| Neuralgic amyotrophy (NA), also referred to as Parsonage-Turner Syndrome (PTS), is a rare disorder consisting of a complex constellation of symptoms with abrupt onset of shoulder pain, usually followed by progressive neurologic deficits of motor weakness and dysesthesias. PTS occurs with an overall reported incidence of1.64cases per100.000people. Although the precise cause of NA has not been clearly established, viral and autoimmune processes have been proposed. In general, the results of basic laboratory investigations are usually normal. The clinical presentation may mirror other pathologies making accurate diagnosis difficult. The diagnosis of the syndrome is based on medical history, physical examination findings, EMG tests, and imaging studies. And electromyography is often crucial in confirmation of the diagnosis.Objective:The study was to analyze the characteristics of Electromyologram in NA and to provide the electrophysiological evidence for diagnosis and differential diagnosis.Method:We studied19cases with NA and25cases of age-matched healthy subjects. Electromyologram was measured with the KEYPOINT myoelectric/evoked potential instrument.1. Electroneurography and F-wave:The recording electrode was placed over the muscle belly and the reference electrode was placed distslly over the muscle tendon. The stimulating electrode was placed over the nerve with the cathode close to the recording electrode and the nerve was stimulated orthodromically. The current was increased until the CMAP no longer increased, then stimulation was increased by further20%-30%. CMAP was recorded with surface disc electrode and its latency and amplitude were analysed. The F-wave latency was obtained by stimulating the distal portion of the median and ulnar nerves using motor nerve conduction setups. SNAP was recorded by stimulation of the distal sensory fibers in the orthodromic sensory conduction test with the recording electrode placed close to the stimulator and its amplitude and SCV were analyzed.2. Needle electromyography:EMG was performed by insertion of a concentric needle in muscle belly. Recordings were made from each muscle at rest, during slight and maximal voluntary contraction. Spontaneous activity and motor unit potentials were analysed. Result:1. Compared patients and the control group, when stimulated at Erb’s point, the amplitude of CMAPs in axillary nerve and musculocutaneous nerve were significantly decreased (P<0.05); their latency were significantly prolonged (P<0.05). whill there was no significant differences in the amplitude and latency of CMAPs in radial, median, ulnar nerves.2. Compared patients and the control group, when stimulated at wrist, the amplitude and latency of CMAPs were no statistically significant (P>0.05), and there was also no significant difference in the latency of F-wave (P>0.05).3. Compared patients and the control group, when stimulated at wrist, the amplitude of SNAPs in median nerve was statistically significant (P<0.05), but there was no statistically significant in ulnar nerve (P>0.05). There was also no significant difference in SCV of both nerves (P>0.05).4. Compared patients caused by upper trunk and the control group, when stimulated at Erb’s point, there were significant differences in the amplitude and latency of CMAPs in radial, median, ulnar nerves.5. The occurance of spontaneous potential and simple phase in recruited activity were higher (P<0.05); The duration and amplitude of MUPs were changed (P<0.05).6. The abnormal rates of electrophysiological studies in different nerves and muscles were significantly different (P<0.05).7. Abnormal rates of the four electrophysiological comparison (MCV, SCV, F-wave, EMG) were statistically significant (P<0.05).Conclusion:1. In patients, the amplitudes of CMAPs in axillary nerve and musculocutaneous nerve were abnormally low, with slightly prolonged distal latencies. And EMG in deltoid and abductor pollicis brevis showed neurologic damage. These results suggested PTS often involved proximal nerves and the pathological change of affected nerves might be axonal degeneration.2. In patients, the amplitudes of SNAPs evoked from median nerves were abnormally low, with normal SCV in patients. These results suggested the pathological change of affected sensory nerves might also be axonal degeneration and the lesion was distal to spinal ganglia3. Normal latencies of F-wave were observed in patients. The results suggested the determination of F-wave latency might not be important for the diagnosis of PTS.4. The abnormal rates of electrophysiological studies in different nerves and muscles were different, with higher abnormal rates in axillary nerve, musculocutaneous nerve and detoid muscle. These results suggested that we should focus on the examination of proximal nerves and muscles for suspected PTS patients.5. The abnormal rates of MCV, SCV, F-wave and EMG in patients were different. |