Abstract
Wernicke’s Encephalopathy is an acute neuro-psychiatric condition caused by an insufficient supply of thiamine (Vitamin B1)
to the brain. If undiagnosed or inadequately treated, it is likely to proceed to Korsakoff’s Syndrome. Wernicke’s Encephalopathy
can result from dietary deficiency alone and this form is usually successfully treated, with little chance of Korsakoff’s
Syndrome supervening. On the other hand, thiamine deficiency associated with alcohol misuse/dependence may require up to 1
gram of thiamine IV in the first 24 hours to be treated successfully. The reasons for this difference in treatment will be
discussed. Thiamine diphosphate acts as a co-factor for a number of thiamine-dependent enzymes. Thiamine deficiency leads
to a reduction in the activity of these enzymes, and this leads to alterations in mitochondrial activity, impairment of oxidative
metabolism, decreased energy status and eventually selective neuronal death. The damage caused by the combination of thiamine
deficiency and alcohol metabolism probably interferes with adequate thiamine transport at a number of sites in the body, including
the blood–brain barrier, as well as causing damage to the apoenzymes which then require higher concentrations of thiamine
to work normally. The accumulated damage is likely to render the use of oral thiamine therapeutically inadequate since the
body is unable to produce high enough concentrations of thiamine in the blood to traverse the blood–brain barrier. Some individuals
are probably genetically predisposed to develop Wernicke’s. Long before individuals with alcohol misuse or dependence develop
Wernicke’s Encephalopathy the neurons and other cells of the body are functioning sub-optimally because of the inadequate
supply of thiamine and the neurotoxic effect of alcohol. This relative deficiency initiates a series of pathological changes
which accumulate and further interfere with the supply of thiamine and its utilisation at a time when the requirements are
increased. The best treatment for Korsakoff’s Syndrome is timely recognition of Wernicke’s Encephalopathy and appropriate
intervention and prevention.
to the brain. If undiagnosed or inadequately treated, it is likely to proceed to Korsakoff’s Syndrome. Wernicke’s Encephalopathy
can result from dietary deficiency alone and this form is usually successfully treated, with little chance of Korsakoff’s
Syndrome supervening. On the other hand, thiamine deficiency associated with alcohol misuse/dependence may require up to 1
gram of thiamine IV in the first 24 hours to be treated successfully. The reasons for this difference in treatment will be
discussed. Thiamine diphosphate acts as a co-factor for a number of thiamine-dependent enzymes. Thiamine deficiency leads
to a reduction in the activity of these enzymes, and this leads to alterations in mitochondrial activity, impairment of oxidative
metabolism, decreased energy status and eventually selective neuronal death. The damage caused by the combination of thiamine
deficiency and alcohol metabolism probably interferes with adequate thiamine transport at a number of sites in the body, including
the blood–brain barrier, as well as causing damage to the apoenzymes which then require higher concentrations of thiamine
to work normally. The accumulated damage is likely to render the use of oral thiamine therapeutically inadequate since the
body is unable to produce high enough concentrations of thiamine in the blood to traverse the blood–brain barrier. Some individuals
are probably genetically predisposed to develop Wernicke’s. Long before individuals with alcohol misuse or dependence develop
Wernicke’s Encephalopathy the neurons and other cells of the body are functioning sub-optimally because of the inadequate
supply of thiamine and the neurotoxic effect of alcohol. This relative deficiency initiates a series of pathological changes
which accumulate and further interfere with the supply of thiamine and its utilisation at a time when the requirements are
increased. The best treatment for Korsakoff’s Syndrome is timely recognition of Wernicke’s Encephalopathy and appropriate
intervention and prevention.
- Content Type Journal Article
- Category Review
- Pages 1-12
- DOI 10.1007/s11065-012-9196-z
- Authors
- A. D. Thomson, Molecular Psychiatry Laboratory, Rockefeller Building, University College London, 21 University Street, London, UK
- Irene Guerrini, Bexley Substance Misuse Service, South London & Maudsley NHS Foundation Trust, London, UK
- E. Jane Marshall, Institute of Psychiatry, King’s College London, London, UK
- Journal Neuropsychology Review
- Online ISSN 1573-6660
- Print ISSN 1040-7308