Thoracic Spine Degeneration Following Microlaminotomy for Spinal Cord Stimulator Placement and Subsequent Removal-a Case Report.
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SUBMITTER: Kueper J
PROVIDER: S-EPMC4916097 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Cervical spinal cord injury (SCI) leads to impaired trunk motor control, negatively impacting the performance of activities of daily living in the affected individuals. Improved trunk control with better sitting posture has been previously observed due to neuromuscular electrical stimulation and transcutaneous spinal stimulation, while improved postural stability has been observed with spinal cord epidural stimulation (scES). Hence, we studied how trunk-specific scES impacts sitting independence and posture. Fourteen individuals with chronic, severe cervical SCI with an implanted neurostimulator performed a 5-min tall-sit task without and with trunk-specific scES. Spine posture was assessed by placing markers on five spine levels and evaluating vertical spine inclination angles. Duration of trunk manual assistance was used to assess independence along with the number of independence changes and average independence score across those changes. With scES, the sacrum-L1 inclination and number of independence changes tended to decrease by 1.64 ± 3.16° (p = 0.07; Cohen's d = 0.53) and 9.86 ± 16.8 (p = 0.047; Cohen's d = 0.59), respectively. Additionally, for the participants who had poor sitting independence without scES, level of independence tended to increase by 12.91% [0%, 31.52%] (p = 0.38; Cohen's d = 0.96) when scES was present. Hence, trunk-specific scES promoted improvements in lower spine posture and lower levels of trunk assistance.
| S-EPMC10525621 | biostudies-literature
Project description:BACKGROUND Spinal cord injury (SCI) is a serious disease with high disability and mortality rates, with no effective therapeutic strategies available. In SCI, abnormal DNA methylation is considered to be associated with axonal regeneration and cell proliferation. However, the roles of key genes in potential molecular mechanisms of SCI are not clear. MATERIAL AND METHODS Subacute spinal cord injury models were established in Wistar rats. Histological observations and motor function assessments were performed separately. Whole-genome bisulfite sequencing (WGBS) was used to detect the methylation of genes. Gene ontology (GO) term enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were performed using the DAVID database. Protein-protein interaction (PPI) networks were analyzed by Cytoscape software. RESULTS After SCI, many cavities, areas of necrotic tissue, and many inflammatory cells were observed, and motor function scores were low. After the whole-genome bisulfite sequencing, approximately 96 DMGs were screened, of which 50 were hypermethylated genes and 46 were hypomethylated genes. KEGG pathway analysis highlighted the Axon Guidance pathway, Endocytosis pathway, T cell receptor signaling pathway, and Hippo signaling pathway. Expression patterns of hypermethylated genes and hypomethylated genes detected by qRT-PCR were the opposite of WGBS data, and the difference was significant. CONCLUSIONS Abnormal methylated genes and key signaling pathways involved in spinal cord injury were identified through histological observation, behavioral assessment, and bioinformatics analysis. This research can serve as a source of additional information to expand understanding of spinal cord-induced epigenetic changes.
| S-EPMC6295140 | biostudies-literature
Project description:BackgroundFollowing spinal cord injury (SCI), disease processes spread gradually along the spinal cord forming a spatial gradient with most pronounced changes located at the lesion site. However, the dynamics of this gradient in SCI patients is not established.ObjectiveThis study tracks the spatiotemporal dynamics of remote anterograde and retrograde spinal tract degeneration in the upper cervical cord following SCI over two years utilizing quantitative MRI.MethodsTwenty-three acute SCI patients (11 paraplegics, 12 tetraplegics) and 21 healthy controls were scanned with a T1-weighted sequence for volumetry and a FLASH sequence for myelin-sensitive magnetization transfer saturation (MTsat) of the upper cervical cord. We estimated myelin content from MTsat maps within the corticospinal tracts (CST) and dorsal columns (DC) and measured spinal cord atrophy by means of left-right width (LRW) and anterior-posterior width (APW) on the T1-weighted images across cervical levels C1-C3. MTsat in the CST and LRW were considered proxies for retrograde degeneration, while MTsat in the DC and APW provided evidence for anterograde degeneration, respectively. Using regression models, we compared the temporal and spatial trajectories of these MRI readouts between tetraplegics, paraplegics, and controls over a 2-year period and assessed their associations with clinical improvement.ResultsLinear rates and absolute differences in myelin-sensitive MTsat indicated retrograde and anterograde neurodegeneration in the CST and DC, respectively. Changes in MTsat within the CST and in LRW progressively developed over time forming a gradient towards lower cervical levels by 2 years after injury, especially in tetraplegics (change per cervical level in MTsat: -0.247 p.u./level, p = 0.034; in LRW: -0.323 mm/level, p = 0.024). MTsat within the DC was already decreased at cervical levels C1-C3 at baseline (1.5 months after injury) in both tetra- and paraplegics, while linear decreases in APW over time were similar across C1-C3, preserving the spatial gradient. The relative improvement in light touch score was associated with MTsat within the DC at baseline (rs = 0.575, p = 0.014).ConclusionRostral and remote to the injury, the CST and DC show ongoing structural changes, indicative of myelin reductions and atrophy within 2 years after SCI. While anterograde degeneration in the DC was already detectable uniformly at C1-C3 early following SCI, retrograde degeneration in the CST developed over time revealing specific spatial and temporal neurodegenerative gradients. Disentangling and quantifying such dynamic pathological processes may provide biomarkers for regenerative and remyelinating therapies along entire spinal pathways.
| S-EPMC9939725 | biostudies-literature
Project description:BackgroundPlacing a spinal stimulator for the purpose of restoring paralysed function is a novel procedure; however, paralysis predisposes people to infection. Preventing surgical site infections is critical to benefit this population.ObjectiveThe objective of this study was to review the root cause analysis of postoperative wound infections by a hospital epidemiology team following implantation of epidural spinal cord neurostimulators in patients with chronic spinal cord injury.MethodsA team was assembled to review the case of every individual who had been enrolled to receive a neurostimulator at the facility. A root cause analysis was performed evaluating five categories: the patient; equipment; facility/environment; procedure; and personnel.FindingsThe root cause analysis included 11 patients. Two patients became infected. Three others dehisced their wound without becoming infected. All patients were given preoperative antibiotics on time. A mean of 17 personnel were in the operating room during surgery. Vancomycin powder was used in the patients who either dehisced their wound or became infected.ConclusionsThe root cause analysis provides guidance for other institutions performing the same novel procedure. This analysis did not reveal a direct association, but did generate several areas for improvement including increasing pre-surgical screening, cleaning transient equipment (e.g., computer screens), limiting traffic in the operating room, using new sterile instruments for each stage of the procedure, not reopening the back incision, not applying vancomycin powder, and using an antimicrobial envelope for the stimulator.
| S-EPMC6683604 | biostudies-literature
Project description:Background and purposetSCH in the absence of spinal trauma or surgery is a rare disorder for which numerous mechanisms have been proposed. Here, we have conducted an analysis of images in all published reports of idiopathic tSCH and identified evidence supporting a pathogenesis in which anterior dural erosion at thoracic levels generates a CSF leak that pushes adjacent spinal tissue to tamponade the dural defect, causing progressive myelopathy. Additionally, we describe a case of tSCH in which postural headache was a significant symptom before myelopathy. This finding suggests that tSCH pathogenesis may be related to spontaneous intracranial hypotension.Materials and methodsPublished imaging from all available prior case reports in the scientific literature was reviewed to determine whether tSCH occurred at the disk or bone level. The presence of EDF, HNP, or an osteophyte in the spinal canal was determined from review of published images. Additionally, 3 previously unreported cases from the teaching files of our department were assessed by using these criteria.ResultsIn greater than two-thirds (47 of 67) of identified cases with published images, tSCH occurred at a disk level. When assessment was possible, EDF, HNP, and osteophytes were present in 26.8%, 30.7%, and 26.2% of cases, respectively. Overall, 52.3% of cases with published images demonstrated evidence of these abnormalities.ConclusionsOur analysis of published imaging indicates that tSCH occurs preferentially at spinal levels and with imaging findings consistent with dural injury that support the proposed etiology of this disorder.
| S-EPMC7966180 | biostudies-literature
Project description:ObjectiveSpinal cord stimulation (SCS) has become a popular nonopioid pain intervention. However, the treatment failure rate for SCS remains significantly high and many of these patients have poor sagittal spinopelvic balance, which has been found to correlate with increased pain and decreased quality of life. The purpose of this study was to determine if poor sagittal alignment is correlated with SCS treatment failure.Materials and methodsComparative retrospective analysis was performed between two cohorts of patients who had undergone SCS placement, those who had either subsequent removal of their SCS system (representing a treatment failure cohort) and those that underwent generator replacement (representing a successful treatment cohort). The electronic medical record was used to collect demographic and surgical characteristics, which included radiographic measurements of lumbar lordosis (LL), pelvic incidence (PI), pelvic tilt (PT), and sacral slope (SS). Also included were data on pain medication usage including opioid and nonopioid therapies.ResultsEighty-one patients met inclusion criteria, 31 had complete removal, and 50 had generator replacements. Measurement of sagittal balance parameters demonstrated that many patients had poor alignment, with 34 outside normal range for LL (10 vs 24 in removal and replacement cohorts, respectively), 30 for PI (12 [38.7%] vs 18 [36.0%]), 46 for PT (18 [58.1%] vs 28 [56.0%]), 38 for SS (18 [58.1%] vs 20 [40.0%]), and 39 for PI-LL mismatch (14 [45.2%] vs 25 [50.0%]). There were no significant differences in sagittal alignment parameters between the two cohorts.ConclusionsThis retrospective cohort analysis of SCS patients did not demonstrate any relationship between poor sagittal alignment and failure of SCS therapy. Further studies of larger databases should be performed to determine how many patients ultimately go on to have additional structural spinal surgery after failure of SCS and whether or not those patients go on to have positive outcomes.
| S-EPMC8655314 | biostudies-literature
Project description:Diffuse large B-cell lymphoma (DLBCL) is one of the most common causes of non-Hodgkin's lymphoma (NHL). Some of these DLBCLs can have genetic mutations as well as protein overexpression. The genes involved are MYC, BCL-2 and BCL-6. These are very aggressive and do not respond well to standard chemotherapy regiment. Lymphomas usually show classic signs and symptoms but rarely can present with little or no symptoms or even mimic other disease processes. Here we will present a case where a spinal lymphoma mimicked a hematoma and the patient developed signs and symptoms only after mechanical fall and hitting his back.
| S-EPMC7155832 | biostudies-literature
Project description:ObjectivesThe burden of pain after spinal cord injury (SCI), which may occur above, at, or below injury level, is high worldwide. Spinal cord stimulation (SCS) is an important neuromodulation pain therapy, but its efficacy in SCI pain remains unclear. In SCI rats, we tested whether conventional SCS (50 Hz, 80% motor threshold [MoT]) and 1200 Hz, low-intensity SCS (40% MoT) inhibit hind paw mechanical hypersensitivity, and whether conventional SCS attenuates evoked responses of wide-dynamic range (WDR) neurons in lumbar spinal cord.Materials and methodsMale rats underwent a moderate contusive injury at the T9 vertebral level. Six to eight weeks later, SCS or sham stimulation (120 min, n = 10) was delivered through epidural miniature electrodes placed at upper-lumbar spinal cord, with using a crossover design. Mechanical hypersensitivity was examined in awake rats by measuring paw withdrawal threshold (PWT) to stimulation with von Frey filaments. WDR neurons were recorded with in vivo electrophysiologic methods in a separate study of anesthetized rats.ResultsBoth conventional SCS and 1200 Hz SCS increased PWTs from prestimulation level in SCI rats, but the effects were modest and short-lived. Sham SCS was not effective. Conventional SCS (10 min) at an intensity that evokes the peak Aα/β waveform of sciatic compound action potential did not inhibit WDR neuronal responses (n = 19) to graded or repeated electrical stimulation that induces windup.ConclusionsConventional SCS and 1200 Hz, low-intensity SCS modestly attenuated below-level mechanical hypersensitivity after SCI. Inhibition of WDR neurons was not associated with pain inhibition from conventional SCS.
| S-EPMC7855640 | biostudies-literature
Project description:BACKGROUND Both spinal cord stimulators (SCS) and interdisciplinary chronic pain rehabilitation program (CPRP) are evidence-based treatments for chronic pain but differ on treatment foci. SCS focuses on decreasing the subjective pain experience as a means of improving function and quality of life. CPRP focuses on addressing the cognitive, emotional, and behavioral factors associated with chronic pain to improve function. Due to experimental constraints, these 2 treatment options are difficult to compare; however, this case report offers a unique opportunity to examine outcomes for both interventions in a sequential manner for changes in pain, function, and mood. CASE REPORT This single case study examined the separate and sequential outcomes of SCS and CPRP in a 26-year-old patient with a work-related injury resulting in chronic upper extremity pain. This patient was treated within an interdisciplinary CPRP following failure and removal of an SCS. Outcomes were measured by psychological assessments and return-to-work through a 6-month post-CPRP follow-up. CONCLUSIONS Pain intensity decreased following SCS placement and CPRP, while pain-related distress, pain interference, and overall affect improved only after CPRP, with sustained improvements at 6-month follow-up. Patient evidenced improvement following treatment with SCS and CPRP. SCS resulted in improvement in subjective pain and modest improved self-reported activity. CPRP demonstrated marked improvement in pain, self-reported function, and mood with patient eventually returning to work and maintaining most of these gains 6-months after completing CPRP treatment.
| S-EPMC6253559 | biostudies-other
Project description:Traumatic spinal cord injury (SCI) often leads to debilitating loss of locomotor function. Neuroplasticity of spinal circuitry underlies some functional recovery and therefore represents a therapeutic target to improve locomotor function following SCI. However, the cellular and molecular mechanisms mediating neuroplasticity below the lesion level are not fully understood. The present study performed a gene expression profiling in the rat lumbar spinal cord at 1 and 3 weeks after contusive SCI at T9. Another group of rats received treadmill locomotor training (TMT) until 3 weeks, and gene expression profiles were compared between animals with and without TMT. Microarray analysis showed that many inflammation-related genes were robustly upregulated in the lumbar spinal cord at both 1 and 3 weeks after thoracic injury. Notably, several components involved in an early complement activation pathway were concurrently upregulated. In line with the microarray finding, the number of microglia substantially increased not only in the white matter but also in the gray matter. C3 and complement receptor 3 were intensely expressed in the ventral horn after injury. Furthermore, synaptic puncta near ventral motor neurons were frequently colocalized with microglia after injury, implicating complement activation and microglial cells in synaptic remodeling in the lumbar locomotor circuitry after SCI. Interestingly, TMT did not influence the injury-induced upregulation of inflammation-related genes. Instead, TMT restored pre-injury expression patterns of several genes that were downregulated by injury. Notably, TMT increased the expression of genes involved in neuroplasticity (Arc, Nrcam) and angiogenesis (Adam8, Tie1), suggesting that TMT may improve locomotor function in part by promoting neurovascular remodeling in the lumbar motor circuitry.
| S-EPMC3919755 | biostudies-literature