The Wernicke‐Korsakoff syndrome: a reappraisal in Queensland with special reference to prevention

Price, John; Kerr, Ray; Hicks, Maureen; Nixon, P.G.F.

doi:10.5694/j.1326-5377.1987.tb133686.x

Cited by 23 publications

(4 citation statements)

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“…18 29 39 Interestingly, in our test population this occurred only in the proportion of alcoholics whose survival time was extended by institutional intervention, as previously suggested. 40 The inclusion of Wernicke's encephalopathy as a prerequisite in our criteria for the Wernicke-Korsakoff syndrome was useful in excluding patients with memory deficits from other causes and did not significantly decrease diagnostic sensitivity. However, the use of Wernicke's encephalopathy as an essential inclusion criterion for Wernicke-Korsakoff syndrome was a source of error for retrospective analysis in a small proportion of patients.…”

Section: Differentiation Of Diagnostic Groupsmentioning

confidence: 93%

Operational criteria for the classification of chronic alcoholics: identification of Wernicke's encephalopathy.

Caine

Halliday

Kril

et al. 1997

Journal of Neurology, Neurosurgery & Psychiatry

411

256

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Results-Despite rater variability with regard to specific symptoms, within and between rater reliability for diagnostic classification using the criteria retrospectively on patient records was 100% for three independent raters. Validity testing showed that Wernicke's encephalopathy was underrecognised only when occurring with hepatic encephalopathy (50% sensitivity).Conclusions-By contrast with current criteria, the proposed operational criteria show that the antemortem identification of Wernicke's encephalopathy can be achieved with a high degree of specificity.

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Section: Differentiation Of Diagnostic Groupsmentioning

confidence: 93%

Operational criteria for the classification of chronic alcoholics: identification of Wernicke's encephalopathy.

Caine

Halliday

Kril

et al. 1997

Journal of Neurology, Neurosurgery & Psychiatry

411

256

View full text Add to dashboard Cite

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“…Although lactate levels exceeding 6 mmol L Ϫ1 in the setting of alcoholic ketoacidosis, should, irrespective of the circulatory status, be appreciated as a sign of severe thiamine deficiency, clinicians should never await the results of any laboratory investigation before administration of an injection of thiamine to any confused, or even only vaguely unwell, alcoholic to prevent the onset or worsening of neurologic and circulatory complications [7,9,20].…”

Section: Discussionmentioning

confidence: 99%

Protection against cardiovascular collapse in an alcoholic patient with thiamine deficiency by concomitant alcoholic ketoacidosis

Bakker¹,

Maaten²,

Hoorntje³

et al. 1997

Journal of Internal Medicine

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Abstract. Bakker SJL, ter Maaten JC, Hoorntje SJ, Gans ROB (University Hospital Vrije Universiteit, Amsterdam, and Catharina Hospital, Eindhoven, The Netherlands). Protection against cardiovascular collapse in an alcoholic patient with thiamine deficiency by concomitant alcoholic ketoacidosis (Case report). J Intern Med 1997; 242: 179-83.Hyperlactataemia due to thiamine deficiency has so far only been reported in the setting of full-blown cardiovascular beriberi with congestive heart failure and systemic vasodilatation. Poor tissue oxygenation and impaired lactate clearance by the liver are generally accepted as underlying causes of the elevated lactate levels. We present an alcoholic patient with thiamine deficiency-induced hyperlactataemia and accompanying alcoholic ketoacidosis, who did not display the circulatory disturbances that are characteristic of cardiovascular beriberi. The hypothesis will be presented that the concomitant presence of alcoholic ketoacidosis has prevented haemodynamic deterioration. Putative mechanisms that could explain such an effect are discussed in detail, with special reference to the role of acetyl-CoA and adenosine.

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“…In the 1980s, the Adelaide psychiatrist Peter Yellowlees, and others, rekindled the fortification debate by pointing out that alcohol‐related brain damage was a major Australian public health problem requiring a national policy for thiamine fortification of flour, bread and alcoholic beverages 16 , 17 . Yellowlees was not aware of the previous studies in Bourke.…”

Section: Thiaminementioning

confidence: 99%

The repeating history of objections to the fortification of bread and alcohol: from iron filings to folic acid

Kamien

2006

Medical Journal of Australia

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The fortification of staple foods has eliminated many deficiency diseases. Despite this, “tampering” with people's food always provokes opposition, much of it from health professionals. Opposition is often based on self‐interest, tunnel vision and theory rather than research. A historical perspective of the patterns of objections to fortification and its outcomes may help resolve the anxieties and opposing ethical positions of advocates and opponents of fortification.

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The Wernicke‐Korsakoff syndrome: a reappraisal in Queensland with special reference to prevention

Cited by 23 publications

References 0 publications

Operational criteria for the classification of chronic alcoholics: identification of Wernicke's encephalopathy.

Operational criteria for the classification of chronic alcoholics: identification of Wernicke's encephalopathy.

Protection against cardiovascular collapse in an alcoholic patient with thiamine deficiency by concomitant alcoholic ketoacidosis

The repeating history of objections to the fortification of bread and alcohol: from iron filings to folic acid

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