Abstract
Long-term occupational exposure to low-frequency whole-body vibration (WBV) is a recognised risk factor for musculoskeletal disorders. Given that mechanical forces are transmitted systemically, similar effects may plausibly extend to the central nervous system (CNS), although this remains insufficiently investigated. Emerging evidence suggests that WBV exposure may act as a source of repetitive subclinical brain microtrauma, described as minimal (mi-TBI). These low-intensity insults do not produce immediate clinical symptoms or detectable abnormalities on conventional neuroimaging (CT or MRI), but may accumulate and contribute to delayed neuronal dysfunction and long-term neurological consequences. Oxidative stress appears to be central to this process. Increased reactive oxygen species production, combined with impaired antioxidant defenses, may induce lipid peroxidation, mitochondrial dysfunction, neuroinflammation, and blood–brain barrier disruption. Similar mechanisms are established in vibration-exposed peripheral tissues, supporting the plausibility of analogous CNS effects. This review examines the hypothesis that chronic WBV exposure contributes to CNS oxidative imbalance and early neurodegenerative processes. Particular emphasis is placed on oxidative stress biomarkers—including malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT)—as potential tools for detecting subclinical brain alterations. Additionally, neurofunctional evaluation and emerging technologies such as virtual reality–based tools, are highlighted for detecting subtle cognitive changes. By integrating mechanistic, molecular, and occupational perspectives, we propose a conceptual framework in which WBV is considered a potential source of subclinical mild traumatic brain injury (m-TBI). However, this hypothesis remains supported primarily by indirect evidence and requires validation in human occupational studies.