Clinical-Neurological Features and Cognitive Deficit in Chronic Alcoholic Encephalopathies

Abstract

The article presents a comprehensive clinical, neurological, and neuropsychological analysis of chronic alcoholic encephalopathy (CAE) as a systemic toxic-metabolic lesion of the central nervous system, characterized by a stage-dependent progressive course that is not a direct equivalent of the stages of alcohol dependence. Based on the examination of 66 patients with CAE of varying severity, the disease is shown to involve a combination of diffuse neurological symptoms (cerebellar, vestibular, pyramidal, sensorimotor, and autonomic disorders, among others) and a systemic cognitive deficit. It has been established that cognitive impairment is one of the early and pathogenetically significant manifestations of CAE and demonstrates a fronto-subcortical regulatory pattern. In the compensated stage, impairments of voluntary attention, neurodynamics, and executive control are already present, with relative preservation of global cognitive status (MMSE). As CAE progresses, cognitive deficits become persistent and multicomponent, involving executive functions, cognitive flexibility, behavioral regulation, and memory, reaching a dementia level in the decompensated stage. The results of specialized neuropsychological methods (FAB, Schulte-Gorbov tables, Pieron-Ruzer test, Clock Drawing Test, 10-word memory test, and “Exclusion of the Superfluous” test) demonstrated high sensitivity to early regulatory disturbances. They allowed for objective assessment of the staged progression of fronto-subcortical dysfunction. It was shown that impairments in memory and constructive activity in CAE are secondary and regulatory, resulting from deficits in programming and control rather than primary amnestic or apraxic disorders. The obtained data support the concept of CAE as a progressive disorder of integrative brain regulatory mechanisms and justify the use of a comprehensive neuropsychological approach for early diagnosis, staging, and prognosis of alcohol-related CNS damage.