Biodegradable polyurethane-decellular extracellular matrix based bioscaffolds promote nerve repair after spinal cord injury

Animal Models of Spinal Cord Repair

Translational Advances in the Management of Acute Spinal Cord Injury

Decision letter: Altered regulation of Ia afferent input during voluntary contraction in humans with spinal cord injury

Editor's evaluation: Altered regulation of Ia afferent input during voluntary contraction in humans with spinal cord injury

The purpose of this study was to determine sleep quality and presence of sleep disorders in participants with spinal cord injury (SCI). A web-based survey, available online from February 2011 to July 2013, using validated sleep questionnaires, advertised via the internet and locally through SCI consumer organizations in the United States, Australia, New Zealand, and Canada, was designed to evaluate sleep in adults with self-reported SCI. Demographic characteristics and medical history were obtained from participant self-report. In our study population, 70% of the 304 participants were male with a mean age of 45 ± 13 years. The mean duration of injury was 16 ± 12 years. Cervical injuries were reported by 49% and thoracic injuries noted in 40% of participants. Increased sleep apnea risk was noted in 31% of participants, with 66% reporting snoring. Insomnia symptoms were reported by 54% of the respondents. Almost 40% of participants ranked their sleep quality as "fairly bad" to "very bad" in the previous month, 29% reported "often" or "almost always" waking up because of pain, and 22% had difficulty falling asleep because of leg cramps. In the past year, 27% of the respondents reported daily uncomfortable leg sensations and 28% found these leg symptoms to be "moderately to extremely distressing." This study increases the awareness that insomnia, sleep apnea, and poor sleep quality are common in individuals with chronic SCI; often coexisting. There is a need for increased screening for sleep problems by healthcare providers taking care of individuals living with SCI.

Our aim was to use 2D convolutional neural networks for automatic segmentation of the spinal cord and traumatic contusion injury from axial T2-weighted MR imaging in a cohort of patients with acute spinal cord injury. Forty-seven patients who underwent 3T MR imaging within 24 hours of spinal cord injury were included. We developed an image-analysis pipeline integrating 2D convolutional neural networks for whole spinal cord and intramedullary spinal cord lesion segmentation. Linear mixed modeling was used to compare test segmentation results between our spinal cord injury convolutional neural network (Brain and Spinal Cord Injury Center segmentation) and current state-of-the-art methods. Volumes of segmented lesions were then used in a linear regression analysis to determine associations with motor scores. Compared with manual labeling, the average test set Dice coefficient for the Brain and Spinal Cord Injury Center segmentation model was 0.93 for spinal cord segmentation versus 0.80 for PropSeg and 0.90 for DeepSeg (both components of the Spinal Cord Toolbox). Linear mixed modeling showed a significant difference between Brain and Spinal Cord Injury Center segmentation compared with PropSeg (P < .001) and DeepSeg (P < .05). Brain and Spinal Cord Injury Center segmentation showed significantly better adaptability to damaged areas compared with PropSeg (P < .001) and DeepSeg (P < .02). The contusion injury volumes based on automated segmentation were significantly associated with motor scores at admission (P = .002) and discharge (P = .009). Brain and Spinal Cord Injury Center segmentation of the spinal cord compares favorably with available segmentation tools in a population with acute spinal cord injury. Volumes of injury derived from automated lesion segmentation with Brain and Spinal Cord Injury Center segmentation correlate with measures of motor impairment in the acute phase. Targeted convolutional neural network training in acute spinal cord injury enhances algorithm performance for this patient population and provides clinically relevant metrics of cord injury.

Spinal cord injury (SCI) is one of the serious central nervous system injuries and the incidence of SCI continues to increase. Previous studies have indicated that electroacupuncture (EA) is beneficial for promoting recovery after SCI. In the present study, we attempted to evaluate how EA can promote the neural repair in SCI model rats by observing changes in the Notch signaling pathway. Experimental rats were randomly divided into four groups. Each group had its own intervention period: 1 day, 7 days, 14 days, and 28 days, and five randomized subgroups: blank control (B) group, blank electroacupuncture (BE) group, sham operation (S) group, model control (M) group and EA group. Animals in the EA group and the BE group were treated with EA at Dazhui (GV14) and Mingmen (GV4) acupoints for 20 min. After the intervention period, the Basso-Beattie-Bresnahan (BBB) score was used to evaluate the neurological function. We found that BBB score increased in EA-treated groups. Hematoxylin and eosin staining was used to observe pathological changes in the injured spinal cord and the results showed that EA therapy could promote the repair of injured spinal cord tissue. Immunohistochemistry and Western blot methods were used to detect the expression of proteins Delta1, Presenilin1, Hes1, and Hes5 in the injured spinal cord. The results showed that the expression levels of Delta1, Presenilin1, Hes1, and Hes5 increased significantly after SCI and decreased after EA treatment. Our study suggested that the possible mechanism by which EA could benefit the recovery after SCI in rats may include inhibiting the Notch signaling pathway and regulating the downstream proteins expression. In addition, our study can provide reference for selecting acupoints and treatment cycle in the treatment of SCI.

Management of Mental Health Disorders, Substance Use Disorders, and Suicide in Adults with Spinal Cord Injury: Clinical Practice Guideline for Healthcare Providers.

Canadian Spine SocietyPresentation CPSS1: Spinal insufficiency fracture in the geriatric pediatric spinePresentation CPSS2: The clinical significance of tether breakages in anterior vertebral body growth modulation: a 2-year postoperative analysisPresentation CPSS3: Anterior vertebral body growth modulation for idiopathic scoliosis: early, mid-term and late complicationsPresentation CPSS4: Ovine model of congenital chest wall and spine deformity with alterations of respiratory mechanics: follow-up from

Neurogenic Lower Urinary Tract Dysfunction in the First Year After Spinal Cord Injury: A Descriptive Study of Urodynamic Findings.

Long-lasting and persistent pain is a frequent consequence of spinal cord and brain injury. Several studies point to a significantly high proportion of patients who experience pain following the trauma. This chapter gives a brief overview of the prevalence, types of persistent pain, animal models that study pain outcomes, and the pertinent mechanisms that underlie the development of neuropathic pain following traumatic spinal cord and brain injury.Traumatic brain injury (TBI) and spinal cord injury (SCI) impose a high personal, social, and economic burden of disability. Although not as common as low back pain, TBI and SCI combined might have an equivalent economic impact mainly because of the young age of patients, the severity of the associated disability, and the major limitations on daily activity (Ma et al., 2014). Research-based estimates of the prevalence of persistent pain are variable and high in patients with SCI and TBI. Most studies indicate that about two-thirds of patients with either SCI or TBI will experience pain after the injury (Nampiaparampil, 2008; Siddall et al., 2003; Stormer et al., 1997; Uomoto and Esselman, 1993). Pain is consistently rated as one of the most difficult problems associated with these types of injuries (Nepomuceno et al., 1979; Rintala et al., 1998; Stensman, 1994; Westgren and Levi, 1998), hinders the ability to participate in rehabilitation programs (Widerstrom-Noga et al., 1999), and is difficult to treat. Chronic pain delays the acquisition of an optimal level of activity (Nicholson Perry et al., 2009) and independence and adversely affects the patients’ mood (Kennedy et al., 1997; Stroud et al., 2006).This chapter reviews and summarizes both clinical and experimental studies that focus on chronic pain after TBI and SCI. The emphasis will be in particular on the prevalence of chronic pain in patients with TBI and SCI. We highlight the specific types of pain that occur after injury. A survey of the different experimental animal models of brain and spinal cord injury evaluating pain as an outcome will be discussed. Finally, we will address the mechanisms responsible for the development of chronic pain following SCI and TBI.

Polysialic Acid Glycomimetic Promotes Functional Recovery and Plasticity After Spinal Cord Injury in Mice

Spinal cord injury models: neurophysiology.

Previous studies have demonstrated changes in urinary bladder neurotrophic factors after bladder dysfunction. We have hypothesized that retrograde transport of neurotrophin(s) from the bladder to lumbosacral dorsal root ganglia (DRG) may play a role in bladder reflex reorganization after spinal cord injury (SCI). In this study, we determined whether the expression of tyrosine kinase receptors (TrkA, TrkB) is altered in lumbosacral DRG after SCI through immunofluorescence techniques. Complete transection of the spinal cord (T8-T10) was performed in female Wistar rats (120-150 g), and animals were studied 5-6 weeks after SCI. One week before killing, Fast Blue (FB) was injected into the bladder to label bladder afferent cells in the L1, L2, L6, and S1 DRG. After SCI, a significant increase in the number of TrkA-immunoreactive (IR) positive cells was detected in the L6-S1 DRG (L6: 1.9-fold, P < or = 0.01; S1: 1.7-fold, P < or = 0.05) and in the L1 DRG (3.0-fold; P < or = 0.01) but not in the L4-L5 DRG compared with spinal-intact (control) rats. After SCI, a significant increase in the number of TrkB-IR cells was also detected in the L6-S1 DRG (L6: 2.2-fold, P < or = 0.01; S1: 1.5-fold, P < or = 0.05) and in the L1-L2 DRG (L1: 1.5-fold, P < or = 0.01; L2: 1.3-fold, P < or = 0.05) but not in the L4-L5 DRG compared with control rats. After SCI, the percentage of FB-labeled cells expressing TrkA immunoreactivity (approximately 68%) or TrkB immunoreactivity (approximately 65%) in L1 and L6 DRG significantly (P < or = 0.01) increased compared with control (20-30%) DRG. After SCI, the percentage of TrkA-IR cells expressing phosphorylated (p)-Trk immunoreactivity significantly increased (1.5- to 2.3-fold increase) in the L1, L6, and S1 DRG. The percentage of TrkB-IR cells expressing p-Trk immunoreactivity after SCI also increased (1.3-fold increase) in the L1 and L6 DRG. These results demonstrate that (1) TrkA and TrkB immunoreactivity is increased in bladder afferent cells after SCI and (2) TrkA and TrkB receptors are phosphorylated in DRG after SCI. Neuroplasticity of lower urinary tract reflexes after SCI may be mediated by both nerve growth factor and brain-derived neurotrophic factor.

Systematic Review of Urological Followup After Spinal Cord Injury