Minutiae of pathophysiology of acute stroke

from corresponding chapter in Continuum late 2008
1. Occlusive infarcts are divided into "white" and "red", the latter of which corresponds to hemorragic transformation due to leaky blood cells into dying brain and are not equivalent to parenchymal hematoma due to vessel burstage. Hemorrhagic transformation occurs in up to 80 %.
2. Pathological stages (garcia, 1998) first 24 hours-- lesion barely visible. Swelling peaks days 3-5. Between days 5-10, the infarcted tissue become sharply demarcated from unaffected brain tissue. The fourth stage , lasting weeks to months, is liquefaction necrosis.

3. Mechanism for low flow stroke may be due to decreased cardiac output, systemic hypotension, increased metabolic demands of tissue (fever, acidosis), or steal of flow from affected to unaffected areas (Alexcandrov, Stroke, 2007). Caplan wonders whether low flow may potentiate emboli due to impaired clearance of emboli with low flow states.

4.