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

Abstract

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 ®ve 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. Spinal Cord (2000) 38, 532 ± 537

Predictors of intramedullary lesion expansion rate on MR images of patients with subaxial spinal cord injury

“…25 Numerous preclinical studies have indicated that immediately after SCI, the disruption of endothelial cells, axons, and the cytoskeleton, in association with molecular cascades and ionic imbalances, results in cytotoxic and vasogenic spinal cord edema, collectively labeled "secondary injury." [11][12][13][17][18][19]26,35,36,43,62,65,67,68 The results of combined MRI and necropsy investigations by Quencer et al, 59 Jimenez et al, 46 and Martin et al 53 of patients who died within a few days after acute traumatic central cord syndrome indicated that axonal swelling and disruption in association with minimal co- agulative necrosis of gray matter are visualized as a highintensity signal IML on T2-weighted MR images. These patients with partial SCI did not show hematomyelia in histological sections.…”

“…These patients have axonal swelling and disruption in conjunction with minimal coagulative necrosis of the spinal cord parenchyma. 1,2,24,26,46,53,59,75 As evident in experimental models of SCI, 20,57,64 IML expansion in humans has yet to be fully validated. 2 At the microscopic level, histopathological studies have shown that IML expansion occurs primarily within the first 24 hours after trauma.…”

Effectiveness of surgical treatment for traumatic central cord syndrome

“…Recent neuropathological studies further suggested that the clinical deficits observed in the early phase of CCS are largely due to the loss of large, monosynaptic, rapidly conducting, myelinated corticospinal fibers. 13 Schneider et al 23 suggested that CCS was associated with a fairly good prognosis, because as the spinal cord edema subsided, motor function would recover, following a definite pattern, and thus, surgical intervention was contraindicated. Furthermore, the condition of some of the patients treated with laminectomy deteriorated dramatically after surgery.…”

Diagnostic criteria of traumatic central cord syndrome. Part 2: A Questionnaire Survey among Spine Specialists

“…In the recent past, the historical report of Schneider et al 1 has been challenged. Not only have the original descriptions of pathogenesis and neuroanatomical basis of TCCS been criticized, [7][8][9][10][11] but optimal treatment of the condition has also been reappraised. 3,[12][13][14][15][16] This survey study challenges the ambiguity of the TCCS definition as introduced by Schneider et al Whereas several physicians assign a diagnosis of TCCS in SCI patients with only 1 motor score point lower in the upper extremities than in the lower extremities, other physicians consider patients with a minimum difference of 15 points as TCCS patients.…”