Porth's Essentials of Pathophysiology, 4e

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Nervous System

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which ischemic but viable brain tissue can be salvaged has led to the use of reperfusion techniques and neuro- protective strategies in the early treatment of ischemic stroke. 18,30–33 Although the results of emergent treatment of hemorrhagic stroke have been less dramatic, contin- ued efforts to reduce disability have been promising. Reperfusion techniques include thrombolytic therapy (administered either intravenously or intra-arterially), catheter-directed mechanical clot disruption, and aug- mentation of cerebral perfusion pressure during acute stroke. 34 The first and only agent approved by the U.S. Food and Drug Administration (FDA) for treatment of acute ischemic stroke is tissue plasminogen activa- tor (tPA). A subcommittee of the Stroke Council of the American Heart Association has developed guidelines for the use of tPA for acute stroke. 20 These guidelines recommend that in persons with suspected stroke, the diagnosis of hemorrhagic stroke be excluded through the use of CT scanning before administration of I.V. throm- bolytic therapy, which must be administered within 3 hours of onset of symptoms, or 4.5 hours in some cases. 34 The major risk of treatment with thrombolytic agents is intracranial hemorrhage of the infarcted brain. A number of conditions, including therapeutic levels of oral anticoagulant medications, a history of gastrointes- tinal or urinary tract bleeding in the previous 21 days, prior stroke or head injury within 3 months, major surgery within the past 14 days, and a blood pressure greater than 185/110 mm Hg, are considered contrain- dications to intravenous thrombolytic therapy. 33 Emerging experimental treatments for ischemic stroke are being increasingly used as alternative methods of reperfusion beyond intravenous thrombolysis. New catheter-based methods allow recanalization of a directly visualized cerebral clot with intra-arterial techniques, often beyond the 4.5-hour window. Patient candidates for invasive reperfusion strategies are generally identified using newer perfusion imaging techniques such as CT or MR perfusion in order to detect a region of reversible injury (ischemic penumbra) and to exclude completed infarcts. Once a penumbra is found, the interventional specialist might mechanically disrupt the clot, extract the clot (thrombectomy), or deliver the thrombolytic drug intra-arterially at the clot surface, or urgently stent intra- cranial vessels to restore flow and rescue the penumbra. Additional methods (drugs, ultrasound, hypothermia) aimed at either extending that therapeutic window until revascularization occurs or improving recanalization rates are under active investigation. 36 These methods require an experienced interventional angiography team, neurocritical care services, and extensive institutional infrastructure, and thus remain limited to tertiary care centers. Poststroke Management and Deficits Poststroke treatment is aimed at preventing recurrent stroke and medical complications while promoting the fullest possible recovery of function. 37 The risk of stroke recurrence is highest in the first week after a stroke or TIA, so the early implementation of antiplatelet agents in

most cases, or warfarin (an anticoagulant) in cardioem- bolic stroke, is imperative. Long-term stroke recurrence is most effectively prevented with aggressive reduction of risk factors, primarily hypertension, diabetes, smok- ing, and hyperlipidemia. In cases of carotid territory stroke with carotid stenosis, revascularization with sur- gery or stenting should be considered. Early hospital care also requires careful prevention of aspiration, deep vein thrombosis, and falls. Recovery is maximized with early and aggressive rehabilitation efforts that include all members of the rehabilitation team—physician, nurse, speech therapist, physical therapist, and occupational therapist—and the family. Poststroke Motor Deficits. Poststroke motor deficits are most common, followed by deficits of language, sensation, and cognition. After a stroke affecting the corticospinal tract such as the motor cortex, posterior limb of the internal capsule, basis pontis, or medullary pyramids, there is profound weakness on the contra- lateral side (hemiparesis; see Chapter 36, Fig. 36-4). Involvement at the level of the motor cortex is most often in the territory of the middle cerebral artery, usu- ally with a sparing of the leg, which is supplied by the anterior cerebral artery. Subcortical lesions of the corti- cospinal tracts cause equal weakness of the face, arm, and leg. Within 6 to 8 weeks, the initial weakness and flaccidity are replaced by hyperreflexia and spasticity. Spasticity involves an increase in the tone of affected muscles and usually an element of weakness. The flexor muscles usually are more strongly affected in the upper extremities and the extensor muscles more strongly affected in the lower extremities. There is a tendency toward foot drop; outward rotation and circumduction of the leg with gait; flexion at the wrist, elbow, and fin- gers; lower facial paresis; slurred speech; an upgoing toe to plantar stimulation (Babinski sign); and dependent edema in the affected extremities. A slight corticospinal lesion may be indicated only by clumsiness in carrying out fine coordinated movements rather than obvious weakness. Passive range-of-motion exercises help to maintain joint function and to prevent edema, shoulder subluxation (i.e., incomplete dislocation), and muscle atrophy, and may help to reestablish motor patterns. If no voluntary movement or movement on command appears within a few months, significant function usu- ally will not return to that extremity. Poststroke Dysarthria and Aphasia. Two key aspects of verbal communication are speech and language. Speech involves the mechanical act of articulating verbal sounds, the “motor act” of verbal expression, whereas language involves the written or spoken use of symbolic formulations, such as words or numbers. 7 Dysarthria is a disorder of speech, which manifests as the imper- fect articulation of speech sounds or changes in voice pitch or quality. It results from a stroke affecting the muscles of the pharynx, palate, tongue, lips, or mouth and does not relate to the content of speech. A person with dysarthria may demonstrate slurred speech while still retaining language ability, or may have a concurrent