Not involved in Wernicke - Korsakoff syndrome:
C i.e. Periventricular grey matter Korsakoff's Psychosis (K P) It is the commonest cause of organic amnestic syndrome. It is also k/ a Wernicke - Korsakov syndrome, because it often follows an acute neurological syndrome called Wernicke's encephalopathy comprising delirium, ataxia, opthalmoplegia, nystagmus & peripheral neuropathy. It is a potentially reversible conditionQ caused by thiamine deficiency most commonly associated with chronic alcohol abuse malnutrition. But other causes of malnutrition eg. starvation, hyperemesis gravidarum, dialysis, cancer, AIDS, gastric plication or prolonged IV hyperalimentation, alone can also result in thiamine deficiency & KP. Neuropathological lesion caused by thiamine deficiency is usually widespread but most consistent changes are seen in bilateral dorsomedial (& anterior) nucleus of thalamus, mammillary bodies, and hippocampus, in form of small vessels hyperplasia; petechial hemorrhages, astrocytic hyperophy & degenerationQ. It disrupts a critical circuit between hippocampus & frontal lobes. The changes are also seen in periventricular (around 3rd ventricle), periaqueductal grey matter, cerebellum, and brain stem (midbrain, pons, medulla fornix) as symmetrical lesions. The cardinal feature is a profound deficit of episodic memory, confabulation and lack of insight into the amnesiaQ. It presents as : Change in personality (frontal lobe like) such that they display lack of initiative, interest or concern & diminished spontaneity. - Executive function deficits involving attention, planning, set shifting, & inferential reasoning. - Apathy, passivity & confabulationQ are often prominent. There is disorientation for time, emotional blunting, & ineia. - There is little impairment in implicit memory and their ability to perform (complete) complex motor procedures remain intactQ. Typically general intelligence, perceptual skills & language remain relatively normalQ. Memory disorder - Profound deficit of episodic type explicit (declarative) memory 1/t loss of autobiographic information (often extending back for many years). Severe anterograde amnesia (learning defect) for verbal & visual material with a lack of insight into the amnesia. Events are recalled immediately after they occur, but forgotten a few minutes later. Thus digit span, testing the sho term memory store, is normal. Storage is mildly impaired but retrieval & learning are severely impairedQ. When patients learn new material they will forget it at a normal rate, but learning the new material is extremely difficult, and in severe cases new learning is impossible. So these patients have difficult encoding & consolidating explicit memory. - Retrograde amnesia back to the onset of illness, is as severe as anterograde loss; but the overall retrograde memory impairment (i.e. before the onset of illness) is not as severe as that of anterograde memory. New learning & recent memory is grossly defective but retrograde (remote) memory is relatively (variably) preserved, and show a temporal gradient, with older memories better preserved. As a result these patients retain more distant memories dramatically more proficiently than they learn new material. - Although remote memory is surprisingly intact, patients are unable to organize them in a temporal context. So they disto the relationship between facts and fill the remote memory gaps by confabulationQ (a vivid & wholly fictitious account of recent activities which the patient believes to be true).
Mammilary body
Thalamus
Periventricular grey matter
Hippocampus