An Electrophysiological Study on the Prevalence of Peripheral Neuropathy in Prediabetics.

Introduction Prediabetes is increasingly recognized as a metabolically active state associated with early microvascular complications. Peripheral neuropathy may develop before the onset of overt diabetes, yet its prevalence and electrophysiological characteristics in prediabetes remain insufficiently defined. To estimate the prevalence of clinical and subclinical peripheral neuropathy in individuals with prediabetes using the Modified Toronto Clinical Neuropathy Score (mTCNS) and nerve conduction studies, and to evaluate associated electrophysiological patterns and metabolic correlations. Methods This cross-sectional study included 60 individuals with prediabetes diagnosed according to standard glycemic criteria. Participants underwent detailed neurological examination, sensory testing, autonomic assessment, and nerve conduction studies of major motor and sensory nerves. Neuropathy severity was graded using mTCNS. Ocular evaluation was also performed. Statistical analysis assessed associations between neuropathy and metabolic parameters. Results The mean age was 46.08 years, and 53.3% were male. Clinical and/or subclinical peripheral neuropathy was identified in 28.4% of participants, with 5% showing severe neuropathy. Nerve conduction studies demonstrated reduced amplitudes, prolonged latencies, and reduced conduction velocities in both motor and sensory nerves. F-wave latencies were significantly prolonged in most nerves. Neuropathy showed significant associations with fasting blood glucose and HbA1c levels, but not with oral glucose tolerance test (OGTT) values, age, or sex. Ocular abnormalities, including cataract, mild diabetic retinopathy, and dry eye disease, were observed in a subset of participants. Conclusion Peripheral neuropathy is detectable in a substantial proportion of individuals with prediabetes, even before the onset of overt diabetes. Both clinical and subclinical neuropathy were observed, with significant associations with fasting blood glucose and HbA1c. These findings indicate early neural involvement in dysglycemia; however, causal relationships cannot be inferred due to the cross-sectional design. Larger prospective studies are required to determine the clinical value of early screening and to evaluate whether early intervention can modify long-term neurological outcomes.