Vascular occlusion, the fundamental underlying cause of ischemic stroke, can be from embolic particles originating in the cardiovascular system distant from the region of the stroke, or thrombotic, in which a clot forms within a vessel in proximity to the area of infarction. Most embolic strokes occur suddenly and the deficit reaches its peak almost at once. Thrombotic strokes tend to evolve somewhat more slowly over a period of minutes or hours and occasionally days; in the latter case, the stroke usually progresses in a saltatory fashion, that is, in a series of steps rather than smoothly. In cerebral hemorrhage, also abrupt in onset, the deficit may be virtually static or steadily progressive over a period of minutes or hours, while subarachnoid hemorrhage is almost instantaneous. It follows that gradual downhill course over a period of several days or weeks will usually be traced to a nonvascular disease. There are, however, many exceptions, such as the additive effects of multiple vascular occlusions and the progression that is caused by secondary brain edema surrounding large infarctions and cerebral hemorrhages. A focal stroke syndrome that reverses itself entirely and dramatically over a period of minutes or up to an hour is called a TIA. The first distinction is to separate ischemic from hemorrhagic stroke; features that are characteristic of the latter such as headache and vomiting at the onset, rapid progression to coma, and severe hypertension are emphasized in the later section on cerebral hemorrhage. Often, however, the distinction is not so clear because sudden onset of a focal neurologic problem is the core syndrome of both processes.
The second essential feature of stroke is its focal signature. The neurologic deficit reflects both the location and the size of the infarct or hemorrhage. Hemiplegia stands as the most typical sign of stroke, whether in the cerebral hemisphere or brainstem, but there are many other manifestations, occurring in recognizable combinations. These include paralysis, numbness, and sensory deficits of many types on one side of the body, aphasia, visual field defects, diplopia, dizziness, dysarthria, and so forth. The neurovascular syndromes enable the physician to localize the lesion—sometimes so precisely that even the affected arterial branch can be specified—and to indicate whether the lesion is an infarct or a hemorrhage. These syndromes are described in the sections that follow. This group of diseases has also provided the most instructive approach to localization in neurology. As our colleague C.M. Fisher aptly remarked, neurology is learned “stroke by stroke.” Also, the focal ischemic lesion has divulged some of our most important ideas about the function of the human brain. Currently, various forms of cerebral imaging have overtaken this traditional, careful clinical approach in order to shorten the time to diagnosis and allow for acute treatment of vascular occlusion.
The severity of the stroke deficit may be partly independent of these factors. Instead, it may reflect some combination of infarcted and ischemic, but not yet infarcted, tissue. The ischemic portion is called the penumbra and current therapy of acute stroke is focused on determining the extent of the size of the region reversible ischemia and reversing it by re-establishing blood flow.
The analysis of a stroke involves several steps. First, the clinician must determine whether the event is a stroke rather than some other process that may have a similar sudden onset, such as migraine, seizure, or syncope. Second, if the event is considered likely to be a stroke or TIA, then the pathophysiology must be ascertained (e.g., cerebral embolism from the heart or a proximal artery, large vessel atherothrombotic occlusion, venous occlusive disease). Third, acute treatment (e.g., tissue plasminogen activator or endovascular thrombectomy) is initiated, if appropriate. Fourth, a plan for the prevention of future strokes is undertaken.