Wernicke-Korsakoff Syndrome Clinical Trial
Official title:
Optimum Thiamine Intervention (OpT In) for Treatment and Prevention of Wernicke-Korsakoff Syndrome (WKS): A Randomised Controlled Trial
Wernicke-Korsakoff syndrome (WKS), once thought to be a rare condition, is now known to be common in people with nutritional deficiencies or alcohol dependence. The primary cause of WKS is thiamine deficiency, and more than 90% of cases are reported in alcohol dependent patients because alcohol dependence predisposes to severe nutritional deficiency. WKS may lead to significant, long-term brain dysfunction with severe effects on work, personal and social function. Whilst effective treatment may greatly reduce severe disability and the human and social costs of this illness, almost no evidence exists on optimal dosing regimens. This project proposes to develop quality evidence for effective treatment of WKS in an Aboriginal setting.
Wernicke-Korsakoff syndrome (WKS), once thought to be a rare condition, is now known to be
common in people with nutritional deficiencies or alcohol dependence. The primary cause of
WKS is thiamine deficiency, and more than 90% of cases are reported in alcohol dependent
patients because alcohol dependence predisposes to severe nutritional deficiency. WKS may
lead to significant, long-term brain dysfunction with severe effects on work, personal and
social function. Whilst effective treatment may greatly reduce severe disability and the
human and social costs of this illness, almost no evidence exists on optimal dosing regimens.
This project proposes to develop quality evidence for effective treatment of WKS in an
Aboriginal setting..
The need for evidence-based thiamine treatment protocols is of great clinical importance for
two related reasons. First, in relation to acute symptomatic WKS, a failure to treat
immediately or adequately may result in profound and often permanent cognitive and
neurological disability. Secondly, the need for evidence-based treatment guidelines is
greatly magnified when it is recognised that milder, subclinical WKS may be preventable with
adequate thiamine treatment.
The aims of this study are to determine the optimal thiamine dose required for:
A. Treatment of acute symptomatic WKS among Aboriginal and non-Aboriginal alcohol dependent
patients.
B. Reducing or preventing subclinical WKS-related brain damage in at-risk Aboriginal and
non-Aboriginal alcohol-dependent patients.
Primary Hypotheses
1. Among alcohol-dependent patients with acute symptomatic WKS, higher doses of parenteral
thiamine (1500mg) will lead to greater improvements in specific cognition and
neurological functions than lower doses (900mg or 300mg).
2. Among alcohol-dependent patients that are at high risk for subclinical WKS-related brain
damage, higher doses of parenteral thiamine (900mg) will lead to greater improvements in
specific cognition and neurological functions compared to lower doses (300mg or 100mg).
Secondary Hypotheses
1. Thiamine deficient patients will show poorer performance on cognitive and neurological
measures.
2. Patients with concurrent magnesium deficiency will show greater impairment at baseline.
3. Nutritional risk and alcohol frequency will correlate with thiamine pyrophosphate
levels.
4. Number of previous admissions with thiamine supplementation in the past 3 months will
correlate with thiamine pyrophosphate levels
;