Wernicke-Korsakoff Psychosis

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WERNICKE-

KORSAKOFF PSYCHOSIS
INTRODUCTION
• Wernicke- Korsakoff psychosis is an alcohol- induced persisting
amnestic disorder.
• Wernicke’s encephalopathy is presented as a set of acute symptoms
and Korsakoff’s syndrome is a chronic condition.
• If Wernicke’s encephalopathy is not treated it will progress to
Korsakoff’s syndrome.
• This is a spectrum of neurologic disease caused by thiamine
deficiency.
ETIOLOGY
• Vitamin B1( thiamine) deficiency –primary cause
• Alcoholism (secondary cause)
• Malnutrition (secondary cause)
PATHOPHYSIOLOGY
• Decrease in vitamin B1  atrophy of mammillary bodies. Associated with
paraventricular hemorrhage in the late stage.
• Thiamine: Absorbed in duodenum
Stored in liver and moves throughout body.

• THIAMINE------------------------------> THIAMINE PYROPHOSPHATE


Thiamine pyrophosphate synthetase
• Thiamine takes part in glucose metabolism and in brain metabolizes lipids and
carbohydrates and maintain normal amino acid and neurotransmitter levels.
• May also be involved in conduction of axon potential along axon and in synaptic
transmission
• Thiamine deficiency –
1. Impairs glucose metabolism ----> decrease cellular energy
2. Brain is vulnerable to impaired glucose ----> hemorrhage and
necrosis of mammillary bodies.
There is difficulty with movement and balance(cerebellum),
heart rate and breathing ( medulla) and brainstem or cranial nerve
issues.
• Ethanol abuse: major cause
1. Interfere with thiamine conversion by blocking action of thiamine
pyrophosphate synthetase.
2. Prevent absorption of thiamine by blocking gene expression for
thiamine transporter
3. Causes cirrhosis – thiamine storage is blocked in liver.
DIAGNOSIS AND CLINICAL FEATURES
• Disturbance in short term memory caused by prolonged heavy use of alcohol.
• Rare in less than 35 years of age.
• Usually occur in persons who have been drinking heavily for many years.
• Wernicke’s encephalopathy is less dangerous than Korsakoff’s syndrome.
Classic triad:
ophthalmoplegia, ataxia and confusion
• The cardinal features of Korsakoff’s syndrome are impaired mental syndrome
(especially recent memory) and anterograde amnesia in an alert and responsive
patient. The patient may or may not have the symptom of confabulation and
personality disorder.
DIFFERENTIAL DIAGNOSIS
• Anoxic encephalopathy
• Alzheimer disease
• Temporal lobe epilepsy
TREATMENT
• In the early stages, Wernicke’s encephalopathy responds rapidly to large
doses of parenteral thiamine.
• Dosage of thiamine : 100mg by mouth 2-3 times daily and is continued
for 1 to 2 weeks. In patients with alcohol-related disorders who are
receiving IV administration of glucose solution, it is good practice to
include 100 mg of thiamine in each liter of the glucose solution.
• Treatment of Korsakoff’s syndrome : thiamine given 100 mg by mouth 2-3
times daily; the treatment regimen should continue for 3 to 12 months.
• Few patients who progress to Korsakoff’s syndrome ever fully recover,
although many have some improvement in their cognitive abilities with
thiamine and nutritional support.
INVESTIGATION
• Labs- CBC, LFT, Thiamine/vitamin B1 levels
• Imaging: MRI- confirm degeneration of mammillary bodies
BLACKOUTS
• Similar to episodes of transient global amnesia discrete episodes of
anterograde amnesia that occur in association with alcohol intoxication.
• The periods of amnesia can be particularly distressing when persons fear
that they have unknowingly harmed someone or behaved imprudently
while intoxicated.
• During a blackout, persons have relatively intact remote memory but
experience a specific short-term memory deficit in which they are unable
to recall events that happened in the previous 5 or 10 minutes. Because
their other intellectual faculties are well preserved, they can perform
complicated tasks and appear normal to casual observers.
• Alcohol blocks the consolidation of new memories into old memories, a
process that is thought to involve the hippocampus and related temporal
lobe structures.
PROGNOSIS
• The Korsakoff state is potentially reversible by early intervention with
thiamine and prompt treatment of Wernicke encephalopathy.
• Unfortunately recovery is incomplete in more than 50% of cases and
individuals may be left with devastating chronic memory deficits.
THANK YOU

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