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Early predictors of developing problematic spasticity following traumatic spinal cord injury: A prospective cohort study.

ABSTRACT: Objective: To identify early predictors and develop reliable, validated prediction models for development of problematic spasticity after traumatic spinal cord injury (SCI).Design: Prospective cohort study of the Rick Hansen Spinal Cord Injury Registry (RHSCIR), retrospective review of inpatient medical charts.Setting: Quaternary trauma center, rehabilitation center, community settings.Participants: Individuals with traumatic SCI between March 1, 2005, and March 31, 2014, prospectively enrolled in the Vancouver site RHSCIR.Interventions: None.Main Outcome Measure: Spasticity limiting function or requiring treatment (problematic spasticity) on the Spinal Cord Injury Health Questionnaire.Results: In 350 patients, variables documented during hospitalization that predicted the development of problematic spasticity up to 5 years post-injury included: initial Glasgow Coma Scale; age at time of injury; admission to rehabilitation center; community discharge anti-spasticity medication prescription, neurological status, Penn Spasm Frequency Scale, and pain interference with quality of life, sleep, activities; greater change in AIS motor scores between admission and discharge. The predictive models had area under the receiver operating characteristic curve of 0.80 (95% CI 0.75, 0.85) in the development set (N?=?244) and 0.84 (95% CI 0.74, 0.92) in the validation set (N?=?106) for spasticity limiting function and 0.81 (95% CI 0.76, 0.85) in the development set and 0.85 (95% CI 0.77, 0.92) in the validation set for spasticity requiring treatment.Conclusions: Our prediction models provide an early prognosis of risk of developing problematic spasticity after traumatic SCI, which can be used to improve clinical spasticity management and assist research (e.g. risk stratification in interventional trials).

SUBMITTER: Mills PB

PROVIDER: S-EPMC7241552 | biostudies-literature | 2020 May

REPOSITORIES: biostudies-literature

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Early predictors of developing problematic spasticity following traumatic spinal cord injury: A prospective cohort study.

Mills Patricia B PB Holtz Kaila A KA Szefer Elena E Noonan Vanessa K VK Kwon Brian K BK

The journal of spinal cord medicine 20181009 3

Objective: To identify early predictors and develop reliable, validated prediction models for development of problematic spasticity after traumatic spinal cord injury (SCI).Design: Prospective cohort study of the Rick Hansen Spinal Cord Injury Registry (RHSCIR), retrospective review of inpatient medical charts.Setting: Quaternary trauma center, rehabilitation center, community settings.Participants: Individuals with traumatic SCI between March 1, 2005, and March 31, 2 ...[more]

PMID: 30299227

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Project description:Background/objectivesWe recently developed techniques to monitor intraspinal pressure (ISP) and spinal cord perfusion pressure (SCPP) from the injury site to compute the optimum SCPP (SCPPopt) in patients with acute traumatic spinal cord injury (TSCI). We hypothesized that ISP and SCPPopt can be predicted using clinical factors instead of ISP monitoring.MethodsSixty-four TSCI patients, grades A-C (American spinal injuries association Impairment Scale, AIS), were analyzed. For 24 h after surgery, we monitored ISP and SCPP and computed SCPPopt (SCPP that optimizes pressure reactivity). We studied how well 28 factors correlate with mean ISP or SCPPopt including 7 patient-related, 3 injury-related, 6 management-related, and 12 preoperative MRI-related factors.ResultsAll patients underwent surgery to restore normal spinal alignment within 72 h of injury. Fifty-one percentage had U-shaped sPRx versus SCPP curves, thus allowing SCPPopt to be computed. Thirteen percentage, all AIS grade A or B, had no U-shaped sPRx versus SCPP curves. Thirty-six percentage (22/64) had U-shaped sPRx versus SCPP curves, but the SCPP did not reach the minimum of the curve, and thus, an exact SCPPopt could not be calculated. In total 5/28 factors were associated with lower ISP: older age, excess alcohol consumption, nonconus medullaris injury, expansion duroplasty, and less intraoperative bleeding. In a multivariate logistic regression model, these 5 factors predicted ISP as normal or high with 73% accuracy. Only 2/28 factors correlated with lower SCPPopt: higher mean ISP and conus medullaris injury. In an ordinal multivariate logistic regression model, these 2 factors predicted SCPPopt as low, medium-low, medium-high, or high with only 42% accuracy. No MRI factors correlated with ISP or SCPPopt.ConclusionsElevated ISP can be predicted by clinical factors. Modifiable factors that may lower ISP are: reducing surgical bleeding and performing expansion duroplasty. No factors accurately predict SCPPopt; thus, invasive monitoring remains the only way to estimate SCPPopt.

Project description:BACKGROUND:Spinal cord injury (SCI) triggers a robust neuroinflammatory response that governs secondary injury mechanisms with both degenerative and pro-regenerative effects. Identifying new immunomodulatory therapies to promote the supportive aspect of immune response is critically needed for the treatment of SCI. We previously demonstrated that SCI results in acute and permanent depletion of the neuronally derived Neuregulin-1 (Nrg-1) in the spinal cord. Increasing the dysregulated level of Nrg-1 through acute intrathecal Nrg-1 treatment enhanced endogenous cell replacement and promoted white matter preservation and functional recovery in rat SCI. Moreover, we identified a neuroprotective role for Nrg-1 in moderating the activity of resident astrocytes and microglia following injury. To date, the impact of Nrg-1 on immune response in SCI has not yet been investigated. In this study, we elucidated the effect of systemic Nrg-1 therapy on the recruitment and function of macrophages, T cells, and B cells, three major leukocyte populations involved in neuroinflammatory processes following SCI. METHODS:We utilized a clinically relevant model of moderately severe compressive SCI in female Sprague-Dawley rats. Nrg-1 (2 μg/day) or saline was delivered subcutaneously through osmotic mini-pumps starting 30 min after SCI. We conducted flow cytometry, quantitative real-time PCR, and immunohistochemistry at acute, subacute, and chronic stages of SCI to investigate the effects of Nrg-1 treatment on systemic and spinal cord immune response as well as cytokine, chemokine, and antibody production. RESULTS:We provide novel evidence that Nrg-1 promotes a pro-regenerative immune response after SCI. Bioavailability of Nrg-1 stimulated a regulatory phenotype in T and B cells and augmented the population of M2 macrophages in the spinal cord and blood during the acute and chronic stages of SCI. Importantly, Nrg-1 fostered a more balanced microenvironment in the injured spinal cord by attenuating antibody deposition and expression of pro-inflammatory cytokines and chemokines while upregulating pro-regenerative mediators. CONCLUSION:We provide the first evidence of a significant regulatory role for Nrg-1 in neuroinflammation after SCI. Importantly, the present study establishes the promise of systemic Nrg-1 treatment as a candidate immunotherapy for traumatic SCI and other CNS neuroinflammatory conditions.

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Early predictors of developing problematic spasticity following traumatic spinal cord injury: A prospective cohort study.

Publications

Early predictors of developing problematic spasticity following traumatic spinal cord injury: A prospective cohort study.

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