Migraine Flashcards
What is the usual treatment for cluster headaches?
nasal or SC triptans/ergots + burst taper steroid like prednisone
What is the usual treatment of tension headaches?
self-medicate w/ NSAIDS
What is the normal treatment for the following headaches?
- mild-moderate or menstrual
- moderate-severe migraine
- prophylaxis of migraine
- NSAIDS
- Short acting Triptan - sumatriptan most effective
- Topiramate, valproate, propranolol, timolol, or metoprolol
Mechanism of migraine?
Peripheral - altered sensittization/neuro-inflammation. 5HT receptors cerebral vessels leads to dilation and sensitization from release of CGRP/SubP and leads to central sensitization (wind up).
- also there is spreading depression wave causing aura.
- all of this is typically happening in CN V
What areas are activated that lead to the symptoms of migraines?
- Dilation of meningeal blood vessel - throbbing
- activation of area postrema - N/V
- activation of hypothalamus - hypersensitivity
- activation of cervical trigeminal system - muscle spasm
- activation of cortex and thalamus - head pain
What what step do the following drugs work in terms of modulating CGRP and SP?
NSAIDS
Triptans
- NSAIDS - decrease inflammatory stimuli, decreasing peripheral sensitization, COX inhibition
- 5HT1 B receptor at blood vessels –> vasoconstriction
- 5HT 1D receptor on nerve terminals –> presynaptic inhibitino of trigemnovascular inflammatory response
ADE of NSAIDS
gastric irritation w/ chronic use
additive nephrotoxicity - fluid retention, HTN, edema, and rarely CHF
Drug interactions of NSAIDS
- ACE/ARB (need the PGs)
- beta blockers
- vasodilators (alpha 2 agonists, and alpha 1 blocker)
When are NSAIDS contraindicated?
late pregnancy b/c of effect on patency of ductus arteriosus, prolonged labor and delivery
What are NSAID combinations?
- Acetaminophen/butalbital/caffeine
2. Aspirin/butabital/caffeine
What are you worried about in terms of acetaminophen?
- G6PD def, but it can be given during the 1st trimester of pregnancy
What is butalbital
barbiturate - has sedative/hypnotic effects via GABA
- drowsiness, sedation, diminished cerebral function
- strongly linked to analgesic overuse syndrome
- CYP inducer and CNS/respiratory depressant
What will caffeine do in the NSAID combo
cerebral vasoconstriction, potential CV interactions
MOA Triptans
5HT1B and 1D agonists
- selective intracranial/extracerebral vasoconstriction
- inhibition of CN 5 activation by vasoactive peptides
- inhibition of trigeminal cervical complex activation
What is the the triptan w/ the shortest onset and the longest onset
- shortest onset : Sumatriptan and Zolmitriptan
- longest onset : Frovatriptan (has longest half life) and Naratriptan
ADE of triptans
dizziness, drowsiness, fatigure, heaviness of tightness of chest
- may cause coronary and peripheral vasospasm
Contraindications for triptans
- heart disease, uncontrolled HTN/ischemica bowel disease
- <24 hrs following ergot/triptan treatment
- propanolol, MAOIs, CYP3A4 drugs, SSRI/SNRI
MOA of ergot alkaloids
- moderate doses - vasoconstriction of small arteries –> used to control hemorrhage and to promote uterine contraction and migraines
- large doses - paralyzes nerve endings of sympathetic fibers
What is ergotism?
mental disorientation, convulsions, muscle cramps, dry gangrene of the extremities
What is a complete contraindication for pregnancy?
Ergots - also don’t use while breast feeding b/c Cat X
When are narcotics ok to use in migraines
- when there is allodynia –> should consider using ketorolac but not opiates b/c there is dependence and other problems
What are the neurotransmitters that are involved in emesis?
- Dopamine - at floor of 4th ventricle
- Ach in vestibular system
- Histamine in peripheral pain receptors
MOA Metoclopramide
Central D2 blocker
Prokinetic by increasing Ach effects
- concern of increasing prolactin levels leading to gynceomastia
MOA Prochlorperazine and Chlorpormazine
Central D2 blocker
Cholinergic and alpha adrenergic blockade
