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