Migraine Headaches--Treatment and Prevention Flashcards
Migraine–neural events provoke
-dilation of cranial blood vessels
Goal of therapeutic agents
-rescue patient from start of a migraine
Medication taken in prodrome phase
- Triptans–5HT1B/1D Receptor agonists
- Ergot alkaloids
Medications taken in headache phase
- NSAIDS
- Acetaminophen
Preventative agents
-B blockers
-Tricyclic antidepressants
-anticonvulsants
-Ca channels
(given in asymptomatic phase)
neurogenic inflammation theory of migraine
-wave of electrical cavity
-stimulates release of neuropeptides (CGRP, substance P) and inflammatory mediators
(NO, histamine, prostaglandins)
-dilate cranial blood vessels and sensitive nerves to pain
step 1
- brainstem dysfunction sparks a wave of excitation/depression in Cortex–H, K, NO discharge from neurons
- cerebral vasoconstriction
step 2
- electrolytes and NO diffuse and dilate cranial arteries and depolarize perivascular trigeminal terminals
- CGRP and neuropeptides promote neurogenic inflammation
step 3
neurogenic inflammation irritates TG n and transmits migraine pain
2 key mediators–interact throughout trigeminal neuromuscular system
-CGRP and NO
used to treat coronary a disease
- Organic nitrates (NO)
- Can provoke migraine
cranial vessels–R
5HT-1B
peripheral neuron R
5HT-1 D
central neuron R
-5HT 1B/iD
serotonin receptor-vascular and synaptic
- vascular-5HT1B R
- synaptic-5HT 1 D R
Triptans mechanism
- selective 5HT1D/1B receptor agonist
- 5HT-1B Receptor stimulates vasoconstriction
- 5HT-1D Receptor inhibits pre-synaptic release of CGRP
Triptan prototype
Sumatriptan