Types Of Lesions A Vascular Lesions

Disturbances of cerebral blood flow are one of the most frequently encountered causes of neurological

Occipital

Basal ganglia

Table IV

Etiology, Morphology, and Consequences of Vascular Malformations

Etiology

Morphology

Consequences

Brain stem aneurysms (1-2% of the population)

Arteriovenous angioma

Cavernous angioma

Abnormal, focal or segmental extension of the brain stem arteries in cases of congenital weakness of the blood vessel walls at section with a high hemodyamic load, resulting in sack- or berry-shaped distensions of the walls, especially in ACA, and exit of ACP from ACI and ACM

Birth defects with the formation of dysplastic arterial and venous vessels as a result of a lack of differential development of the blood vessel plexus in the embryo into a capillary network with persisting arteriovenous short-cuts. This results in convolutions of the blood vessels of various sizes in the cerebral hemispheres. Regressive changes may be found in the blood vessel walls with fibers, calcification, and signs of thrombosis.

Vessels show sinusoidal convoluted distensions of variable size and a lack of the typical layering of the structure of the walls. Frequently clinically apparent are small sources of bleeding surrounded by gliosis.

Rupture, frequently seen as a potentially letal event resulting in SAB, ICB, vasospasms, and residual bleeding

Widespread intracerebral bleeding, bleeding in the ventricles, and infarct as a consequence of steal effect accompanying high shunt volumes

Residual small sources of bleeding but frequently free of obvious clinical symptoms illness. The sudden appearance of paralysis to one side of the body is clinically described as a stroke. This term does not immediately imply that the pathology underlying the symptomatology is pathogenetic due to an ischemic lesion or is directly associated with an intracerebral bleeding. Vascular lesions may occur as a result of an occlusion or stenosis in the branches or network of the arteries leading from the origin of the aorta from the left ventricle to the affected region. They can also reflect a chronic or subacute arterial hypertension (e.g., arteriosclerosis, status lacunaris, and hypertonic encephalopathy) or derive from defects in the development of the blood vessels (basal aneur-ysms, arteriovenous angioma, and cavernous angio-ma; Table IV).

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