Cause Of Spinal Cord Dysfunction Research Articles

The Prevalence and Phenotype of Activated Microglia/Macrophages within the Spinal Cord of the Hyperostotic Mouse (twy/twy) Changes in Response to Chronic Progressive Spinal Cord Compression: Implications for Human Cervical Compressive Myelopathy

BackgroundCervical compressive myelopathy, e.g. due to spondylosis or ossification of the posterior longitudinal ligament is a common cause of spinal cord dysfunction. Although human pathological studies have reported neuronal loss and demyelination in the chronically compressed spinal cord, little is known about the mechanisms involved. In particular, the neuroinflammatory processes that are thought to underlie the condition are poorly understood. The present study assessed the localized prevalence of activated M1 and M2 microglia/macrophages in twy/twy mice that develop spontaneous cervical spinal cord compression, as a model of human disease.MethodsInflammatory cells and cytokines were assessed in compressed lesions of the spinal cords in 12-, 18- and 24-weeks old twy/twy mice by immunohistochemical, immunoblot and flow cytometric analysis. Computed tomography and standard histology confirmed a progressive spinal cord compression through the spontaneously development of an impinging calcified mass.ResultsThe prevalence of CD11b-positive cells, in the compressed spinal cord increased over time with a concurrent decrease in neurons. The CD11b-positive cell population was initially formed of arginase-1- and CD206-positive M2 microglia/macrophages, which later shifted towards iNOS- and CD16/32-positive M1 microglia/macrophages. There was a transient increase in levels of T helper 2 (Th2) cytokines at 18 weeks, whereas levels of Th1 cytokines as well as brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF) and macrophage antigen (Mac) −2 progressively increased.ConclusionsSpinal cord compression was associated with a temporal M2 microglia/macrophage response, which may act as a possible repair or neuroprotective mechanism. However, the persistence of the neural insult also associated with persistent expression of Th1 cytokines and increased prevalence of activated M1 microglia/macrophages, which may lead to neuronal loss and demyelination despite the presence of neurotrophic factors. This understanding of the aetiopathology of chronic spinal cord compression is of importance in the development of new treatment targets in human disease.

Dynamic MRI Reveals Soft-Tissue Compression Causing Progressive Myelopathy in Postlaminectomy Patients: A Report of Three Cases.

Cervical spondylotic myelopathy has been reported as the most common cause of spinal cord dysfunction in individuals older than age fifty-five, although the rate of occurrence is blurred by the difficulty of making a precise and timely diagnosis. The symptoms that patients present with can be inconsistent and show high variability from patient to patient1-4. Magnetic resonance imaging (MRI) has been a beneficial tool for evaluating anteroposterior sagittal diameter, the compression ratio, and the canal-occupying ratio5,6. According to numerous biomechanical and cadaveric studies, cervical flexion results in tension forces on the spinal cord and can cause ventral spinal cord compression against osteophytes and discs. In neck extension, the cervical cord shortens, and there is an increase in the cross-sectional area of the anteroposterior diameter of the spinal cord. In addition, the space available to the spinal cord is reduced as the ligamentum flavum folds inward7,8. We report three cases of progressive myelopathy. The first patient had undergone a previous multilevel cervical laminectomy. Although an initial MRI with the neck in the neutral position showed no spinal cord compression, the patient subsequently underwent dynamic MRI with the neck in extension, which revealed flattening of the spinal cord by soft tissues buckling into the laminectomy defect. The second patient had undergone a previous cervical laminectomy and arthrodesis with lateral mass internal fixation. He presented with progressive myelopathy and exhibited cord flattening on extension MRI, similar to that seen in the first patient. The third patient presented with myelopathic symptoms, had undergone a prior multilevel laminectomy, and had been followed for a syrinx; a cervical MRI with the neck in extension revealed severe stenosis. All three patients were informed that data concerning their cases would be submitted for publication, and they …

Immunohistochemical Profile of NF-κB/p50, NF-κB/p65, MMP-9, MMP-2, and u-PA in Experimental Cervical Spondylotic Myelopathy

The immunohistochemical profile of nuclear factor-κ B (NF-κB)/p50, NF-κB/p65, matrix metalloproteinase (MMP)-9, MMP-2, and urokinase-type plasminogen activator (u-PA) proteins was examined in spinal cord tissues coming from rabbits, which underwent chronic cervical spinal cord compression. To study the potential role of NF-κB and extracellular matrix proteins under the chronic mechanical compression of the cervical spinal cord. Cervical spondylotic myelopathy (CSM) is the most common cause of spinal cord dysfunction among adults older than 55 years. Neuronal loss, myelin destruction, axonal degeneration, and glial scar formation are the principal neuropathological features of CSM. However, the biologic pathways that lead to these features remain unclear. In this study, we used a new animal experimental model of CSM developed in our laboratory. Briefly, after posterior cervical laminectomy, gradual and progressive compression (during 20 weeks) was achieved by introducing a piece of aromatic polyether (0.07 mm thick) under the C6 lamina in 15 New Zealand rabbits. In control animals (n = 15), the aromatic polyether was implanted and then removed after 60 seconds (sham operation). The immunoreactivity of p50 and p65 subunits of NF-kB, as well as that of MMP-2, MMP-9, and u-PA, was evaluated in paraffin-embedded spinal cord sections coming from both groups. The evaluation was performed using immunohistochemistry technique and the results were analyzed using SPSS for Windows, release 12.0 (SPSS Inc., Chicago, IL). Increased immunoreactivity of both NF-κB subunits, p50 and p65, as well as MMP-2, MMP-9, and u-PA was demonstrated in animals with CSM in comparison with controls. Statistical analysis of the results revealed strong positive correlation between NF-κB subunits immunoreactivity and that of MMP-9, MMP-2, and u-PA. There is a strong correlation between the immunoexpression of NF-κB/p50, NF-κB/p65, MMP-2, MMP-9, u-PA, and CSM.

Risk factors for development of cervical spondylotic myelopathy: results of a systematic review

Study design: Systematic review.Study rationale: Cervical spondylotic myelopathy (CSM) is a common cause of spinal cord dysfunction that may be asymptomatic or may present with severe symptoms. Since CSM has an insidious manifestation, identification of risk factors associated with this condition may aid clinicians in monitoring high-risk patients and implementing appropriate management strategies.Objective: To assess sociodemographic, clinical, radiographic, and genetic risk factors associated with presence of CSM in patients 18 years or older.Methods: A systematic review of the literature was performed using PubMed, the National Guideline Clearinghouse Databases, and bibliographies of key articles to assess risk factors associated with CSM. Articles were reviewed by two independent reviewers based on predetermined inclusion and exclusion criteria. Each article was evaluated using a predefined quality-rating scheme.Results: From 486 citations, eight articles met all inclusion and exclusion criteria. Larger vertebral body and smaller spinal canal and Torg/Pavlov ratio were associated with CSM diagnosis, while gender was not associated with a CSM diagnosis across multiple studies. There were inconsistent reports with respect to increased age as a risk factor for CSM diagnosis.Conclusion: The limited data available suggests that inherent anatomical features that may contribute to congenital cervical stenosis may be associated with CSM. This systematic review is limited by the small number of high-quality studies evaluating prognostic factors for CSM. The overall strength of evidence for all risk factors evaluated is low.

Surgical management of cervical spondylotic myelopathy

Cervical spondylotic myelopathy (CSM) is emerging as the most common cause of spinal cord dysfunction in the elderly worldwide. In the past decade, our understanding of the biomechanics of the spine has improved along with advances in spinal instrumentation and this has led to significant changes in the surgical management of CSM. This review will discuss the indications, advantages and limitations of different operative approaches as well as the complications and prognosis of surgery for cervical spondylotic myelopathy. Choice of surgical approach for CSM should be based on the clinical and radiological characteristics of the individual patient and not on the preferences of the surgeon.

Steroids have no place in the management of cervical myelopathy

Cervical spondylotic myelopathy (CSM) is the most common cause of spinal cord dysfunction in adults in Western society. Very little has been written about it in Nigeria. This would give the impression that it is rare in Nigeria. Unfortunately, this is not the case and having seen a few patients now in Abuja, we can appreciate some of the real issues. Patients with cervical spondylotic myelopathy are not being properly diagnosed and managed. It is often thought to be a disease of old age and part of life. Others feel that old age and infirmity preclude management and so patients are not referred to hospital. Families also at times prefer local management with traditional healers. Finally, patients are often treated only by general practitioners, general medicine physicians and neurologists. We have now seen a few patients who have been treated long term for CSM by neurologists without referral for surgical intervention. Patients having been seen are placed on long term steroid therapy, vitamin C and analgesics and neuropathic pain medicines such as Carbamazepine, Gabapentin and Pregabalin. Our perspective is that such treatment especially for moderate or severe CSM is of little benefit to address the fundamental and underlying problem in CSM. In our opinion, steroid use is not necessary and predisposes patients to diabetes, osteoporosis and avascular necrosis of the head of femur. The other two key problems in the past were poor availability of MRI scans and spine trained neurosurgeons.

Apoptosis of neurons and oligodendrocytes in the spinal cord of spinal hyperostotic mouse (twy/twy): possible pathomechanism of human cervical compressive myelopathy

IntroductionCervical compressive myelopathy is the most serious complication of cervical spondylosis or ossification of the posterior longitudinal ligament (OPLL) and the most frequent cause of spinal cord dysfunction. There is little information on the exact pathophysiological mechanism responsible for the progressive loss of neural tissue in the spinal cord of such patients. In this study, we used the spinal hyperostotic mouse (twy/twy) as a suitable model of human spondylosis, and OPLL to investigate the cellular and molecular changes in the spinal cord. Mutant twy/twy mouse developed ossification of the ligamentum flavum at C2–C3 and exhibited progressive paralysis.Materials and methodsThe mutant twy/twy mice, aged 16 and 24 weeks, were used in the present study. The cervical spinal cord was analyzed histologically and immunohistochemically.ResultsWe observed that a significant correlation between the proportion of apoptotic oligodendrocytes in the compressed area of the spinal cord and the magnitude of cord compression. Immunohistochemical analysis indicated overexpression of TNFR1, CD95, and p75NTR in the twy/twy mice, which was localized by the immunofluorescence in the neurons and oligodendrocytes.ConclusionThe expression of such factors seems to play at least some role in the apoptotic process, which probably contributes to axonal degeneration and demyelination in the twy/twy mice spinal cords with severe compression.Electronic supplementary materialThe online version of this article (doi:10.1007/s00586-011-2025-x) contains supplementary material, which is available to authorized users.

New experimental rabbit animal model for cervical spondylotic myelopathy

Cervical spondylotic myelopathy (CSM) represents the most commonly acquired cause of spinal cord dysfunction among individuals over 55 years old. The pathophysiology of the disease involves static and dynamic mechanical factors, which are the result of chronic degeneration. The clinical course of the disease remains unpredictable. In the past, many experimental animal models have been developed to study the cellular and molecular mechanisms underlining the pathophysiology of the disease. To create a new animal model of CSM, which will reproduce the temporal course of the disease and the local microenvironment at the site of spinal cord compression. We performed posterior laminectomy to New Zealand rabbits at the level of C7, and a thin sheet (5-7 μm) of aromatic polyether was implanted with microsurgical technique at the epidural space underneath C5-C6 laminae. Motor function evaluation was performed after the operation and once a week thereafter. After 20 weeks, the animals were killed, and the histological evaluation of spinal cord at the site of compression above and below it, using eosin hematoxylin, immonohistochemistry and Kluver-Barrera techniques reveals axonal swelling and demyelination, interstitial edema and myelin sheet fragmentation. Moreover, histological evaluation of C5 and C6 laminae reveals osteophyte formation. We believe that this CSM model reproduces the temporal evolution of the disease and creates a local microenvironment at the site of spinal cord compression, which shares the same characteristics with that of human disease.

Comparative Effectiveness of Ventral vs Dorsal Surgery for Cervical Spondylotic Myelopathy

Cervical spondylotic myelopathy (CSM) is the most common cause of spinal cord dysfunction. To determine the feasibility of a randomized clinical trial comparing the clinical effectiveness and costs of ventral vs dorsal decompression with fusion surgery for treating CSM. A nonrandomized, prospective, clinical pilot trial was conducted. Patients ages 40 to 85 years with degenerative CSM were enrolled at 7 sites over 2 years (2007-2009). Outcome assessments were obtained preoperatively and at 3 months, 6 months, and 1 year postoperatively. A hospital-based economic analysis used costs derived from hospital charges and Medicare cost-to-charge ratios. The pilot study enrolled 50 patients. Twenty-eight were treated with ventral fusion surgery and 22 with dorsal fusion surgery. The average age was 61.6 years. Baseline demographics and health-related quality of life (HR-QOL) scores were comparable between groups; however, dorsal surgery patients had significantly more severe myelopathy (P<.01). Comprehensive 1-year follow-up was obtained in 46 of 50 patients (92%). Greater HR-QOL improvement (Short-Form 36 Physical Component Summary) was observed after ventral surgery (P=.05). The complication rate (16.6% overall) was comparable between groups. Significant improvement in the modified Japanese Orthopedic Association scale score was observed in both groups (P<.01). Dorsal fusion surgery had significantly greater mean hospital costs ($29 465 vs $19 245; P<.01) and longer average length of hospital stay (4.0 vs 2.6 days; P<.01) compared with ventral fusion surgery. Surgery for treating CSM was followed by significant improvement in disease-specific symptoms and in HR-QOL. Greater improvement in HR-QOL was observed after ventral surgery. Dorsal fusion surgery was associated with longer length of hospital stay and higher hospital costs. The pilot study demonstrated feasibility for a larger randomized clinical trial.

Laminoplasty versus Laminectomy and Fusion for Multilevel Cervical Spondylotic Myelopathy

Cervical spondylotic myelopathy is increasingly prevalent in the elderly and is the leading cause of spinal cord dysfunction in this population. Laminectomy with fusion and laminoplasty halt progression of myelopathy in these patients; however, both procedures have well-documented complications and associated morbidity and it is unclear which might be most advantageous. We therefore compared the pain, function and alignment of patients who underwent laminectomy with fusion to those with laminoplasty for the treatment of multilevel cervical spondylotic myelopathy. We performed a retrospective matched cohort analysis on all 121 patients from 2002 to 2007 who underwent laminectomy with fusion (82) or laminoplasty (39) for multilevel cervical spondylotic myelopathy. We determined change in preoperative and postoperative sagittal alignment using Cobb measurement, development of junctional stenosis, and subjective improvements in pain and gait. Complications were recorded for both cohorts. The majority of patients in both cohorts reported improvements in pain and gait postoperatively. There were seven complications in the laminectomy and fusion cohort (9%) with two patients requiring formal revision surgery (2%). There were five complications in the laminoplasty cohort (13%) with two formal revision procedures (5%). Patients in both the laminectomy with fusion and laminoplasty cohorts reported similar functional improvements after treatment for cervical spondylotic myelopathy. Prospective randomized control trials are needed to determine whether one procedure is truly superior. Level IV, therapeutic study. See Guidelines for Authors for a complete description of levels of evidence.

Spinal cord herniation: a misdiagnosed and treatable cause of thoracic myelopathy

This study is a case report and review of the literature. Spinal cord herniation is a rare, although increasingly recognized, cause of spinal cord dysfunction. It is due to an anterior dural defect, through which the spinal cord herniates. The purpose of this article is to report the authors' experience and to provide insight on clinical presentation and radiological signs to make the reader aware of this entity and then to prevent misdiagnosis. The authors conducted a retrospective review of patients who underwent surgery for spinal cord herniation at their institution between 2000 and 2008. Three patients were treated (all women) and the interval between the onset of symptoms and surgery ranged from 24 to 48months. All patients had progressive signs of thoracic myelopathy, and two of them were initially misdiagnosed. In all cases, the herniation was reduced and the defect repaired using different methods. The results and complications of our cases were compared with that of the reported literature. According to the results in these cases and the review of the literature, the authors believe that spinal cord herniation should be treated by using a dural patch to close the dural defect and to prevent retethering of the spinal cord.

Cervical Laminoplasty as a Management Option for Patients With Cervical Spondylotic Myelopathy

Cervical spondylotic myelopathy (CSM) is one of the leading causes of spinal cord dysfunction in the adult population. Laminoplasty is an effective decompressive procedure for the treatment of CSM. We present our experience with 40 patients who underwent cervical laminoplasty using titanium miniplates for CSM. We performed a retrospective review of the medical records of a consecutive series of patients with CSM treated with laminoplasty at the University of Rochester Medical Center or Rochester General Hospital. We documented patient demographic data, presenting symptoms, and postoperative outcome. Data are also presented regarding the general cost of constructs for a hypothetical 3-level fusion. Forty patients underwent cervical laminoplasty; all were available for follow-up. The mean number of levels was 4. All patients were myelopathic, and 17 (42.5%) had signs of radiculopathy preoperatively. Preoperatively, 62.5% of patients had a Nurick grade of 2 or worse. The average follow-up was 31.3 months. The median length of stay was 48 hours. On clinical evaluation, 36 of 40 patients demonstrated an improvement in their myelopathic symptoms; 4 were unchanged. Postoperative kyphosis did not develop in any patients. The management of CSM for each of its etiologies remains controversial. As demonstrated in our series, laminoplasty is a cost-effective, decompressive procedure for the treatment of CSM, providing a less destabilizing alternative to laminectomy while preserving mobility. Cervical laminoplasty should be considered in the management of multilevel spondylosis because of its ease of exposure, ability to decompress, effective preservation of motion, maintenance of spinal stability, and overall cost.

Molecular mechanisms of spinal cord dysfunction and cell death in the spinal hyperostotic mouse: Implications for the pathophysiology of human cervical spondylotic myelopathy

Cervical spondylotic myelopathy (CSM) is the most common cause of spinal cord dysfunction in adults in Western society. Paradoxically, relatively little is known about the pathobiological mechanisms associated with the progressive loss of neural tissue in the spinal cord of CSM patients. In this report we have utilized the twy/twy mutant mouse, which develops ossification of the ligamentum flavum at C2–C3 and exhibits progressive paralysis. This animal model represents an excellent in vivo model of CSM. This study reports novel evidence, which demonstrates that chronic extrinsic cervical spinal cord compression leads to Fas-mediated apoptosis of neurons and oligodendrocytes which is associated with activation of caspase-8, -9 and -3 and progressive neurological deficits. While surgical decompression will remain the mainstay of management of CSM, molecular therapies, which target Fas-mediated apoptosis could show promise as a complementary approach to maximize neurological recovery in this common spinal cord condition.

Incidence of Fractures in a Cohort of Veterans With Chronic Multiple Sclerosis or Traumatic Spinal Cord Injury

Logan WC Jr, Sloane R, Lyles KW, Goldstein B, Hoenig HM. Incidence of fractures in a cohort of veterans with chronic multiple sclerosis or traumatic spinal cord injury. Objective To measure skeletal fractures in a cohort of veterans with spinal cord dysfunction (SCD) due to multiple sclerosis (MS) or trauma-related spinal cord injury (SCI). Design Retrospective cohort analysis. Setting Database search. Participants Study subjects were a subset of the 1996 Veterans Health Administration (VHA) National Spinal Cord Dysfunction Registry, from which 8150 patients were identified with either MS (n=1789) or SCI (n=6361). Inpatient and outpatient encounters for nonaxial fractures, based on International Classification of Diseases, Ninth Revision, Clinical Modification codes, were identified through VHA administrative databases between October 1996 and June 2005. VHA Beneficiary Identification Records Locator Subsystem death file identified time of death. Interventions Not applicable. Main Outcome Measures Data from the 1996 VHA National Spinal Cord Dysfunction Registry survey was used to determine duration of disease and motor impairment (4 categories of motor impairment based on self-report of the number of limbs involved and degree of motor loss). Proportional hazard modeling evaluated the time to first fracture and Poisson regression evaluated relative risk (RR) of fracture by cause of SCD and degree of motor impairment, adjusting for age, sex, race, and duration of SCD. Results Subjects were, on average, 52.5 years of age, acquired their SCD 22 years prior, and 386 of 8150 were deceased. During the study period, 4021 fracture encounters were identified representing 1738 unique fractures for 1085 of 7832 subjects, for a mean per-person fracture rate of 3.1 per 100 patient-years at risk. The RR of fracture differed according to cause of SCD and motor impairment. Fracture risk was increased by more than 2-fold in those with some motor impairment (RR=2.33, P<.001), by more than 80% with moderate motor impairment (RR=1.87, P<.001), and almost 70% for those with severe motor impairment (RR=1.67, P<.001), compared with those with little motor impairment. Trauma-related SCI increased the RR of fracture 80% (RR=1.82, P<.001) compared with MS. Conclusions Persons with SCD have high rates of skeletal fractures. The highest fracture rates occurred in those with some to moderate motor impairment. There were significant differences in risk of fracture according to causal disease, controlling for motor impairment and duration. There appear to be unique contributors to risk of fracture beyond simply disuse.

Acute flaccid paraplegia: a rare complication of meningococcal meningitis

A case report of spinal cord dysfunction following meningococcal meningitis. To describe a rare complication of meningococcal meningitis. Spinal Unit, Armed Forces Institute of Rehabilitation Medicine, Rawalpindi, Pakistan. A young healthy male developed meningococcal meningitis followed by acute onset low thoracic flaccid paraplegia with complete motor and sensory loss and sphincter disturbance. He responded well to antibiotics but was not investigated for causes of paraplegia. While at home in a rural area, he developed pressure ulcers, anemia and depression. Magnetic resonance imaging of the whole spine and computed tomography scan of the brain performed after 4 and 10 weeks were normal. The patient had a comprehensive rehabilitation at our institute. Recovery was complicated by ossification in the right thigh, which responded well to radiotherapy. At 1-year follow-up, the motor deficit and neurogenic bladder and bowel persisted and the patient remained wheelchair dependent for mobility. Several mechanisms have been proposed to explain spinal cord damage after meningitis. These include spinal cord infarction; autoimmune-mediated inflammatory myelopathy and direct infection of the cord. Most probable cause of spinal cord dysfunction in this case was thoracic myelopathy.

Clinical and MRI Predictors of Outcome After Surgical Intervention for Cervical Spondylotic Myelopathy

Cervical spondylotic myelopathy (CSM) is the most common cause of spinal cord dysfunction in older individuals. Controversy remains in terms of the optimal timing and indications for surgical intervention. In this context, it would be of benefit to define clinical and magnetic resonance imaging (MRI) predictors of outcome after intervention for CSM. We studied subjects with clinically documented cervical myelopathy to evaluate the relationship among preoperative MRI signal change, clinical findings, and outcome after surgical intervention. We performed a retrospective case study of 76 CSM patients who underwent cervical decompressive surgery and who had pre- and postoperative MRI studies available for review. Preoperative clinical findings and MRI abnormalities on T1- (T1WI) and T2-weighted (T2WI) images were correlated with outcomes (Nurick scores; Odom's criteria) following surgical intervention. Postoperative MRIs were performed 2-4 months postsurgery to assess for adequacy of decompression and resolution of preoperative signal changes. The pattern of spinal cord signal intensity was classified as: Group A (MRI N/N), no intramedullary signal intensity abnormality on T1WI or T2WI; Group B (MRI N/Hi), no intramedullary signal intensity abnormality on T1WI and high intramedullary signal intensity on T2WI; Group C (MRI Lo/Hi), low intensity intramedullary signal abnormality on T1WI and high intensity intramedullary signal abnormality on T2WI. Statistical analyses were performed using SAS (version 8.2). We evaluated 76 patients (57% males, mean age 62 years, range 30-89) who experienced preoperative symptoms for an average of 6.5 months (range 1 month to 9 years). Preoperative MRI studies demonstrated the following: Group A (MRI N/N) = 45; Group B (MRI N/Hi) = 23; and Group C (MRI Lo/Hi) = 8. The mean postoperative follow-up period was 2.5 years (range 2 months to 8.5 years). A positive Babinski sign and the presence of intrinsic hand muscle atrophy showed the greatest association with abnormal preoperative MRI signal change. High preoperative Nurick score, clonus, and leg spasticity were associated with a less favorable postoperative outcome. In Group B (MRI N/Hi), 11/23 (52.17%) patients had recovery to MRI N/N (P < .0001) at their follow-up scan. Patients with high intramedullary signal change on T2WI who do not have clonus or spasticity may experience a good surgical outcome and may have reversal of the MRI abnormality. A less favorable surgical outcome is predicted by the presence of low intramedullary signal on T1WI, clonus, or spasticity. These data suggest that there may be a window of opportunity to obtain optimal surgical outcomes in patients with CSM.

Magnetic resonance imaging of traumatic intervertebral disc extension in dogs

This retrospective study evaluated the magnetic resonance (mr) images of traumatic disc extrusions in 11 dogs. The findings included a reduction in the volume and signal intensity of the nucleus...

Operative Treatment of Cervical Spondylotic Myelopathy

Cervical spondylotic myelopathy is a leading cause of spinal cord dysfunction in the adult population. Affected patients represent a large subset of individuals who undergo operative treatment of degenerative cervical conditions. In a study of 450 patients undergoing anterior neck surgery for the treatment of degenerative disc disease, 61% presented with radicular symptoms, 16% had pure myelopathic symptoms, and the remaining 23% had a combination of myelopathy and radiculopathy1. The subtle clinical findings of early cervical spondylotic myelopathy make diagnosis difficult, and true natural history studies are unavailable. The patients or their relatives notice increasing awkwardness with gait and balance that they attribute to old age or arthritis of the lower extremity joints. Patients may report an insidious onset of clumsiness or diffuse numbness in the hands, resulting in worsening of handwriting or …

Spinal cord compression

Compression of the spinal cord may present to general physicians, orthopaedic surgeons, neurologists or, if radicular pain is mistaken for intra-abdominal pathology, general surgeons. The causes of spinal cord dysfunction are diverse and range from anterior spinal artery ischaemia through a range of inflammatory insults to structural compressive pathology. The purpose of this article is to discuss the diagnosis of spinal cord compression, how to localise it clinically and how best to manage it.

Spinal Fracture or Luxation

Spinal trauma is a common cause of spinal cord dysfunction in dogs and cats. When the spine is injured by exogenous injury, the impact often results in vertebral fracture or luxation. As each injury is unique, treatment guidelines have to be individualized to the animal. This article reviews the clinical management including surgical and nonsurgical treatments for animals with vertebral fracture/luxation.