Migraines Flashcards
How far in advance of a migraine does the prodromal phase occur?
- 24-48 hours in advance
Can MOH ever come before another type of headache?
- no!
always presents after a tension type headache or a migraine
What are some of the factors that would lead you to think the person is experiencing a MOH?
- > 15 headaches per month
- untreated headaches that last over 4 months
What is one characteristic of a MOH that distinguishes it from other headaches?
- usually are present first thing in the morning - migraines sx typically develop throughout the day and they will have disappeared by the morning
What is considered to be a chronic migraine?
- headache occurring on 15 or more days for more than 3 months
What are the typical s/s of a migraine headache?
- unilateral (most often) - but not always on the same side
- throbbing, pulsating
- attack progressively worsens over hours
- often n/v
- photophobia/phonophobia
- osmophobia and cutaneous allodynia
What are some of the main red flag symptoms associated with migraines?
- age > 50 y/o
- severe and abrupt
- worsening over days-weeks
- stiff neck, focal signs, reduced consciousness, abnormal speech, motor reflex, cognitive impairment
- fever, rash, n/v
What are the risk factors associated with medication overuse headaches?
- anxiety/depression
- smoking
- women ( <50 y/o)
- high caffeine intake ( >2 cups of coffee/day)
- physical inactivity
What ar the most typical signs and symptoms associated with a MOH?
- am symptoms
- poor acute tx response
- > 15 headache days per month (often daily with a pre-existing migraine)
- overuse of acute meds (>3 months)
- neck pain
- increased variability
What meds are considered to be “low risk” for MOH?
used >15 days/month
- NSAIDS
- acetaminophen
- ASA
What meds are considered to be “moderate risk” for MOH?
used >10 days/month
- triptans
- ergotamine
what meds are considered to be “high risk” for MOH?
used > 5-10 days/month
- opioids
- butalbital products (5 days)
- ASA/acetaminophen
- use of >1 acute medication
What is a type 1 (uncomplicated) type of MOH?
- no hx of drug misuse
- not using opioids, barbiturates
- no significant and/or uncontrolled psychological concerns
What is a type 2 (complicated) MOH?
- previous withdrawal failure
- significant/uncontrolled psychological concerns
- hx of drug misuse
- using opioids and/or barbiturates
Who would benefit most from a slow taper of there migraine medications?
- patients using opioids/barbiturates (caffeine?); previous unsuccessful abrupt weans, significant anxiety over medication removal
- psychiatric co-morbidities
Who would benefit most from an abrupt wean of migraine medications?
- patients using acute medications other than opioids/barbiturates, motivated and accepting of process
How long is bridge therapy typically for?
- 5-10 days
What is bridge therapy?
- purpose of it is to get the person over to their prophylactic therapy with the least amount of pain possible
What medications are typically used for bridge therapy?
- NSAIDS
- corticosteroids (dexamethasone, prednisone)
- asa
- triptans
- DHE (nasal spray)
Once back to episodic migraines, you can reintroduce what?
- migraine specific prn medications (need to only be used <2 days a week)
What are some possible withdrawal symptoms after medication removal for headaches?
- increase in headaches
- n/v
- tachycardia
- restlessness
- insomnia
- anxiety
How long do withdrawal sx of medications typically last?
3-10 days (up to 4 weeks)
What are the main principles of prophylactic migraine therapy?
- start low and titrate slowly (for max dose, or to intolerable effects)
- trial drug for adequate period of time (delayed response)
- consider patient specific characteristics
- discuss expected benefits with patients
- in treatment failure, try drug from different therapeutic class
- lifestyle measures are also important
What is valproate CI’ed in?
- pregnancy
- nausea
- weight gain
- alopecia
- transaminitis
- pancreatitis
- agranulocytosis
What are the main SE associated with topiramate?
- parasthesias
- change in taste
- cognitive SE
- anorexia/weight loss
- aggravates depression
- category D in pregnancy
What is the MOA of beta- blockers?
- raises the migraine threshold by modulating the adrenergic system and 5HT transmission in cortical pathways of the brain
When are beta-blockers first line?
- especially in patients <60 years, hypertension or CVD
Beta-blockers with ___________ may not be effective
intrinsic sympathomimetic activity
What are the main SE associated with beta blockers?
- fatigue
- bradycardia
- hypotension
- coldness of extremities
- vivid dreams
- depression
- impotence
- bronchospasm
In what illnesses are beta blockers CI’ed?
- asthma
- heart block
- uncompensated heart failure
- peripheral vascular disease
What is the MOA with antidepressants in migraines?
- down regulates central 5HT receptors, increases synaptic NE levels, enhances endogenous opioid receptor action
- consider in those with comorbidities: depression, insomnia, neuropathic pain, tension-type headache
What antidepressant is used first line?
- tricyclic antidepressants (amitripyline, nortriptyline)
What antidepressants are typically chosen second line?
- venlafaxine, duloxetine
(2nd line with less evidence) - once daily dosing, beneficial if co-morbid anxiety/mood disorders
What ar the main SE associated with TCAs?
- anticholinergics (avoid in BPH, glaucoma), sedation, increased appetite, weight gain, orthostatic hypotension, cardiac toxicity (slowed atrioventricular conduction)
When should antidepressants NOT be used?
- avoid in heart block
- significant CVD
- urinary retention
- uncontrolled glaucoma
- prostate disease
- mania
What are the main SE associated with venlafaxine?
- n/v
- drowsiness
- sexual dysfunction
When should venlafaxine not be used?
- avoid in hypertension
- avoid in kidney failure
What is a CGRP antagonist?
- mABs for the preventative tx for migraine for target CGRP (calcitonin gene-related peptide)»_space;> CGRP is a vasodilatory neuropeptide w/ NB role for migraines
Do CGRP antagonists work much better with migraines than other prophylactic therapy?
- no- do not appear to be more significantly effective than other prophylactic treatment
- some patients had significantly better responses than others
What is the main CGRP antagonist available?
- erenumab
What are the main SE associated with CGRP antagonists?
- GI: constipation
- immunologic: antibody development
- local: injection site reaction
- neuromuscular and skeletal: muscle cramps, muscle spasms
Who should CGRP antagonists be considered for?
- severe disability and lack of benefit from or unable to tolerate existing alternatives
- difficulty adhering to daily medication regimens
- polypharmacy (antibodies =low risk of DIs)
Who should CGRP antagonists be avoided in?
- infrequent h/a’s and/or h/a’s that respond to abortive treatment
- pregnancy or possibility of becoming pregnant (long duration of action; levels of CGRP are lower in women with preeclampsia)
- known cardiovascular disease or high risk (CGRP may have a cardioprotective effect during ischemic emergencies)
CGRP antagonists - exercise caution with patients who are:
- concomitantly, regularly exposed to vasoconstrictive drugs or substances (CGRP blockade may be risky)
When should women not be using oral contraceptives when they have migraines?
- when they have an aura- should be encouraged to try an alternative form of contraception (no estrogen)
