Headache Pharmacotherapy Flashcards
What is a primary vs secondary headache?
Primary - one of the three main types: Tension, migraine, and cluster headache
Secondary - pain secondary to an identifiable head pathology, i.e. tumor, subarachnoid hemorrhage
Who tends to get migraine, tension, and cluster headaches? How long does each last?
Migraine - 4-72 hours, most common in women
Tension - usually 4-6 hours, variable
Cluster - brief, 15-180 min, much more common in men
What are common triggers for migraines?
Menstruation, stress, alcohol, caffeine withdrawal, nitrates, sulfates in food (i.e. hot dogs), loss of sleep, noise, exercise, etc
What are prodromal syndromes / auras?
Prodromal syndromes - happen before most migraines, patients may have anxity, depression, photophobia, or constitutional symptoms
Auras - much rarer (only 10%), last 5-60 minutes, often visual auras or flashing lights (perceptual disturbances)
How are many drugs for migraine administered and why?
Cutaneous, subcutaneous, rectal, parenteral or intranasal
-> many patients with migraine experience nausea / vomiting as well as decreased GI emptying, so oral treatments will be less effective
What is the firstline treatment for acute migraine?
Acetaminophen or NSAIDs + triptan (if severe)
Consider ergot alkaloids
What are the first and second line suggestions for migraine prophylaxis?
First line: Beta blockers or topiramate
-Tricyclics like amitryptyline if h/o depression
Second line: Verapamil, if beta blockers not tolerated.
Valproic acid also an option
What are the symptoms of cluster headache?
Unilateral headaches occurring repetitively in clusters of days to weeks
Sharp pain associated with autonomic symptoms
-> Lacrimation, rhinorrhea, periorbital swelling
What is used for acute treatment and prophylaxis in cluster headache?
Acute - 100% oxygen therapy and sumatriptan
Prophylaxis - Verapamil preferred > lithium
What is the neurovascular hypothesis for how migraine is generated?
Trigeminovascular system is a network of nerve fibers innervating cranial vessels in meninges
Sensitization of vessels occurs which causes release of substance P, calcitonin gene-related peptide (CGRP), and vasoactive peptides, and irritative vasodilation
How exactly are triptans thought to combat migraine?
5HT-1B = Blood vessels, agonism causes vasoconstriction
5HT-1D = trigeminal nerve, agonism causes reduction of release of inflammatory mediators (i.e. SP, CGRP)
Why is it important to treat headaches early?
The longer the neural activation and degrandulation of inflammatory chemicals occurs, causing the vasodilation, the more “sensitized” the system becomes
-> need to rapidly terminate this cycle with triptans and an NSAID
What is the threshold at which you should consider prophylactic headache therapy?
If attacks occur more frequently than 2 times per week (except cluster), or attacks are extremely severe (prophylaxis is worth it despite the infrequency)
What causes a menstrual migraine?
Rapid changes in estrogen levels, which occurs especially before or during menstruation
Serotonergic systems are suppressed during late luteal phase (important in downregulating migraine) -> affects many women with migraine
What can be used as prophylaxis for menstrual migraine?
- Birth control pills - keeps estrogen more level and constant
- Standard prophylaxis
- “Miniprophylaxis” - taking triptans right before you think a migraine is likely to happen during your menstrual cycle (only time triptans are used prophylactically)
