Abstract
Pathogenetic mechanisms and cellular pathology of common metabolic encephalopathies are discussed. Clinical considerations and anatomic bases are summarized as foundational points. Hypertensive, hypoxic/ischemic, uremic, hepatic, septic, hypoglycemic, diabetic, thiamin deficiency, osmotic demyelinative and traumatic forms of metabolic encephalopathies are considered, with relevant clinical, imaging correlates, biochemical bases and histopathological manifestations.