Mechanisms of Changes in the Segmental Neuromotor Apparatus in Patients with Posttraumatic Cervical Myelopathy
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Mechanisms of Changes in the Segmental Neuromotor Apparatus in Patients with Posttraumatic Cervical Myelopathy F. A. Bushkov and M. A. Bzhilyansky
Translated from Zhurnal Nevrologii i Psikhiatrii imeni S. S. Korsakova, Vol. 120, No. 4, Iss. 1, pp. 7–13, April, 2020. Original article submitted July 5, 2019. Accepted August 7, 2019. Objectives. To study the neurophysiological mechanisms of formation of motor deficit in patients with posttraumatic cervical myelopathy. Materials and methods. A retrospective clinical-neurophysiological study was performed from 2008 to 2018 involving 190 patients undergoing rehabilitation therapy at the Preodolenie Rehabilitation Center; the study included 39 women and 151 men, mean age 27 [21.0; 36.0] years, at 3 [1.0; 8.0] years after spinal cord trauma. On admission for rehabilitation therapy, all patients underwent investigations of neurological status with assessments on the International Standards for Neurological Classification of Spinal Cord Injury (ISNSCI) and nerve conduction studies. A total of 160 left and 145 right median nerves were investigated, along with 161 left and 151 right tibial nerves and 90 left and 66 right ulnar nerves. Total muscle potential (TMP) amplitudes were assessed, along with M responses and excitation conduction velocities (ECV) for the distal parts of motor fibers, repeat investigations were carried out (n = 95) at 6 [3.0; 10.0] years after trauma, the time between investigations being 2.9 [1.0; 4.0] years. The reference group for TMP and ECV of the median nerve consisted of 10 patients with traumatic paraplegia and the reference group for the tibial nerve consisted of 12 patients; there were no significant differences in age and sex composition. Results. In the study group, TMP amplitude in the median nerve was 4.1 [1.6; 6.1] mV and ECV was 56 [51.0; 61.0] m/sec, compared with TMP 11 [7.50; 16.40] mV (p = 0.00) and ECV 59 [58.0; 62.0] m/sec (p = 0.00) in the reference group; analysis of data for the tibial nerve in the study group gave TMP 4.3 [0.65; 7.95] mV and ECV 43 [39.0; 48.0] m/sec, with the reference group giving TMP 8.4 [6.4; 10.1] mV (p = 0.00) and ECV 50 [47.0; 51.0] m/sec (p = 0.00). Marked denervation changes were seen in 20% of patients. Signs of axonal neuropathy were more marked in all nerves in patients with complete spinal cord injury as compared with patients with partial injuries, while both tibial nerves showed decreased ECV. Studies of the median nerves in patients with lesions at C7–T1 showed significant reductions in TMP amplitude on the left (2.5 [0.55; 5.65] mV) and right (2.7 [0.80; 6.30] mV) as compared with patients with the clinical signs of lesions at C4–C6, in whom M responses on the left were 4.6 [2.30; 6.20] mV (p = 0.03) and on the right were 4.7 [2.80; 6.10] mV (p = 0.03). Conclusions. The main mechanism of peripheral nervous system damage in patients with posttraumatic cervical myelopathy was a combination of neuron damage at the level of the primary spinal cord lesions with secondary axonal neuropathy caudal to
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