Wernicke Korsakoff Psycosis

Ans:C-Normal pupillary response

Symptoms of Wernicke encephalopathy include:

• Confusion and loss of mental activity that can progress to coma and death
• Loss of muscle coordination (ataxia) that can cause leg tremor
• Vision changes such as abnormal eye movements (back and forth movements called nystagmus), double vision, eyelid drooping
• Alcohol withdrawal

Symptoms of Korsakoff syndrome:

• Inability to form new memories
• Loss of memory, can be severe
• Making up stories (confabulation)
• Seeing or hearing things that are not really there (hallucinations)

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 hypertrophy & degenerationQ. It disrupts a critical circuit between hippocampus & frontal lobes. The changes are also seen in periventricular (around 3^rd 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, & inertia.

– 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 short 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 distort 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).

Answer is D (Hippocampus):

Hippocamous is not involved in Wernicke’s Korsakoff syndrome.

Wernicke–Korsakoff syndrome (WKS)

• It is the combined presence of Wernicke’s encephalopathy (WE) and Korsakoff’s syndrome.
• The cause of the disorder is thiamine (vitamin B1) deficiency, which can cause a range of disorders including beriberi, Wernicke’s encephalopathy, and Korsakoff’s psychosis.
• WKS is usually secondary to alcohol abuse.
• WE is characterized by the presence of a triad of symptoms;
  • Ocular disturbances (ophthalmoplegia)
  • Changes in mental state (confusion)
  • Unsteady stance and gait (ataxia)
• KS is described as an acute onset of severe memory impairment without any dysfunction in intellectual abilities.The DSM IV lists the following criteria for the diagnosis of Korsakoff’s Syndrome:
  • anterograde amnesia
  • Variable presentation of retrograde amnesia
  • One of:
    • Aphasia
    • Apraxia
    • Agnosia
    • A deficit in executive functions.
• Wernicke–Korsakoff syndrome in alcoholics particularly is associated with atrophy/infarction of specific regions of the brain, especially the mamillary bodies.
• Other regions include the anterior region of the thalamus (accounting for amnesic symptoms), the medial dorsal thalamus, the basal forebrain, the median and dorsal raphe nuclei, periventricular gray matter, inferior and superior colliculi and the cerebellum.

Answer is B (Thalamus):

The Amnestic effect in Wernicke’s Korsakoff Syndrome is related to lesions in the dorso-medial nuclei of the thalamus.

`Lesions in the dorsomedial nucleus of the thalamus seem to be the best correlate of the memory disturbance and confabulation’ – Robbins

Ans. Thiamine

Ans. Hippocampus