Migraine Flashcards
(25 cards)
Features of a migraine
- duration (4-72 hours)
- Pulsating, more less unilateral
- moderate to severe pain
- impair function
- nausea/vomiting more less photo/photophobia
Consistently two major issues
- Vascular
- Neurogenic
Vascular theory on migraines
- begins with vasoconstriction of cerebral vessels
- the subsequent reduction in blood flow causes the ‘aura’
- then there is a compensatory dilation of vessels, which leads to pain
Neurogenic theory on migraines
- attacks precipitated by excess excitation in neocortex
- followed by ‘cortical spreading depression’ (CSD): rapid and profound depolarization of neurons
- this CSD leads to the aura and this triggers the pain
Pharmacology of migraines
- dilation/inflammation of cerebral vessels
- release of pain mediators
- serotonin seems to play a role in both
Treatment of migraines
Triptans
Ergots
Sumatriptan mechanism
Agonist at 5HT-1B and 5HT-1D
Vasoconstrictor
Reduced release of pain transmitters
Sumatriptan pharmacokinetics and ROA
Onset varies depending on route Routes of administration - Oral - Nasal spray - Subcutaneous
Triptans side effects related to vasoconstriction
Related to vasoconstriction - chest/neck discomfort Rare, serious: - myocardial ischemia/infarction - Avoid in patients with cardio-/cerebrovasscular disease
Triptans side effects due to serotonin
Nausea
Caution: serotonin syndrome
Ergot alkaloids example
Dihydroergotamine
Dihydroergotamine mechanism
Agonist at 5HT-1B, 5HT-1D, and alpha 1
- vasoconstrictor
- reduced release of pain mediators
Route of administration of ergot alkaloids
Injectable
Nasal Spray
Acute Migraine treatment
Anti-inflammatory: NSAIDs Acetaminophen Opioids - codeine containing products - Butorphanol
Opioids in migraine
- not addressing main issues, no vasoconstriction effects, no anti-inflammatory effects
- tolerance/withdrawal/dependence
Butorphanol mechanism
- partial agonist/mixed agonist-antagonist at opioid receptors
- more likely to see dysphoria
- kappa agonist
Butorphanol route of administration
Nasal spray
- definite potential for dependence
Medication overuse headache
Frequent headaches (>15/month) - Can occur with any drugs for migraine: some drugs are higher risk than others
MOH mechanism
- unknown
- effects of chronic drug use for headache: changes in neurotransmitter levels, decreases threshold for developing a subsequent headaches
MOH management
- discontinue headache medication
- switch to prophylaxis
Migraine prophylaxis
Reuptake inhibitors (tricyclic antidepressants) Na+ channel blockers (Valproic Acid) Calcium alpha 2 delta channel blockers (Gabapentin)
Pain mechanism
- Increase number of Na+ channels
- Facilitates propagation of action potentials (noxious stimuli no longer necessary
- Calcium channel opens
- prompts release of pain mediators
Beta blockers for migraine
Propranolol
Beta blockers mechanism
Inhibit SNS activity - may modulate hyperexcitability
Some beta blockers may also modulate 5HT: off target effects
