The modern study of neurovascular function owes much of its success to important, early contributors to the field. Some of the earliest drawings of the cerebral circulation were done in the 1500s by Andreas Vesalius. y Gabriel Fallopius provided a detailed description of the cerebral vasculature, including a description of what was later called the circle of Willis. [1 Thomas Willis was the first to describe the function of the circle that bears his name. [1 Vascular anatomy was transformed into physiology through the work of William Harvey in the early 1600s. [1 The most important early advances in the study of "apoplexy" were a result of meticulous studies of the cerebral blood vessels of patients with apoplexy by Johann Jakob Wepfer. y The actual demonstration that the paralysis was on the side opposite the brain lesion in "apoplexy" was through the work of Domenico Mistichelli, and Francois Bayle was among the first to relate atherosclerosis in cerebral arteries to "apoplexy."
A transient ischemic attack (TIA) is an episode of focal, nonconvulsive neurological dysfunction caused by a reversible interference of the blood supply to an area of the retina or brain that lasts less than 24 hours, and often lasts less than 30 minutes. The episodes are sudden and often are unprovoked. They reach a maximum intensity almost immediately. The duration of a TIA was determined on an arbitrary basis. Subsequent studies have revealed that the typical carotid distribution TIA lasts less than 10 to 20 minutes.y , [4
A reversible ischemic neurologic deficit (RIND) is a focal neurological deficit that lasts longer than 24 hours but resolves with complete recovery within 3 weeks. [5 This term has not been used much because this division does not represent a unique group prognostically or therapeutically. [5
A completed (established) stroke is the preferred term to describe an acute episode of focal brain ischemia that lasts longer than 24 hours. Most completed strokes reach a maximal neurological deficit within an hour of onset. Older terms that have been used in the past include apoplexy (literally meaning "struck with violence" or "being thunderstruck") and cerebrovascular accident. Both of these older terms imply a random, unpredictable, or uncertain nature to these events, which often is not the case.
Stroke in evolution or progressive stroke describes a temporal profile in which the neurological deficit occurs in a stepwise or progressive pattern. In the carotid artery distribution, there is usually little likelihood of progression after 24 hours. In the vertebrobasilar distribution, progression may continue for up to 72 hours. y There are numerous causes to consider (, Table.., .22:1 ) when there is "progression" of an ischemic event.
Stroke may be divided into ischemic infarctions, which may be bland or hemorrhagic, and hemorrhages, including intracerebral hemorrhages and subarachnoid hemorrhages. Ischemic infarctions can be due to intrinsic vascular occlusion (thrombus) or an occlusion from intravascular material that originates elsewhere, such as heart or other vessels (embolism).
Common focal sites of cerebrovascular atherosclerosis include the proximal common carotid artery, the origin of the internal carotid artery, the carotid siphon, and the proximal middle cerebral and vertebral arteries. The aortic arch has been recognized as a source for atheroembolism.
Small arteries are also susceptible to atherosclerotic changes. Examples of these small arteries would be the lenticulostriate arteries, thalamoperforating arteries, the basilar paramedian penetrating arteries, and the medullary arteries. These arteries supply deep cerebral white matter. The most frequent sites of lacunar infarcts are the putamen, basis pontis, thalamus, posterior limb of the internal capsule, and caudate nucleus. They may also occur in the anterior limb of the internal capsule, subcortical cerebral white matter, and cerebellar white matter.
Overall, embolism accounts for between 15 and 30 percent of strokes. '7] y Emboli that cause brain ischemia may arise from the heart, the aorta, the venous system in combination with a transcardiac defect, or from other intracerebral or extracerebral arteries (artery-to-artery embolism).
_TABLE 22-1 -- CAUSES OF NEUROLOGICAL WORSENING AFTER AN ISCHEMIC EVENT_
Occlusion of a stenotic artery due to thrombus Recurrent embolism Hemorrhagic transformation Failure of collateral blood supply Hypoperfusion due to systemic hypotension Hypovolemia or decreased cardiac output Hypoxia
Medical conditions such as pneumonia, pulmonary embolus, myocardial ischemia, congestive heart failure, electrolyte disturbances, or urosepsis
Diffuse perfusion deficits may lead to brain ischemia and may occur with severe hypotensive crises due to sepsis, anaphylaxis, acute blood loss, pharmacologic alterations, cardiac surgery, and other acute medical crises. These situations may lead to infarctions, typically in the border zone regions (watershed areas) between the anterior, middle, and posterior cerebral arteries.
Hemorrhages may be subarachnoid, intraparenchymal, or a combination of both. Intraparenchymal hemorrhages are the result of bleeding from an arterial source directly into the brain. Subarachnoid hemorrhages are the result of bleeding into the subarachnoid spaces.
Another distinction needs to be made between hematomas within the brain parenchyma, which are referred to as intracerebral, and those outside the brain parenchyma, which are referred to as extracerebral. Examples of extracerebral hematomas are subdural and epidural hematomas.
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