Neurological, nutritional and alcohol consumption factors underlie cognitive and motor deficits in chronic alcoholism

Abstract

Variations in pattern and extent of cognitive and motor impairment occur in alcoholism (ALC). Causes of such heterogeneity are elusive and inconsistently accounted for by demographic or alcohol consumption differences. We examined neurological and nutritional factors as possible contributors to heterogeneity in impairment. Participants with ALC (n = 96) and a normal comparison group (n = 41) were examined on six cognitive and motor domains. Signs of historically determined subclinical Wernicke's encephalopathy were detected using the Caine et al. criteria, which were based on postmortem examination and chart review of antemortem data of alcoholic cases with postmortem evidence for Wernicke's encephalopathy. Herein, four Caine criteria provided quantification of dietary deficiency, cerebellar dysfunction, low general cognitive functioning and oculomotor abnormalities in 86 of the 96 ALC participants. Subgroups based on Caine criteria yielded a graded effect, where those meeting more criteria exhibited greater impairment than those meeting no to fewer criteria. These results could not be accounted for by history of drug dependence. Multiple regression indicated that compromised performance on ataxia, indicative of cerebellar dysfunction, predicted non-mnemonic and upper motor deficits, whereas low whole blood thiamine level, consistent with limbic circuit dysfunction, predicted mnemonic deficits. This double dissociation indicates biological markers that contribute to heterogeneity in expression of functional impairment in ALC. That non-mnemonic and mnemonic deficits are subserved by the dissociable neural systems of frontocerebellar and limbic circuitry, both commonly disrupted in ALC, suggests neural mechanisms that can differentially affect selective functions, thereby contributing to heterogeneity in pattern and extent of dysfunction in ALC.

Prevalence of Low Plasma Vitamin B1 in the Stroke Population Admitted to Acute Inpatient Rehabilitation

“…The current reference ranges may not be valid in a post-stroke patient cohort, and the authors agree with the proposal that current reference data for thiamine deficiency should be called into question as they may not accurately describe VitB1 inadequacy in a pathological state as they were based on normalized values in healthy populations [27]. Given the increasing literature describing the importance of VitB1 in brain function among not only patients suffering from alcoholism [28,29] but also the geriatric population suffering from cognitive deficits [30], critically ill patients [17,31,32], post-bariatric procedures [33], and those suffering from conditions such as Alzhemers [34], HIV/AIDS [35], malignancy [36], diabetes [37], and obesity [5,38], it is important to consider the potential role of low and low normal levels of VitB1 in the population recovering from acute stroke.…”

Cigarette smoking history is associated with poorer recovery in multiple neurocognitive domains following treatment for an alcohol use disorder

“…Despite recovery with sobriety, deficiencies in several neurocognitive domains may persist with extended abstinence, principally in executive functions, processing speed, learning and memory, visuospatial skills, and postural stability (Durazzo & Meyerhoff, 2007;Durazzo, Pennington, Schmidt, & Meyerhoff, 2014;Rourke & Grant, 2009;Schmidt, Pennington, Durazzo, & Meyerhoff, 2014;Stavro, Pelletier, & Potvin, 2012). Multiple biopsychosocial factors including age, sex, alcohol consumption history, number of detoxifications, nutritional status, and comorbid psychiatric, substance and biomedical disorders are associated with the magnitude of neurocognitive dysfunction apparent following detoxification, and the rate and extent of recovery during abstinence (Durazzo & Meyerhoff, 2007;Fama et al, 2019;Loeber et al, 2010;Oscar-Berman & Marinkovic, 2007;Rourke & Grant, 2009).…”

Neurocognitive Functioning in Alcohol Use Disorder: Cognitive Test Results Do not Tell the Whole Story

“…Cognitive deficits in severe alcoholism are usually attributed to brain damage in the frontal and limbic regions [4,5], particularly due to thiamine deficiency/malnutrition and the consequences of liver damage [6][7][8]. Yet, a direct neurotoxic effect of alcohol consumption for neurocognitive deficits in humans is not fully established, and there is an ongoing debate regarding whether mild to moderate alcohol consumption is harmful [9] or even neuroprotective [10,11].…”