STUDY DESIGN: A retrospective comparative study. PURPOSE: To clarify the risk factors related to the development of postoperative C5 palsy through radiological studies after cervical double-door laminoplasty (DDL). OVERVIEW OF LITERATURE: Although postoperative C5 palsy is generally considered to be the result of damage to the nerve root or segmental spinal cord, the associated pathology remains controversial. METHODS: A consecutive case series of 47 patients with cervical spondylotic myelopathy treated by DDL at our institution between April 2008 and April 2015 were reviewed. Postoperative C5 palsy occurred in 5 of 47 cases after DDL. We investigated 9 radiologic factors that have been reported to be risk factors for C5 palsy in various studies, and statistically examined these between the two groups of palsy and the non-palsy patients. RESULTS: We found a significant difference between patients with and without postoperative C5 palsy with regards to the posterior shift of spinal cord at C4/5 (p=0.008). The logistic regression analyses revealed posterior shift of the spinal cord at C4/5 (odds ratio, 12.066; p=0.029; 95% confidence interval, 1.295–112.378). For the other radiologic factors, there were no statistically significant differences between the two groups. CONCLUSIONS: In the present study, we showed a significant difference in the posterior shift of the spinal cord at C4/5 between the palsy and the non-palsy groups, indicating that the "tethering phenomenon" was likely a greater risk factor for postoperative C5 palsy.
Humans ; Logistic Models ; Paralysis* ; Pathology ; Retrospective Studies ; Risk Factors* ; Spinal Cord ; Spinal Cord Diseases*

Arthritis, Gouty ; complications ; Epidural Space ; Humans ; Lipoma ; pathology ; Spinal Cord ; Spinal Cord Compression ; etiology

Nerve regeneration in adult mammalian spinal cord is poor because of the lack of intrinsic regeneration of neurons and extrinsic factors - the glial scar is triggered by injury and inhibits or promotes regeneration. Recent technological advances in spatial transcriptomics (ST) provide a unique opportunity to decipher most genes systematically throughout scar formation, which remains poorly understood. Here, we first constructed the tissue-wide gene expression patterns of mouse spinal cords over the course of scar formation using ST after spinal cord injury from 32 samples. Locally, we profiled gene expression gradients from the leading edge to the core of the scar areas to further understand the scar microenvironment, such as neurotransmitter disorders, activation of the pro-inflammatory response, neurotoxic saturated lipids, angiogenesis, obstructed axon extension, and extracellular structure re-organization. In addition, we described 21 cell transcriptional states during scar formation and delineated the origins, functional diversity, and possible trajectories of subpopulations of fibroblasts, glia, and immune cells. Specifically, we found some regulators in special cell types, such as Thbs1 and Col1a2 in macrophages, CD36 and Postn in fibroblasts, Plxnb2 and Nxpe3 in microglia, Clu in astrocytes, and CD74 in oligodendrocytes. Furthermore, salvianolic acid B, a blood-brain barrier permeation and CD36 inhibitor, was administered after surgery and found to remedy fibrosis. Subsequently, we described the extent of the scar boundary and profiled the bidirectional ligand-receptor interactions at the neighboring cluster boundary, contributing to maintain scar architecture during gliosis and fibrosis, and found that GPR37L1_PSAP, and GPR37_PSAP were the most significant gene-pairs among microglia, fibroblasts, and astrocytes. Last, we quantified the fraction of scar-resident cells and proposed four possible phases of scar formation: macrophage infiltration, proliferation and differentiation of scar-resident cells, scar emergence, and scar stationary. Together, these profiles delineated the spatial heterogeneity of the scar, confirmed the previous concepts about scar architecture, provided some new clues for scar formation, and served as a valuable resource for the treatment of central nervous system injury.
Mice ; Animals ; Gliosis/pathology* ; Cicatrix/pathology* ; Spinal Cord Injuries ; Astrocytes/metabolism* ; Spinal Cord/pathology* ; Fibrosis ; Mammals ; Receptors, G-Protein-Coupled

In recent years, the study of autophagy in spinal cord injury (SCI) gradually becomes the hot spot. However, the function of autophagy in the injured spinal cord is still controversial. In order to further understand the role of autophagy after SCI, we summarized the activation of autophagy, autophagic cell death, the relationship between autophagy and apoptosis, the function of autophagy in promoting the molecular metabolism and the role of autophagy after spinal cord injury. We concluded that the role of autophagy after SCI is a double-edged sword. Upregulating the level of autophagy appropriately can promote damaged proteins metabolism and inhibit apoptosis. However, excessive activation of antophagy may induce autophagic cell dealth. So we consider that the proper regulation of autophagy will be a new target in the treatment of SCI.
Animals ; Apoptosis ; Autophagy ; physiology ; Humans ; Spinal Cord Injuries ; etiology ; pathology

Two cases of thoracic intramedullary schwannoma confirmed by surgery and pathology are reported. These tumors were hypointense on T1WI, and hyperintense on T2WI with good enhancement on MRI. One case showed typical intramendullary tumor, associated with peritumoral cord swelling and syrinx, and another showed both intramedullary and extramedullary location. Schwannomas of the spinal cord, although very rare, Should be included in the differential diagnosis of intramedullary tumor.
Diagnosis, Differential ; Magnetic Resonance Imaging ; Neurilemmoma* ; Pathology ; Spinal Cord

Adult ; Hemangiopericytoma ; diagnosis ; Humans ; Male ; Spinal Cord ; pathology

BACKGROUNDThe incidence of spinal injury with spinal cord contusion is high in developed countries and is now growing in China. Furthermore, spinal cord injury happens mostly in young people who have a long life expectance. A large number of patients thus are wheelchair bound for the rest of their lives. Therefore, spinal cord injury has aroused great concern worldwide. Despite great efforts, recovery from spinal cord injury remains unsatisfactory. Based on the pathology of spinal cord contusion, an idea of early neurosurgical intervention has been formulated in this study.

METHODSA total of 30 patients with "complete" spinal cord injury or classified as American Spinal Injury Association (ASIA)-A were studied. Orthopedic treatment of the injured vertebra (e), internal fixation of the vertebral column, and bilateral laminectomy for epidural decompression were followed directly by neurosurgical management, including separation of the arachnoid adhesion to restore cerebrospinal fluid flow and debridement of the spinal cord necrotic tissue with concomitant intramedullary decompression. Rehabilitation started 17 days after the operation. The final outcome was evaluated after 3 months of rehabilitation. Pearson chi-square analysis was used for statistical analysis.

RESULTSAll the patients recovered some ability to walk. The least recovered patients were able to walk with a wheeled weight support and help in stabilizing the weight bearing knee joint (12 cases, 40%). Thirteen patients (43%) were able to walk with a pair of crutches, a stick or without any support. The timing of the operation after injury was important. An optimal operation time window was identified at 4 - 14 days after injury.

CONCLUSIONSEarly neurosurgical intervention of spinal cord contusion followed by rehabilitation can significantly improve the locomotion of the patients. It is a new idea of a therapeutic approach for spinal cord contusion and has been proven to be very successful.

Adolescent ; Adult ; Humans ; Male ; Middle Aged ; Spinal Cord ; pathology ; surgery ; Spinal Cord Injuries ; pathology ; surgery ; Treatment Outcome ; Young Adult

Child ; Child, Preschool ; Female ; Humans ; Magnetic Resonance Imaging ; Male ; Spinal Cord ; abnormalities ; pathology ; Spinal Cord Diseases ; diagnosis ; pathology ; surgery ; Syndrome

OBJECTIVETo investigate the protective effect of antler polypeptide on the rats with spinal cord injury (SCI).

METHODSThe model rats were treated with different doses of antler polypeptide, and its effect on motor function, ethology and pathological changes of spinal cord of the rats observed.

RESULTSSeven days after treatment with different doses of antler polypeptide, rat's motor activity was recovered in some extent. Significant difference (P < 0.001)was found between the antler polypeptide treatment group and operation group. The effect could be enhanced by increase of the doses. We observerd the effect on the pathological change of spinal cord in rat, and found the tissue edema and inflammatory infiltration were relieved after treatment with different doses of antler polypeptide, especially in the dose of 15 mg antler polypeptide.

CONCLUSIONAntler polypeptide can promote the motor function recovery in SCI rats, and its action is dose-dependent.

Animals ; Antlers ; chemistry ; Male ; Peptides ; therapeutic use ; Rats ; Rats, Wistar ; Spinal Cord ; pathology ; Spinal Cord Injuries ; drug therapy ; pathology

OBJECTIVETo observe the pathological changes of axonal injury in a rat model of experimental allergic encephalomyelitis (EAE).

METHODSWith HE, luxol fast blue and Bielschowsky staining, the expression of APP, MBP, SMI-32 and MBP in the brain and spinal cord of EAE rats using double-labeling indirect immunofluorescence.

RESULTSExtensive cuffing lesions of inflammatory cell infiltrations were found in the brain and spinal cord of the rats, accompanied by multiple lesions of demyelination, axonal disarrangement with vesicular loss. SMI-32 staining identified numerous nonphosphorylated neurofilament, indicating the presence of axonal injury. Axonal oval bodies formed by APP accumulation were found in the white matters of the spinal cord 14 days after EAE, suggesting that neuraxial damage occurred in the early stage of EAE which was not synchronous with myelin loss.

CONCLUSIONDifferent levels of inflammation occur in different stages of EAE, and inflammatory cell infiltration is the most obvious at the peak of EAE. Axonal injury occurs in the early stage of EAE and progresses over the entire disease course.

Animals ; Axons ; pathology ; Brain ; pathology ; Encephalomyelitis, Autoimmune, Experimental ; pathology ; Female ; Rats ; Rats, Wistar ; Spinal Cord ; pathology