Non-alcoholic Wernicke's Encephalopathy Research Articles

Corpus Callosum Atrophy in Wernicke's Encephalopathy

Neuropathologic changes in Wernicke's encephalopathy (WE) involve variable brain structures. Corpus callosum involvement in WE, however, is largely unknown. The authors investigated the degree and the pattern of corpus callosum changes in WE according to the etiologies. Nineteen patients with WE (between 34 and 81 years) and 19 age- and sex-matched control participants were included. The total cross-sectional callosal area and 5 callosal subregions (C1-C5) were measured by tracing outer margins in the midsagittal sections. Subregions were determined by placing radial dividers with 10 rays. The pixel numbers for corpus callosums were calculated, and the values obtained were adjusted for head size variations. The causes of WE were alcoholism (10), intestinal surgery (5), anorexia (3), and hyperemesis gravidarum (1). The mean size of the total corpus callosum was significantly reduced in alcoholic WE (P< .001; 527.8 +/- 70.8 mm2 for alcoholic WE; 664.6 +/- 58.1 mm2 for the corresponding controls), but not in nonalcoholic WE. In subregion analysis, prefrontal callosum (C2) atrophy was the most prominent in alcoholic WE. In contrast, only splenium (C5) was atrophied in nonalcoholic WE. The degree of atrophy did not change throughout the follow-up period (mean 5.3 weeks). This study suggests that the extent and location of corpus callosum atrophy differs between alcoholic WE and nonalcoholic WE, implying separate contribution of alcohol neurotoxicity and nutritional deficiency.

Corpus Callosum Atrophy in Wernicke's Encephalopathy

ABSTRACTBackground and Purpose. Neuropathologic changes in Wernicke's encephalopathy (WE) involve variable brain structures. Corpus callosum involvement in WE, however, is largely unknown. The authors investigated the degree and the pattern of corpus callosum changes in WE according to the etiologies. Methods. Nineteen patients with WE (between 34 and 81 years) and 19 age‐ and sex‐matched control participants were included. The total cross‐sectional callosal area and 5 callosal subregions (C1‐C5) were measured by tracing outer margins in the midsagittal sections. Subregions were determined by placing radial dividers with 10 rays. The pixel numbers for corpus callosums were calculated, and the values obtained were adjusted for head size variations. Results. The causes of WE were alcoholism (10), intestinal surgery (5), anorexia (3), and hyperemesis gravidarum (1). The mean size of the total corpus callosum was significantly reduced in alcoholic WE (P&lt; .001; 527.8 ± 70.8 mm 2for alcoholic WE; 664.6 ± 58.1 mm 2for the corresponding controls), but not in nonalcoholic WE. In subregion analysis, prefrontal callosum (C2) atrophy was the most prominent in alcoholic WE. In contrast, only splenium (C5) was atrophied in nonalcoholic WE. The degree of atrophy did not change throughout the follow‐up period (mean 5.3 weeks). Conclusion. This study suggests that the extent and location of corpus callosum atrophy differs between alcoholic WE and nonalcoholic WE, implying separate contribution of alcohol neurotoxicity and nutritional deficiency.

Non-alcoholic Wernicke's encephalopathy — unusual clinical findings

Wernicke's encephalopathy is a common complication of thiamine deficiency among alcoholics. However, there are few reports of this disorder in non-alcoholics. We present a case of Wernicke's encephalopathy in a non-alcoholic, 68-year-old patient with recurrent vomiting attributed to biliary colics. Establishing the diagnosis in this patient was complicated by our finding of positive 14-3-3 protein in the cerebrospinal fluid (CSF). This is typically elevated in prion disease, but it has not previously been reported to be elevated in this entity. Compatible clinical presentation in combination with typical magnetic resonance imaging (MRI) findings and exclusion of other possible causes finally established the diagnosis.

Thiamin Deficiency and Korsakoff's Syndrome: Failure to Find Memory Impairments Following Nonalcoholic Wernicke's Encephalopathy

Prolonged alcohol consumption is associated with a variety of neuropsychiatric conditions, including the dense amnesic disorder known as Korsakoff's syndrome. Korsakoff's syndrome is frequently diagnosed in alcoholics after an episode of acute thiamin deficiency. The accepted view within the medical literature is that the etiology of this disorder lies in thiamin deficiency or Wernicke's encephalopathy. However, examination of the published reports of pure thiamin deficiency unaccompanied by chronic and excessive consumption of alcohol shows that, in this group of patients, the rate of progression to Korsakoff's syndrome is low. This result suggests that the memory impairments associated with alcohol-related brain damage cannot be attributed to thiamin deficiency alone. The etiology of alcohol-related cognitive impairments such as Korsakoff's syndrome is still poorly understood but several lines of evidence suggest multiple causal factors interact to produce deficits in performance. Animal models that manipulate only a single putative etiological factor are unlikely to elucidate the multiple influences that lead to Korsakoff's syndrome. A study of the natural history of alcohol-related brain damage is needed that will allow an assessment of individual risk factors and their interactions.

Brain lesions in alcoholics.

Brain lesions in alcoholics are multifactorial in origin. Ethanol neurotoxicity, Wernicke's encephalopathy, hepatocerebral degeneration, head trauma, central pontine myelinolysis, Marchiafava-Bignami syndrome, pellagra, and premorbid pathological conditions, such as fetal alcohol syndrome, may all contribute to cognitive dysfunction in alcoholics. With the exception of ethanol neurotoxicity, all of these conditions are associated with specific neuropathological lesions. Wernicke's encephalopathy, the neurological syndrome of thiamine deficiency, is frequently overlooked during life and may cause global dementia as well as the more familiar Korsakoff's amnestic syndrome. Distinguishing ethanol neurotoxicity from nutritional deficiency can be facilitated by magnetic resonance imaging, which can visualize some of the specific macroscopic lesions of Wernicke's encephalopathy, central pontine myelinolysis, cerebellar degeneration, and Marchiafava-Bignami syndrome. Computerized morphometric studies of alcoholic brains have revealed ventricular enlargement, selective loss of subcortical white matter, and alterations in neuronal size, number, architecture, and synaptic complexity. These lesions tend to be more severe when there is coexisting nutritional deficiency or liver disease, suggesting that ethanol neurotoxicity may not be the sole cause. A search for similar lesions in nonalcoholic Wernicke's encephalopathy and nonalcoholic liver disease will help determine the specificity of these lesions.