Objective. To study the neurophysiological mechanisms of motor deficit in patients with post-traumatic cervical myelopathy. Material and methods. A retrospective clinical and neurophysiological study was conducted for the period 2008—2018. The study included 190 patients with post-traumatic cervical myelopathy (39 women and 159 men, mean age 27 (21,0; 36,0) years, time after spinal cord injury 3 [1,0; 8,0] years). A spinal cord injury was the cause of cervical myelopathy in 92,5% of the patients. The International Standards for Neurological Classification of Spinal Cord Injury (ISNCSCI) was administered at admission and during rehabilitation. A motor nerve conduction study (NCS) was conducted as well. Compound muscle action potentials (CMAP) amplitude and nerve conduction velocity (NCV) in the distal segment of 160 left and 145 right median nerves, 161 left and 151 right tibial nerves, 90 left and 66 right ulnar nerves were recorded. Re-examination (n=95 patients) was performed 6 (3,0; 10,0) years after injury. The time between examinations was 2,9 (1,0; 4,0) years. The control groups for the median nerve and the tibial nerve consisted of age- and sex-matched 10 patients with traumatic paraplelegia and 12 healthy subjects, respectively. Results. In the main group, the SMAP amplitude for the median nerve was 4,1 [1,6; 6,1] mV, NCV 56 [51,0; 61,0] m/s; in the control group the SMAP was 11 [7,50; 16,40] mV (p=00), NCV 59 [58,0; 6,0] m/s (p=00), in the main group the SMAP amplitude for the tibial nerve was 4,3 [0,65; 7,95] mV, NCV 43 [39,0; 48,0] m/s, in the control group SMAP was 8,4 [6,4; 10,1] mV (p=00), NCV 50 [47,0 ; 51,0] m/s (p=00). About 20% of patients had severe denervation changes. In patients with clinically complete spinal cord injury, axonal neuropathy (a decrease in SMAP) was more pronounced in all nerves than in incomplete patients, and a decrease in NCV was observed in both tibial nerves. In patients with C7—Th1 level, the SMAP amplitude was reduced on the left (2,5 [0,55; 5,65] mV) and right (2,7 [0,80; 6,30] mV) sides compared to those with C4—C6, in which CMAP was 4,6 [2,30; 6,20] mV on the left (p=0.03) and 4,7 [2,80; 6,10] mV on the right sides (p=0.03). Conclusions. The main neurophysiological mechanisms of motor deficit in patients with post-traumatic cervical myelopathy are the combination of the primary neuronal damage at the level of spinal cord injury and the development of secondary axonal neuropathy more caudally at the first three years after spinal cord injury.