1Assistant Professor, Department of Physiology, Gandhi Medical College
2Corresponding Author & Associate Professor, Department of Physiology, Gandhi Medical College
3Professor and Head, Department of Physiology, Chirayu Medical College
4JR III, Department of Physiology Gandhi Medical College, Bhopal
*Corresponding Author: Dr. Sanjeev Kumar Shrivastava, Associate Professor, Department of Physiology, Gandhi Medical College, Bhopal-462001, e-mail: sanjeevshrivastava8@gmail.com
Online published on 21 November, 2019.
Present study was aimed to assess abnormalities of ulnar nerve in stable COPD patients.
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.
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.
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 impairment.
Nerve conduction study, hypoxemia, demyelination, axonal loss
