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Harrison's Principles of Internal Medicine, 18e
| Part 17. Neurologic Disorders > Section 2. Diseases of the Central Nervous System > |
Ischemic Stroke
Sections: Pathophysiology of Ischemic Stroke, Treatment: Acute Ischemic Stroke, Medical Support, Intravenous Thrombolysis, Endovascular Techniques, Antithrombotic Treatment, Platelet Inhibition, Anticoagulation, Neuroprotection, Stroke Centers and Rehabilitation, Etiology of Ischemic Stroke, Cardioembolic Stroke, Artery-to-Artery Embolic Stroke, Carotid Atherosclerosis, Other Causes of Artery-to-Artery Embolic Stroke, Small-Vessel Stroke, Pathophysiology, Clinical Manifestations, Less Common Causes of Stroke, Transient Ischemic Attacks, Treatment: Primary and Secondary Prevention of Stroke and TIA, General Principles, Atherosclerosis Risk Factors, Antiplatelet Agents, Anticoagulation Therapy and Embolic Stroke, Anticoagulation Therapy and Noncardiogenic Stroke, Treatment: Carotid Atherosclerosis, Surgical Therapy, Endovascular Therapy, Bypass Surgery, Intracranial Atherosclerosis, Dural Sinus Thrombosis, Stroke Syndromes, Stroke Within the Anterior Circulation, Middle Cerebral Artery, Anterior Cerebral Artery, Anterior Choroidal Artery, Internal Carotid Artery, Common Carotid Artery, Stroke Within the Posterior Circulation, Posterior Cerebral Artery, P1 Syndromes, P2 Syndromes, Vertebral and Posterior Inferior Cerebellar Arteries, Basilar Artery, Imaging Studies, CT Scans, MRI, Cerebral Angiography, Ultrasound Techniques, Perfusion Techniques.
Topics Discussed: abcd2 score; acute cerebral ischemia; acute cerebrovascular accidents; alteplase; amaurosis fugax; amphetamine; aneurysm, dissecting; anterior cerebral artery occlusion; anterior choroidal artery infarction; anticoagulants; anticoagulation; anticoagulation, chronic; antiplatelet agents; antithrombin iii; anton syndrome; atherosclerosis; atrial fibrillation; basilar artery insufficiency; basilar artery occlusion; blindness, cortical; blood pressure; brain; brain ct; brain mri; broca area; cadasil; cardiac embolism; cardioembolic stroke; carotid angioplasty and stenting; carotid artery, common; carotid artery, internal, occlusion; carotid atherosclerosis; carotid stenosis; cerebral angiography; cerebral ischemia; cerebrovascular accident in children; cerebrovascular accident, cocaine induced; cerebrovascular disorders; cerebrum; claude syndrome; cocaine; corpus callosum; dejerine-roussy syndrome; drugs affecting blood and blood formation; drugs affecting cardiovascular function; echoencephalography; embolic stroke; endarterectomy, carotid; extracranial to intracranial bypass; fibrinolytic agents; fibromuscular dysplasia; focal neurologic deficits; frontal lobe; frontal lobe syndrome; giant cell arteritis; glucose; heparin; infarction, anterior cerebral artery; infarction, lacunar; infarction, middle cerebral artery; infarction, posterior cerebral artery; internal carotid artery; intracranial atherosclerosis; ischemic stroke; lateral medullary syndrome; leukoaraiosis; leukoencephalopathies; medial medullary syndrome; medulla oblongata; midbrain; midbrain infarction; middle cerebral artery occlusion; motor cortex; moyamoya disease; necrotizing arteritis; neuroanatomy; neuroprotection; neuroprotective agents; occipital lobe; oral contraceptives; parietal lobe; pathophysiology of cardiovascular disorders: vascular disease; peduncular hallucinosis; perfusion computed tomography; pharmacotherapy of cardiovascular disorders; pons; pontine syndrome; posterior cerebral artery occlusion; posterior circulation intracranial artery; posterior circulation stroke of uncertain pathology; primary cns vasculitis; sickle cell disease; sinus thrombosis, intracranial; somatosensory cortex; stroke; stroke center; stroke prevention; stroke rehabilitation; stroke risk; temporal lobe; thrombectomy; thromboembolic stroke; thrombolytic therapy; transcranial doppler; transient ischemic attack; us brain scan; vertebral artery stenosis; vertebrobasilar insufficiency; warfarin.
Excerpt:"Acute occlusion of an intracranial vessel causes reduction in blood flow to the brain region it supplies. The magnitude of flow reduction is a function of collateral blood flow and this depends on individual vascular anatomy, the site of occlusion, and likely systemic blood pressure. A decrease in cerebral blood flow to zero causes death of brain tissue within 4–10 minutes; values <16–18 mL/100 g tissue per minute cause infarction within an hour; and values <20 mL/100 g tissue per minute cause ischemia without infarction unless prolonged for several hours or days. If blood flow is restored prior to a significant amount of cell death, the patient may experience only transient symptoms, and the clinical syndrome is called a TIA. Tissue surrounding the core region of infarction is ischemic but reversibly dysfunctional and is referred to as the ischemic penumbra. The penumbra may be imaged by using perfusion-diffusion imaging with MRI or CT (see below and Figs. 370-15 and 370-16). The ischemic penumbra will eventually infarct if no change in flow occurs, and hence saving the ischemic penumbra is the goal of revascularization therapies.When ischemic stroke occurs, the immediate goal is to optimize cerebral perfusion in the surrounding ischemic penumbra...."
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