Neuropathology of cerebrovascular diseases
Section snippets
Cerebrovascular accident (stroke)
The most common consequence of cerebral vascular disease is cerebrovascular accident or stroke, which typically is a sudden unexpected intracranial catastrophe that leads to different symptoms depending on the anatomical site affected. It may cause prompt but rarely sudden or immediate death. It is subdivided pathologically into two entities: ischemic cerebral infarction and hemorrhagic cerebral infarction. The cause for ischemic cerebral infarction is usually the sudden blockage or significant
Cerebrovascular atherosclerosis
The underlying pathogenesis of cerebral atherosclerosis is probably not very different from that in any other arteries. Indeed, the risk factors that have been recognized, including smoking, hyperlipidemia, diabetes, obesity, and hypertension, probably apply as well to brain vessels as any other organ.49 Precisely how these various risk factors produce CVD is still the subject of research and may involve complex interacting factors, such as genes and environment. There is recent interest in the
Neuropathology of infarcts and hemorrhages
A cerebral infarct is a well-circumscribed area of necrosis in the distribution of a specific vascular territory resulting from occlusion or severe hypoperfusion in the feeding artery (Figure 1). Atherosclerosis is the most common cause of cerebral infarct and may be due to plaque enlargement (usually with a superimposed thrombus), embolization of the thrombus or plaque material, or hemodynamic alterations when a proximal vessel is partly or totally occluded and collateral blood flow is
Hypertensive cerebrovascular disease
Arterial hypertension is a universally accepted risk factor for cerebral vascular disease. However, there is still considerable debate on the mechanisms involved in the production of its pathology.62 The high prevalence of this disease makes it a major public health problem in different parts of the world but mainly in affluent societies. This is clearly true among the black population in the USA, who suffer the ravage of this disease more than any other group. Hypertension is thought to be the
Cerebral aneurysms and subarachnoid hemorrhage
Cerebral vascular aneurysms can be divided into saccular (berry aneurysms), atherosclerotic (fusiform), mycotic, traumatic, dissecting aneurysms, and microaneurysms. The most common aneurysms of the intracranial arteries are saccular or berry aneurysms. Cerebral berry aneurysms are typically saccular outpouchings occurring at the branching points of intracranial cerebral arteries. They may vary in size from less than a millimeter to a centimeter or more in diameter, may be spherical or
Vascular malformations
Vascular malformations are congenital lesions of cerebral vessels and include arteriovenous malformations (AVMs), cavernous hemangiomas, capillary telangiectasias, and venous angiomas. They arise during early fetal life when the usual division into arteries, veins, and capillaries is interrupted, resulting in the formation of direct arterial–venous communications.
Cerebral amyloid angiopathy
Cerebral amyloid angiopathy (CAA) is confined to intracranial arteries and arterioles in the leptomeninges and the superficial cortex of the cerebral (and cerebellar) hemispheres, although the amyloid protein itself may be present systematically88 (Figure 5). It is a sporadic disease in patients over 70 years of age but may be familial in younger patients.89, 90, 91 By microscopic examination, involved vessels are dilated and their walls thickened and replaced by pink amorphous material.
Vasculitis of central nervous system
Vasculitis of the intracranial blood vessels may have an infectious or noninfectious origin.
Cerebral autosomal dominant arteriopathy and leukoencephalopathy (CADASIL)
The main symptoms of CADASIL are migraine with aura, often very severe, sometimes causing hemiparesis, recurrent ischemic stroke, psychiatric symptoms, and cognitive decline with eventual dementia. The patients may experience their first stroke before the age of 30, but the peak is around the fourth and fifth decades of life.119 MRI detects white matter changes in the poles of the temporal lobes before the clinical symptoms become apparent.120 The disease is due to NOTCH3 gene mutation on
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