BUS 17 Lecture Notes - Lecture 16: Citric Acid Cycle, White Matter, Orbitofrontal Cortex
Document Summary
E-reader: clinical and pathological features of alcohol-related brain damage (zahr): Aim: describe a potential continuum between arbd, we and ks with respect to changes in human behaviour and brain structure alcohol consumption can lead to hepatic encephalopathy, wernicke encephalopathy (we), 12. 5% in patients with alcoholism treatment with thiamine can result in rapid clinical development if untreated: 80% of patients with we develop ks. Most salient: global amnesia: deficits in memory for new material and in gait and balance, despite sparing of general intelligence, short term memory and visuoperceptual implicit learning. Deficits in executive functions: problem solving, working memory, cognitive flexibility, self regulation . Patients with uncomplicated alcoholism: deficits in explicit memory, visuospatial processes and motor control. But working memory was associated with damage in frontocerebellar circuitries: postmortem pathological features: in wks: include lesions in periventricular regions around the third and fourth ventricles and atrophy of the mamillary bodies.
