RT Book, Section A1 Nestler, Eric J. A1 Hyman, Steven E. A1 Holtzman, David M. A1 Malenka, Robert C. SR Print(0) ID 1105917214 T1 Stroke and Migraine T2 Molecular Neuropharmacology: A Foundation for Clinical Neuroscience, 3e YR 2015 FD 2015 PB McGraw-Hill Education PP New York, NY SN 9780071827690 LK neurology.mhmedical.com/content.aspx?aid=1105917214 RD 2024/03/28 AB Stroke occurs when blood flow to the brain is disrupted and the areas of brain deprived of oxygen die. This can be caused by obstruction or hemorrhage of blood vessels.Loss of oxygenation causes death of neurons through complex processes, which include excitotoxicity, mediated by excessive release of glutamate from damaged neurons, and subsequent increases in intracellular calcium levels and overactivation of calcium-dependent enzymes.Loss of oxygenation also causes neuronal death through the formation of free radicals and through genetically programmed cell death, called apoptosis.Despite increased understanding of the biochemical processes underlying neuronal death, the best therapy for stroke remains rapidly restoring the brain’s blood supply and preventing the formation of clots and emboli.This includes the use of antiplatelet agents such as aspirin and clopidogrel, and oral anticoagulants such as warfarin and dabigatran, as well as thrombolytic agents such as tissue plasminogen activator (tPA), which target different steps of coagulation cascades.Migraine headaches are believed to result from waves of inhibitory neuronal activity called “cortical spreading depression” that stimulate trigeminal nerve endings innervating the brain’s vasculature. This causes release of proinflammatory substances, such as calcitonin gene–related peptide (CGRP), into and around the vessels, resulting in vasodilation and pain.Treatment regimes for migraine headaches typically employ both prophylactic and abortive strategies.The mainstay in abortive treatment is the triptan drugs, such as sumatriptan, which are agonists at serotonin 5HT1B and 5HT1D receptors.