Abstract
Background & Objectives Present study was aimed to assess abnormalities of ulnar nerve in stable COPD patients. Method Study comprised of 60 healthy adults and 60 stable COPD patients (40–50 years) with no clinical neuropathy. Duration of illness and spirometric indices (FEV1%, FEV1/FVC, PEFR %) were assessed. Nerve conduction study of motor and sensory component of ulnar nerve was recorded bilaterally using RMS EMG MKII. Distal latency, nerve conduction velocity and compound motor action potential (CMAP) and sensory nerve action potential (SNAP) were analysed. Significant abnormality was defined as variations beyond mean ± 2SD from healthy adults. Results Observations revealed significantly prolonged distal latency and decreased conduction velocity (demyelination), decreased CMAP (axonal loss) bilaterally of both sensory and motor components of ulnar nerve in COPD patients compared with controls. Interpretation & conclusion Observation suggests that hypoxemia of COPD, by inducing direct action on nerve fibres or pontomedullary portion of brain or by enhancing effect of other neurotoxic substances causes nerve impairmen
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