A Clinical Perspective on Adult Cerebral Atrophy in Chronic Alcohol Use: Considering the Role of Neurotropic TORCH-Related Viruses (CMV, HSV-1, and Rubella)

Chronic alcohol use is a well-recognized cause of cerebral atrophy and ventricular enlargement in adults.Neurotropic viral infections, including cytomegalovirus (CMV), herpes simplex virus type 1 (HSV-1), and rubella virus-pathogens traditionally grouped within the TORCH framework-may also contribute to central nervous system injury, particularly in states of immune dysfunction.This descriptive observational study draws on routine clinical observations of eight adults aged 42-65 years with long-standing alcohol use who presented with neurological symptoms at a district-level hospital with referral access to tertiary care.Non-contrast computed tomography imaging demonstrated diffuse cerebral atrophy with proportional ventricular enlargement consistent with hydrocephalus ex vacuo rather than true hydrocephalus.Clinical history and available serological data suggested prior exposure to CMV, HSV-1, and/or rubella in several patients, without evidence of acute viral encephalitis.Integrating these observations with a narrative review of the literature, this article explores plausible mechanisms through which alcohol-related neurotoxicity, immune dysregulation, and latent or prior neurotropic viral exposure may interact to accelerating neuronal injury, with particular vulnerability of temporal lobe structures.These mechanisms are discussed as hypothesized associations rather than proven causal relationships.Recognition of these interactions is clinically relevant for practitioners evaluating alcohol-exposed adults with cerebral atrophy and ventricular enlargement, especially in resource-limited settings where advanced neuroimaging and molecular viral diagnostics are not readily available.