Clinical and Biological Risk Factors for Neuropsychological Impairment in Alcohol Use Disorder

Abstract

The effects of alcoholism on cognitive and motor functioning are heterogeneous. While the role of some factors (patterns of alcohol consumption, eating habits or associated liver disease) has been hypothesized, the origins of this heterogeneity remain difficult to establish. The goals of the present study were thus to identify the clinical and biological risk factors for alcohol-related neuropsychological impairments and to determine the threshold beyond which these risk factors can be considered significant. Thirty alcoholic patients and 15 healthy controls had a blood test and underwent a neuropsychological examination. Alcohol severity measures, and liver, thiamine and malnutrition variables, were included in logistic regression models to determine the risk factors for cognitive and motor impairments (executive functions, visuospatial abilities, verbal episodic memory, ataxia), as well as those related to the severity of patients’ overall neuropsychological profile (moderate or severe impairments). Liver fibrosis was found to be a risk factor for executive impairments and also for ataxia, when it was associated with long-term alcohol misuse and symptoms of withdrawal. Altered thiamine metabolism was solely predictive of verbal episodic memory impairments. This combination of biological abnormalities was associated with a profile of moderate neuropsychological impairments. Malnutrition was associated with a profile of more severe impairments. Malnutrition, altered liver function and thiamine metabolism explain, at least partially, the heterogeneity of alcohol-related neuropsychological impairments. Our findings could allow clinicians to identify patients at particular risk of severe neuropsychological impairments before the onset of irreversible and debilitating neurological complications.

Addiction Biomarkers: Dimensional Approaches to Understanding Addiction

“…One way in which addiction-related biomarkers may be particularly useful is by diagnosing addiction without the traditional social outcomes (e.g., family discord, drug use in unsafe conditions, etc. ), as in DSM-5, and also independently of whether patients have experienced tolerance or withdrawal to an addictive agent; indeed, some individuals may experience alterations in other domains of neuroscience function regardless of physical tolerance and withdrawal [43]. This concept is consistent with the belief that many addicted individuals consider themselves addicted to a given agent regardless of whether they are currently active users [17].…”

The Regulatory Role of the Human Mediodorsal Thalamus

“…These causative studies in rodents have established that chronic and heavy alcohol intake is not mandatory to mimic the specific thalamic alterations observed in KS [131] , but alcohol may potentiate the effects of TD [132] . In AUD patients, altered thiamine metabolism was solely predictive of episodic memory impairments [133] and lower levels of circulating thiamine diphosphate selectively correlated with poorer episodic memory performance [134] . The thalamus is not homogeneously affected by TD.…”

“…By contrast, the MD is damaged in AUD patients, but not especially in KS patients, or in animal models of KS. Thus, the fronto-cerebellar circuit, including the MD, may not be especially vulnerable to TD, but rather to other comorbid alcohol-related brain dysfunction [133] . Alt-text: Box 4 …”

<p>Cognitive Impairments in Early-Detoxified Alcohol-Dependent Inpatients and Their Associations with Socio-Demographic, Clinical and Psychological Factors: An Exploratory Study</p>

“…10 More recent views have proposed different potential causes, such as recent alcohol consumption, length of the dependence, number of withdrawals or malnutrition. [11][12][13][14][15][16] This shows a substantial lack of general agreement on this topic.…”