Evidence that impaired motor conduction in the bilateral ulnar and tibial nerves underlies cervical spondylotic amyotrophy in patients with unilateral deltoid muscle atrophy

Abstract

Abstract:Introduction: The clinical entity of cervical spondylotic amyotrophy (CSA) is characterized by severe muscle atrophy in the upper extremities with insignificant sensory deficits in patients with cervical spondylosis. However, the pathogenesis of CSA is still unclear.Methods: We assessed electrophysiological motor conduction through the corticospinal tract and ulnar and tibial nerves, which do not supply the deltoid or biceps muscles, of 18 patients with CSA, 12 patients with compressive cervical myelopathy, and 18 control subjects with cervical spondylotic radiculopathy. Motor evoked potentials following transcranial magnetic stimulation and M-waves and F-waves following electrical stimulation were measured from the bilateral abductor digiti minimi muscles (ADMs) and abductor hallucis muscles (AHs). The peripheral conduction time (PCT) was calculated from the latencies of the CMAPs and F-waves as follows: (latency of CMAPs + latency of F-waves -1) / 2. The central motor conduction time (CMCT) was calculated by subtracting the PCT from the onset latency of the MEPs.Results: The M-wave (M) latency and minimum F-wave (Fmin) latency from the ADM, and Fmin-M latency from the ADM/AH were significantly longer in the CSA group than in the other groups, on both the affected (p = 0.000-0.007) and unaffected sides (p = 0.000-0.033). F-wave persistence from the bilateral ADMs was significantly lower in the CSA group than in the other groups (p = 0.000-0.002). Among the CSA patients, there were no significant differences in these parameters between the affected and unaffected sides. The CMCT showed no significant differences between the CSA and control groups, but significant differences between the CSA and CCM groups (p = 0.000-0.004).Conclusions: CSA patients with unilateral deltoid muscle atrophy had subclinical impairments of lower motor neurons and/or peripheral axons in the ulnar nerve, and subclinical impairments of peripheral axons in the tibial nerve. These motor impairments may have originally existed in these individuals before the onset of CSA.

[Retracted] Clinical Application of Evoked Potentials in the Operation of Cervical Spondylotic Myelopathy with Different Imaging

“…With the deepening of clinical and imaging technology cooperation and the study of many cases, many scholars have found that high signal does not necessarily indicate a poor prognosis. [17,[35][36][37][38][39] It is proposed that patients with high signal after surgery are better than those with low signal or no signal, and some scholars have found that whether there is high signal before surgery is not directly related to the degree of spinal cord compression or the efficacy of surgery. Some cases of hyperintensity can have reversible changes and have a good prognosis [40][41][42].…”

Differentiating Neurodegenerative Disease from Compressive Cervical Myelopathy Using Motor Evoked Potentials

“…MEP measurements were performed in a manner similar to previous reports 8–10 . MEP measurements were performed when the participants were awake.…”

“…MEP measurements were performed in a manner similar to previous reports. [8][9][10] MEP measurements were performed when the participants were awake. Surface recording electrodes were placed on the bilateral abductor digiti minimi (ADM) and abductor hallucis (AH) muscles.…”

“…7 In our group, motor evoked potential (MEP) measurements with transcranial magnetic stimulation (TMS) and electrical stimulation of peripheral nerves have been used to assess spinal cord dysfunction in CCM. [8][9][10][11] In addition, MEP measurements have been performed under the same conditions in patients with suspected neurodegenerative diseases. Although there have been reports of evaluation of ALS and MS using MEP, no previous study has compared CCM with neurodegenerative diseases.…”