Background/aim: Although ulnar neuropathy at the elbow (UNE) is the second most common entrapment mononeuropathy, there are few reports on its neurophysiological classification. In this study, we tried to find out the role of needle electromyography (EMG) in the neurophysiological classification of UNE. Materials and methods: UNE patients who met the clinical and neurophysiological diagnostic criteria and healthy individuals were included in this study. Reference values of nerve conduction studies were obtained from healthy individuals. Needle EMG was performed to all UNE patients. According to the neurophysiological classification proposed by Padua, UNE patients were classified as mild, moderate, and severe. Results: Thirty-one controls and thirty-five UNE patients were included in the study. There was mild UNE in 23 patients, moderate UNE in 8, and severe UNE in 4. Abnormal needle EMG findings were present in all patients with moderate and severe UNE and in 12 patients with mild UNE. Conclusion: Abnormal needle EMG findings are seen in most of the UNE patients. Therefore, it is not practical to use needle EMG findings in the neurophysiological classification. Needle EMG abnormalities may also be present in patients with mild UNE due to axonal degeneration or motor conduction block.

Objectives: Although compound muscle action potential (CMAP) and sensory nerve action potential (SNAP) amplitudes of the nerves are reduced in sciatic nerve injury due to intramuscular injection (SNIII), they may still be higher than the reference values if there is a mild axonal degeneration. In this case, comparing the outcomes of nerve conduction studies of intact and affected lower extremities becomes important. We aimed to determine the role of this comparison in the diagnosis of SNIII. Methods: Patients with SNIII were included. Reference values for lower extremity nerve conduction studies were obtained from healthy participants. Peroneal, posterior tibial, superficial peroneal, and sural nerve conduction studies were performed in both lower extremities. In the first analysis, the CMAP or SNAP amplitude of the nerve was considered abnormal if it was less than the reference value. In the second analysis, the CMAP or SNAP amplitude of the nerve was considered abnormal if it was less than the reference value or <50% of the CMAP or SNAP amplitude obtained from the intact limb nerve. Results: Thirty patients and 31 controls were included in the study. Compared with those found in the first analysis, the number of posterior tibial nerve CMAPs with reduced amplitudes, and the sural and superficial peroneal nerve SNAPs with reduced amplitudes were higher in the second analysis (P = 0.008, P < 0.001, and P = 0.031; respectively). Conclusion: This study showed that nerve conduction studies should be performed in both the intact and affected extremities in SNIII.

Introduction: To test the hypothesis of impaired cholinergic activity in amyotrophic lateral sclerosis (ALS), we studied short‐ and long‐latency afferent inhibition (SAI and LAI). Methods: The ulnar nerve was stimulated at the wrist preceding transcranial magnetic stimulation (TMS), 21 ms for SAI and 200 ms for LAI, in 21 patients and 17 control subjects. Short‐interval intracortical inhibition (SICI) and cognitive function was assessed in ALS patients using automatic threshold tracking and the Montreal Cognitive Assessment (MoCA). Results: The SAI paradigm resulted in inhibition in all control subjects, whereas inhibition was observed in 13 of 21 (62%) patients. Mean SAI and LAI values were significantly reduced in ALS. No significant correlation existed between afferent inhibition and other neurophysiological data. The MoCA was normal in all but 1 patient. Discussion: LAI and SAI are both impaired in ALS, probably unrelated to increased cortical excitability or cognitive dysfunction. Muscle Nerve 59:699–704, 2019

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