Porth's Essentials of Pathophysiology, 4e

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Nervous System

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monocular blindness (amaurosis fugax). In most cases of stroke, a single cerebral artery and its territories are affected. Usually, thrombotic strokes are seen in older persons and frequently are accompanied by evidence of atherosclerotic heart or peripheral arterial disease. The thrombotic stroke is not associated with activity and may occur in a person at rest. SmallVessel Stroke (Lacunar Infarct). Lacunar infarcts are small (<15 mm wide) infarcts located in the deep, noncortical parts of the brain or in the brain stem. 1 They are found in the territory of single, deep, penetrating arteries supplying the internal capsule, basal ganglia, or brain stem. They result from occlusion of the smaller penetrating branches of large cerebral arteries, com- monly the middle cerebral and posterior cerebral arter- ies. The infarcted tissue eventually scars to leave small, rounded cavities, or lacunae (“lakes”). They are thought to result from arteriosclerosis, commonly in the settings of chronic hypertension or diabetes. Because of their size and location, lacunar infarcts usually do not cause cortical deficits such as aphasia or apraxia. Instead, they produce classic recognizable “lacunar syndromes” such as pure motor hemiplegia, pure sensory hemiplegia, and dysarthria with clumsy hand syndrome. Because CT scans are not sensitive enough to detect these tiny infarcts, diagnosis used to depend on clinical features alone. The use of MRI has allowed frequent visualiza- tion of small vessel infarcts and is obligatory to confirm such a lesion. Embolic Stroke. An embolic stroke is caused by a mov- ing blood clot that travels from its origin to the brain. It usually affects the larger proximal cerebral vessels, with emboli often lodging at bifurcations. The most frequent site of embolic strokes is the middle cerebral artery, reflecting the large territory of this vessel and its position at the terminus of the carotid artery. Although most cere- bral emboli originate from a thrombus in the left heart, they also may originate in an atherosclerotic plaque in the carotid arteries. The embolus travels quickly to the brain and becomes lodged in a smaller artery through which it cannot pass. Embolic stroke usually has a sud- den onset with immediate maximum deficit. Various cardiac conditions predispose to formation of emboli that produce embolic stroke, including rheumatic heart disease, atrial fibrillation, recent myocardial infarc- tion, ventricular aneurysm, and bacterial endocarditis. More recently, the use of transesophageal echocardiog- raphy, which better images the interatrial septum, has implicated a patent foramen ovale as a source for para- doxical venous emboli to the arterial system. Advances in the diagnosis and treatment of heart disease can be expected to favorably alter the incidence of embolic stroke. Hemorrhagic Stroke The most frequently fatal stroke is caused by the spon- taneous rupture of an intracerebral vessel. 27,28 With rup- ture of a blood vessel, hemorrhage into the brain tissue

occurs, resulting in a focal hematoma and sometimes intraventricular hemorrhage, edema, compression of the brain contents, or spasm of the adjacent blood ves- sels. The most common predisposing factors are advanc- ing age and hypertension. Other causes of hemorrhage are aneurysm, trauma, erosion of the vessels by tumors, arteriovenous malformations, blood coagulation dis- orders, vasculitis, and drugs. A cerebral hemorrhage occurs suddenly, usually when the person is active. Vomiting commonly occurs at the onset, and headache is common. Focal symptoms depend on which vessel is involved. In the most common situation, hemorrhage into the basal ganglia results in contralateral hemiple- gia, with initial flaccidity progressing to spasticity. The hemorrhage and resultant edema exert great pressure on the brain substance, and the clinical course progresses rapidly to coma and frequently to death. Treatment of hemorrhagic stroke focuses on inten- sive management of the increased arterial and intracra- nial pressures, and prevention of hematoma expansion. Initial promising results with use of recombinant fac- tor VII to limit hematoma expansion were deflated by the occurrence of thromboembolic complications. 28 In patients with anticoagulant-associated hemorrhages, use of prothrombin complex concentrate has been more successful than vitamin K administration. 29 Acute Stroke Management The specific manifestations of stroke or TIA are deter- mined by the cerebral artery that is affected, by the area of brain tissue that is supplied by that vessel, and by the adequacy of the collateral circulation. 7,18 Symptoms of stroke/TIA always are sudden in onset and focal, and usually are one-sided. The most common symptom is weakness of the face and arm, and sometimes also of the leg. Other frequent stroke symptoms are unilateral numbness, vision loss in one eye (amaurosis fugax) or to one side (hemianopia), language disturbance (aphasia), slurred speech (dysarthria), and sudden, unexplained imbalance or ataxia. In the event of TIA, symptoms rapidly resolve spontaneously, usually within minutes, although the underlying mechanisms are the same as for stroke. Stroke signs depend on the specific vascular terri- tory compromised (Table 37-5). As a generalization, carotid ischemia causes monocular visual loss or apha- sia (dominant hemisphere) or hemineglect (nondomi- nant hemisphere), contralateral sensory or motor loss, or other discrete cortical signs such as apraxia and agnosia. Vertebrobasilar ischemia induces ataxia, diplo- pia, hemianopia, vertigo, cranial nerve deficits, contra- lateral hemiplegia, sensory deficits (either contralateral or crossed, i.e., contralateral body and ipsilateral face), and arousal defects. Discrete subsets of these vascular syndromes usually occur, depending on which branches of the involved artery are blocked. Diagnosis. Accurate diagnosis of acute stroke, based on a complete history and thorough physical and neurologic examination, is designed to determine the presence of