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  • Stroke occurs when blood flow to the brain is disrupted and cells in the areas of brain deprived of oxygen die. This can be caused by obstruction or hemorrhage of blood vessels. Brain cells can die within minutes under conditions of zero blood flow.

  • Neuronal death occurs in part through excitotoxicity, mediated by excessive release of glutamate from damaged neurons and subsequent increases in intracellular calcium levels and overactivation of calcium–dependent enzymes, and by free radical formation that causes genetically programmed cell death, called apoptosis.

  • Stroke symptoms differ greatly based on the neuroanatomic location of the compromised brain tissue. Symptoms can be caused by a slowing of blood flow that leaves cells alive but not functioning normally, or when cells have died.

  • Treatments for stroke are divided into preventive measures, therapies used during the acute phase of stroke, and longer–term therapies employed during recovery.

  • The most effective preventive therapy for stroke is to reduce the formation of blood clots and emboli by use of antiplatelet agents such as aspirin and clopidogrel, and oral anticoagulants such as warfarin and dabigatran. Treating general cardiovascular risk factors such as hypercholesterolemia, hypertension, and diabetes also significantly reduces the risk for stroke.

  • Acute stroke treatments are centered on selectively restoring the brain’s blood supply to tissue that is not functioning but is not yet irreversibly damaged. This includes the use of thrombolytic agents such as tissue plasminogen activator (tPA) and mechanical thrombectomy with intravascular devices.

  • Prorecovery treatments focus primarily around physical therapy. Treatment of depression and spasticity are also important during longer–term stroke recovery. Pharmacologic agents that promote recovery remain an active area of research.

  • Migraine headaches are believed to result from the activation of the trigeminovascular system. Release of proinflammatory substances, such as calcitonin gene–related peptide (CGRP), into and around the vessels results in vasodilation and pain.

  • Activation of the trigeminovascular system may be triggered by cortical spreading depression, a slowly propagating wave of depolarization followed by inhibition of brain activity, which might be the electrophysiologic correlate of migraine aura.

  • Treatment regimens 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.

  • Antagonists of CGRP or its receptor are a more recently introduced alternative for treatment of a migraine headache.


Vertebrate neurons are exquisitely specialized for the functions they perform. As explained in previous chapters, a single neuron may receive information from and relay information to thousands of other neurons; consequently, the nervous system is capable of remarkably complex functions. Moreover, the brisk flux of ions across neural membranes permits extremely rapid interneuronal signaling. However, this specialization comes at a cost. A tremendous amount of energy is required to maintain ionic gradients across the membranes of the approximately 100 billion neurons that comprise the human brain. And a roughly equal ...

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