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A Randomized Controlled Trial of Early versus Late Surgical Decompression for Thoracic and Thoracolumbar Spinal Cord Injury in 73 Patients.

ABSTRACT: Convincing clinical evidence exists to support early surgical decompression in the setting of cervical spinal cord injury (SCI). However, clinical evidence on the effect of early surgery in patients with thoracic and thoracolumbar (from T1 to L1 [T1-L1]) SCI is lacking and a critical knowledge gap remains. This randomized controlled trial (RCT) sought to evaluate the safety and efficacy of early (<24 h) compared with late (24-72 h) decompressive surgery after T1-L1 SCI. From 2010 to 2018, patients (≥16 years of age) with acute T1-L1 SCI presenting to a single trauma center were randomized to receive either early (<24 h) or late (24-72 h) surgical decompression. The primary outcome was an ordinal change in American Spinal Injury Association (ASIA) Impairment Scale (AIS) grade at 12-month follow-up. Secondary outcomes included complications and change in ASIA motor score (AMS) at 12 months. Outcome assessors were blinded to treatment assignment. Of 73 individuals whose treatment followed the study protocol, 37 received early surgery and 36 underwent late surgery. The mean age was 29.74 ± 11.4 years. In the early group 45.9% of patients and in the late group 33.3% of patients had a ≥1-grade improvement in AIS (odds ratio [OR] 1.70, 95% confidence interval [CI]: 0.66-4.39, p = 0.271); significantly more patients in the early (24.3%) than late (5.6%) surgery group had a ≥2-grade improvement in AIS (OR 5.46, 95% CI: 1.09-27.38, p = 0.025). There was no statistically significant difference in the secondary outcome measures. Surgical decompression within 24 h of acute traumatic T1-L1 SCI is safe and is associated with improved neurological outcome, defined as at least a 2-grade improvement in AIS at 12 months.

SUBMITTER: Haghnegahdar A

PROVIDER: S-EPMC8240887 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:The role of decompressing the intradural space through a durotomy as a treatment option for acute traumatic cervical spinal cord injury has not been explored in an animal model, to our knowledge. We sought to determine the role of durotomy and duraplasty in the treatment of acute cervical spinal cord injury and its effects on inflammation, scar formation, and functional recovery.Seventy-two adult female Sprague-Dawley rats were assigned to three groups: contusion injury alone, contusion injury with a decompressive durotomy, and contusion injury with a decompressive durotomy followed by placement of a dural allograft. A mild (200-kdyn [2-N]) contusive injury was delivered to the exposed spinal cord at C5. The injured segment was reexposed four hours after injury, and a durotomy with decompression was performed. When a dural allograft was used it was affixed to the surrounding intact dura with use of a fibrin sealant. The Grip Strength Meter was used to assess forelimb function. Animals were killed at two and four weeks, and immunohistochemical analysis was performed to assess scar formation, inflammatory cell infiltration, and lesional volume.Immunohistochemical analysis revealed increased scar formation, cavitation, and inflammatory response in the animals treated only with a decompressive durotomy. Relative to the group with a contusion injury alone, the animals treated with a durotomy followed by a dural allograft had decreased cavitation and scar formation. Lesional volume measurements showed a significantly increased cavitation size at four weeks in both the contusion-only (mean and standard deviation, 12.6 +/- 0.5 mm(3)) and durotomy-only (15.1 +/- 1 mm(3)) groups relative to the animals that had received a dural allograft following durotomy (6.8 +/- 1.4 mm(3)).Functional recovery after acute cervical spinal cord injury was better in animals treated with decompression of the intradural space and placement of a dural allograft than it was in animals treated with decompression alone. These functional data correlated directly with histological evidence of a decrease in spinal cord cavitation, inflammation, and scar formation.

Project description:Purpose To evaluate whether noninvasive molecular imaging technologies targeting myeloperoxidase (MPO) can reveal early inflammation associated with spinal cord injury after thoracic aortic ischemia-reperfusion (TAR) in mice. Materials and Methods The study was approved by the institutional animal care and use committee. C57BL6 mice that were 8-10 weeks old underwent TAR (n = 55) or sham (n = 26) surgery. Magnetic resonance (MR) imaging (n = 6) or single photon emission computed tomography (SPECT)/computed tomography (CT) (n = 15) studies targeting MPO activity were performed after intravenous injection of MPO sensors (bis-5-hydroxytryptamide-tetraazacyclododecane [HT]-diethyneletriaminepentaacetic acid [DTPA]-gadolinium or indium 111-bis-5-HT-DTPA, respectively). Immunohistochemistry and flow cytometry were used to identify myeloid cells and neuronal loss. Proinflammatory cytokines, keratinocyte chemoattractant (KC), and interleukin 6 (IL-6) were measured with enzyme-linked immunosorbent assay. Statistical analyses were performed by using nonparametric tests and the Pearson correlation coefficient. P < .05 was considered to indicate a significant difference. Results Myeloid cells infiltrated into the injured cord at 6 and 24 hours after TAR. MR imaging confirmed the presence of ischemic lesions associated with mild MPO-mediated enhancement in the thoracolumbar spine at 24 hours compared with the sham procedure. SPECT/CT imaging of MPO activity showed marked MPO-sensor retention at 6 hours (P = .003) that continued to increase at 24 hours after TAR (P = .0001). The number of motor neurons decreased substantially at 24 hours after TAR (P < .01), which correlated inversely with in vivo inflammatory changes detected at molecular imaging (r = 0.64, P = .0099). MPO was primarily secreted by neutrophils, followed by lymphocyte antigen 6 complexhigh monocytes and/or macrophages. There were corresponding increased levels of proinflammatory cytokines KC (P = .0001) and IL-6 (P = .0001) that mirrored changes in MPO activity. Conclusion MPO is a suitable imaging biomarker for identifying and tracking inflammatory damage in the spinal cord after TAR in a mouse model. © RSNA, 2016 Online supplemental material is available for this article.

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A Randomized Controlled Trial of Early versus Late Surgical Decompression for Thoracic and Thoracolumbar Spinal Cord Injury in 73 Patients.

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