Z Unlusoy Acar1, P Yalinay Dikmen2, V Yayla3, K Başaran4, U Emekli4, A E Öge5. 1. Department of Neurology, TDV 29 May Hospital, 34091 Istanbul, Turkey. 2. Department of Neurology, Acıbadem University School of Medicine, 34140 Istanbul, Turkey. Electronic address: pinarya@hotmail.com. 3. Department of Neurology, Dr. Sadi Konuk Bakırköy Education and Research Hospital, 34147 Istanbul, Turkey. 4. Department of Plastic and Reconstructive Surgery, Istanbul University, Istanbul Faculty of Medicine, 34390 Istanbul, Turkey. 5. Department of Neurology, Istanbul University, Istanbul Faculty of Medicine, 34390 Istanbul, Turkey.
Abstract
AIM OF THE STUDY: In two previous studies, we found that the compound muscle action potential (CMAP) amplitude loss was significantly higher than the loss of estimated motor unit numbers in the course of Wallerian degeneration (WD). In order to overcome some drawbacks of the method previously used, we performed a similar CMAP vs MUNE comparison by using the statistical motor unit number estimation (MUNE) method. PATIENTS AND METHODS: Initial electrophysiological studies on 6 patients were performed between 22 and 98 hours after the injuries; it was possible to make repeated examinations, four times in 1 nerve, twice in 1 nerve and three times in 4 nerves, before the eventual complete disappearance of the CMAPs. RESULTS: The transected/intact (T/I) side CMAP ratios declined steeply as WD evolved. They were significantly lower than the relatively stable MUNE ratios 48 hours after the injury. CONCLUSION: This study, performed with the use of statistical MUNE, strengthens our previous observation by the incremental method that might have some relevance to the pathophysiology of early WD. CMAP amplitude loss that is more than expected from the amount of axonal degeneration may indicate a considerable amount of inactive muscle fibers in the motor units innervated by the nerve fibers, which are undergoing degeneration but still retain their excitability. Although technical sources of error cannot be totally excluded, our findings could more likely be explained by the failing of neuromuscular synapses in an asynchronous order before complete unresponsiveness of the motor unit ensues.
AIM OF THE STUDY: In two previous studies, we found that the compound muscle action potential (CMAP) amplitude loss was significantly higher than the loss of estimated motor unit numbers in the course of Wallerian degeneration (WD). In order to overcome some drawbacks of the method previously used, we performed a similar CMAP vs MUNE comparison by using the statistical motor unit number estimation (MUNE) method. PATIENTS AND METHODS: Initial electrophysiological studies on 6 patients were performed between 22 and 98 hours after the injuries; it was possible to make repeated examinations, four times in 1 nerve, twice in 1 nerve and three times in 4 nerves, before the eventual complete disappearance of the CMAPs. RESULTS: The transected/intact (T/I) side CMAP ratios declined steeply as WD evolved. They were significantly lower than the relatively stable MUNE ratios 48 hours after the injury. CONCLUSION: This study, performed with the use of statistical MUNE, strengthens our previous observation by the incremental method that might have some relevance to the pathophysiology of early WD. CMAP amplitude loss that is more than expected from the amount of axonal degeneration may indicate a considerable amount of inactive muscle fibers in the motor units innervated by the nerve fibers, which are undergoing degeneration but still retain their excitability. Although technical sources of error cannot be totally excluded, our findings could more likely be explained by the failing of neuromuscular synapses in an asynchronous order before complete unresponsiveness of the motor unit ensues.