A histopathological analysis of the human cervical spinal cord in patients with acute traumatic central cord syndrome

Study design: We have applied conventional histochemical and morphometric techniques to study the changes within the human spinal 'hand' motor neuron pool after spinal cord injury in patients who presented with acute traumatic central cord syndrome (ATCCS). Objective: To determine whether a reduction of large alpha motor neurons at the C7, C8 and T1 spinal cord levels underlies the mechanism which causes hand dysfunction seen in patients with (ATCCS). Background: The etiology of upper extremity weakness in ATCCS is debated and injury and/or degeneration of motor neurons within the central gray matter of the cervical enlargement has been advanced as one potential etiology of hand weakness. Methods: The spinal cords of five individuals with documented clinical evidence of ATCCS and three age-matched controls were obtained. The ATCCS spinal cords were divided into acute/sub-acute (two cases) and chronic (three cases) groups depending on the time to death after their injury; the chronic group was further subdivided according to the epicenter of injury. We counted the motor neurons using light microscopy in 10 randomly selected axial sections at the C7, C8 and T1 spinal cord levels for each group. We also analyzed the lateral and ventral corticospinal tracts (CST) in all groups for evidence of Wallerian degeneration and compared them to controls. Results: A primary injury to the lateral CST was present in each case of ATCCS with evidence of Wallerian degeneration distal to the epicenter of injury. There was minimal Wallerian degeneration within the ventral corticospinal tracts. In the chronic low cervical injury group, there was a decrease in motor neurons supplying hand musculature relative to the other injury groups where the motor neurons sampled at the time of death were not reduced in number when compared to the control group. Conclusions: We hypothesize that hand dysfunction in ATCCS can be observed after spinal cord injury without any apparent loss in the number of motor neurons supplying the hand musculature as seen in our acute/sub-acute (n = 2) and our chronic high injury (n = 1) groups. The motor neuron loss seen in the chronic low level injury was felt to be secondary to the loss of C7, C8, and T1 neurons adjacent to the injury epicenter.