading depression phenomenom

A

self propagating wave of enuronal and glial depol that spreads across the cerebral cortex
suppression of brain activity across the cortex

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

what does cortical spreading depression cause

A

migraine aura
activate trigeminal nerve afferents
disrupt BBB permeability

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

how does sensitization contribute to migrains

A

nerves becomes more responsive to stimuli

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

peripheral vs ccentral sensitization

A

peripheral occurs in primary afferent neurons causing greater migrain symptoms
central in 2nd order neurons resulting in greater conversion of episodic to chornic migrain?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what role does serotonin have in migrains

A

just know activation of serotonin receptors is important for acute migraines

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

migrain subtypes

A
acute episodic 
chronic 
vestibular
menstrual
retinal 
hemiplegic (paralysis of one side of body)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

signs of migrain headache

A
stable pattern 
positive fmaily history 
normal neurologic exam
food triggers
menstrual association 
improve with sleep 
long standing history
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

prodrome features

A

1-2 days before onset of headache
neurologic - allodynia, photophobis, ponophobia, difficult concentrating
psychological - anxiety, depression, euphoria, dwosy, restless
autonominc - polyuria, diarrhea, constipation
stiff neck, thirst

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

migrain aura time frame and symptoms

A
can precede or be present during headache
<60min duration 
completely reversible 
mix of positive and negative focal neurologic symptoms 
positive - flickering lights, spots
negative - numb, lack of vision 
tingling 
muscle weakness 
dizziness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

describe a typical migrain headache

A
unilateral 
throbbing, pulsating 
attack progressively and worsens
NV 
photophobia/phonophobia 
osmophobia(sensitive to smell) and cutaneous allodynia 
mod - sev pain intensity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

red flags

A

onset age >50 (lesion, meningitis)
severe abrupt onset (hemorrage)
worsenign (lesion)
stiff neck, abnormal speech (meningitis, stroke)
fever, rahs (meningitis)
cancer, lyme disease, HIV (metastatis, opportunistic infection)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

symptoms warranting meuroimaging

A
first or worst headache
recent significant change
new unexplained eurological symptoms
headache always on the same side
unresponsive headaches
new onset after 50 
new onset in patients with cancer or HIV..
fever, stiff neck, papilledema, cognitive impairment, change in personality
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is migrainous infarction

A

rare complication of migrain
mostly occurs in the posterior circulation in younger women with a history of migraine with aura
ischemic stroke??

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

risk of ischemic stroke significantly increased in which type of people with migraines

A
women 
<45yoa
smokers who have aura
oral contraceptives who have aura 
previous hostory of stroke 
>12 headaches per year
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

examples of migrain triggers

A
stress
hormones
weather
sleep disturbance
odor
heat
food
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

non pharms

A
avoid triggers
rest in dark quiet room 
headache diary 
relaxation techniques
cbt 
cold/heat packs 
hydration 
routine 
regular meals
caffiene balance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

goals of acute therapy

A

relieve pain and associated symptoms
functional headache free state in 2hr with no recurrence in 24 hours
no AE
relieve disability
avoid medicatio overuse headache
avoid development of central sensitization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

reasons to treat the headache early

A

reduce overal burden of migrain

reduce likelihood of central sensitization

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

challenges to treating headaches early

A

some avoid meds unless headache is severe

fear of overuse

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

drugs for acute and when to take them

A
triptan 
ergot derivative
nsaids
acetaminopehn
domperidone, metoclopramide 
best taken at onset of head pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

role of triptans

A

mod-sev migraines first line

reduce NV, photo and phonophobia

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

if dont respond is there a benefit in switching

A

yes

space 24h

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

triptans CI in

A

CAD
severe liver disease
some caution in renal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

triptan MOA

A

vasoconstrictor

inhibits neurogenic inflammation peripherally prevents central sensitization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

most common triptan coverage

A

EDS2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

when would you use subcutaneous sumatriptan

A

use if headache builds rapidly or is accompanied by early NV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

which formulations are good in NV

A

ODT
intranasal
SC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

oral triptan onset and duration

A

start working in 30-60min

last 2-4 hr

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

which triptans have a slower onset (better tolerated) and longer duration

A

naratriptan
frovatriptan
use if have long migraines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

triptans with sulfonamide moiety

A

suma

nara

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

triptans with sulfonyl group

A

ele

frova

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

summary of tri[tan drug interactions

A

dont take within 24 hr of ergot alkaloid due to additive vasoconstriction
avoid within 2 weeks of MAOIs
caution with SSRI -serotonin syndrome
cyp3A4 inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

triptan common SE

A
paresthesia 
fatigue 
dizzy 
fatigue 
warm 
somnolence
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

triptan sensations are

A

mild transient burning, tingling, tightness, pressure, heaviness, pain

36
Q

serious rare triptan SE

A

MI, cornoary vasospasm with ischemia
serotonin syndrome
see doctor if lasts more than 20 min

37
Q

triptan contraindications

A
cerebrovascular disease
IHD
uncontrolled HTN 
PVD 
hemiplegic or basilar migraine
38
Q

ergot actions

A

non selectiv serotonin agonist
alpha and beta agonist
dopamine D! and D2 agonist

39
Q

dihydroergotamine dosage forms

A

SC
IM
IV

40
Q

common ergot SE

A
NV - pretreat with antiemetic 
ab pain 
weak, fatigue 
paresthesias
muscle pain 
diarrhea
chest tightness 
NAUSEA!!
41
Q

serious ergot SE

A

severe peripheral ischemia - cold numb, pain, claudication
gangerenous extremities
MI
bowel and brain ischemia

42
Q

ergot CI

A

cardiac/cerebrovascular disease
uncontrolled HTN
pregnant
hemiplegic or basilar migrani

43
Q

role of acetaminopehn

A

acute treatment fo mild to mod
contraidications to nsaids
best if taken early
better than placebo

44
Q

acetaminophen MOA

A

may block prostaglandin synthesis in CNS and pain impulse generation in the periphery

45
Q

NSAIDs role

A

acute migrain treatment of mild-mod severity

46
Q

nsaids MOA

A

prevent inflammation in the trigeminovascular system via prostaglandin synthesis inhibition

47
Q

why avoid fiorinal

A

contains butalbital which causes rebound headaches

48
Q

why avoid routine use of opioids for migraine

A

lack of evidence of superiority
increase risk of chronic headache
reduce response to other drugs
SE abuse

49
Q

what is medication overuse headache

A

acute meds used lots over several months

50
Q

prevent MOH by limiting use of

A

tylenol, asa, nsaids <15days/month
triptan, opioids(8), combo, ergot <10days/month
should be acute med free for >20days/month**

51
Q

management of MOH

A

taper down and stop drug (would just stop unless an opioid)
watch for refractory rebound headache and withdrawal
prophylactic treatment may help reduce rebound and withdrawal
renewed response to therapy usually occur within 2months of med withdrawal

52
Q

treatmetn algorithm for mild-mod

mod-sev start at 2

A
  1. asa, ibuprofen, diclofenac, naproxen, acetaminophen
  2. triptan (try at least 3 diff triptans)
  3. triptan +nsaid
  4. DHE + antinauseant
  5. acet + codiene/tramadol
53
Q

of nausea occurs or to improve efficacy use

A

metoclopramide or domperidone 10mg

54
Q

treatment in pregnancy

A
non pharm 
acet
metrocolopramide
sumtriptan sometimes 
breast feeding the same except can use nsaids
55
Q

when to consider prophylaxis

A

frequent, long lasting, severe
CI or failure to acute therapu
>2attacks per week (risk of MOH)

56
Q

goals of migraine prophylaxis

A

reduce frequency by 50%

prevent transition from acute to chronic

57
Q

prophylaxtic treatments

A

beta blockers
antidepressant
antiepileptic
butterbur

58
Q

beta blocker MOA

A

raises migrain threshold by modulating adrenergic system and serotonin transmission in cortical pathways of brain

59
Q

first line beta blockers

A

propranolol 80-160mg
metoprolol
timolol

60
Q

beta blocker SE and CI

A

fatigue, bradycardia, hypotension, cold, vivid dreams, bronchospasm
asthma, heart block, heart failure, peripheral vascular disease

61
Q

antidepressant MOA

A

downregulate central serotonin receptors
increase synaptic NE
enhances endogenous opioid receptor action

62
Q

consider antidepressants in

A

comorbidities

depression, insomnia, neuropathic pain, tension headache

63
Q

first line antidepressant

A

amitriptyline

venlafaxine

64
Q

TCA SE

A
anticholinergic 
sedation 
weight gain 
orthostatic hypotension 
cardiac toxicity
65
Q

TCA CI

A
heart block 
CVD 
urinary retention
glaucoma
prostate disease
mani
66
Q

avoid venlafaxine in

A

hypertension
kidney failure
serotonin syndrome risk

67
Q

serotonin syndrome symptoms

A
agitation 
rapid HR 
confusion 
dilated pupils 
muscle rigid
diarrhea
shivering
68
Q

effective anticonvulsant drugs

A

valproate
topiramate
gabapentin maybe

69
Q

anticonvulsant MOA

A

enhance GAB
modulate glutamate
inhibit Na/Ca ion channel activity

70
Q

role for anticonvulsants

A

second line prophylaxis

pateitns with bipolar, seizures, anxiety

71
Q

valproic acid safety

A
NV
alopecia
tremor
weight gain 
avoid in liver disease, bleeding disorder, pregnancy, obesity
72
Q

topiramate safety

A

weight loss, paresthesia , fatigue, memory impairment

avoid in kidney problem, pregnancy, cognitive impairment, glaucoma

73
Q

NHP with low-mod quality evidence for efficacy

A
butterbur - long term safety unknown 
coenzyme q10
magnesium 
riboflavin 
not a lto of SE
74
Q

prophylactic treatment algorithm

A

beta blocker or antidepressant
if one doesnt work try the other
combo BB with anticonvulsant or TCA

75
Q

pregnant prophylaxis

A
non drug 
magnesium 
propranolol
nortriptyline 
lactation same but can use valproate
76
Q

initiation of prophylactic treatment

A

start low and titrate to max dose

77
Q

prodrome stage occurs when

A

24-48 hours before onset of headache

78
Q

prodrome symptoms

A
neurological - difficulty concentraion 
anxiety, depression, fatigue
food cravings, anorexia
NVD
just feel off
79
Q

women with migraine with aura should be encouraged to

A

stop smoking
control their BP
use alternative method of contraception

80
Q

migraine triggers

A
stress
hormones
weather
sleep 
odor
lights
alcohol
smoke
heat
 food or no food
sexual activity 
exercise
81
Q

why take and antiemetic in acute therapy

A

(antiemetic bc gastric motility and drug absorption delayed during attack resulting in NV
effect will be slower if delayed motility

82
Q

counseling for SC triptan

A

to outside of thigh/upper arm
do not load autoinjection until ready
should see effect in 10min

83
Q

counselling for intranasal triptan

A

do not prime
2.5mg in one nostril only
onset in 10 min

84
Q

ODT triptan counselling

A
may be taken without water
keep in foli
dont split
may repeat after 2hr
onset 30 min 
has aspartame
85
Q

migranal nasal spray counseling

A

pump 4x into the air before first use
5.mg in each nostril
may repeat in 15 minutes
max4 sprays per attack

86
Q

signs and symptoms of MOH

A
AM symptoms
poor sleep quality 
neck pain 
poor response to acute meds
using meds for 3 months
>15 hedaache days per month