Headache Pharmacotherapy Flashcards
(34 cards)
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)
What should be used and avoided in patients with migraines during pregnancy? Is it common to have migraines in pregnancy?
Less common -> estrogen levels stable
Tylenol and caffeine are probably the best
Avoid:
NSAIDs - prevent PGE2, especially in third trimester is important
Ergots - cause vasoconstriction which can cause intrauterine contraction
Triptans - uterine vasospasm
What is a drug-induced migraine and how are they treated?
Medication misuse and excessive prophylaxis with analgesics leads to rebound headaches whenever a patient isn’t on peak dose. Probably due to suppression of natural opioid systems.
-> removal of offending medication (i.e. excedrin) leads to dramatic symptom removal
What is the mechanism of action of ergot alkaloids?
Structurally related to monoamines, can cause potent vasoconstriction or dilation
- > mechanism of action is sympathomimetic vasoconstriction of cranial arteries, or stimulation of 5HT-1 receptors
- > very nonselective, dirty drugs
What is the most commonly used ergot alkaloid and what should be given with it?
Dihydroergotamine
Commonly used with metoclopramide (antiemetic)
What are the most serious adverse effects of ergot alkaloids?
- Nausea / vomiting - dopamine agonism stimulates area postrema. Reason it’s given with metoclopramide
- Peripheral vasoconstriction -> can lead to gangrene, sympathomimetic properties
What are the important contraindications of ergotamines?
- Peripheral vascular disease
- Renal impairment - may cause diversion of blood flow from kidneys
- Coronary artery disease -vasospasm
- Pregnancy (as mentioned early)
- Concomitant triptan use
Are triptans used to treat tension headaches?
No, they are thought to be just effective against cluster and migraine headaches.
Tension headaches should be treated with analgesic, NSAIDs, or acetaminophen
What are the most common adverse events of triptans?
Chest tightness - due to coronary artery vasospasm
Drowsiness - may be beneficial
Tingling and numbness due to vasoconstriction (paresthesias)
What are the most serious adverse events of triptans and hence contraindications?
Coronary vasospasm -> MI, arrhythmias, and strokes
Contraindicated in Prinzmetal angina, coronary artery disease, and uncontrolled HTN
Avoid in hepatic disease. Don’t use with a MAO-A inhibitor within 2 weeks -> serotonin syndrome
