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Degenerative cervical myelopathy (DCM) is the leading cause of spinal cord dysfunction in adults worldwide. DCM encompasses various acquired (age-related) and congenital pathologies related to degeneration of the cervical spinal column, including hypertrophy and/or calcification of the ligaments, intervertebral discs and osseous tissues. These pathologies narrow the spinal canal, leading to chronic spinal cord compression and disability. Owing to the ageing population, rates of DCM are increasing. Expeditious diagnosis and treatment of DCM are needed to avoid permanent disability. Over the past 10 years, advances in basic science and in translational and clinical research have improved our understanding of the pathophysiology of DCM and helped delineate evidence-based practices for diagnosis and treatment. Surgical decompression is recommended for moderate and severe DCM; the best strategy for mild myelopathy remains unclear. Next-generation quantitative microstructural MRI and neurophysiological recordings promise to enable quantification of spinal cord tissue damage and help predict clinical outcomes. Here, we provide a comprehensive, evidence-based review of DCM, including its definition, epidemiology, pathophysiology, clinical presentation, diagnosis and differential diagnosis, and non-operative and operative management. With this Review, we aim to equip physicians across broad disciplines with the knowledge necessary to make a timely diagnosis of DCM, recognize the clinical features that influence management and identify when urgent surgical intervention is warranted.Degenerative cervical myelopathy is the leading cause of spinal cord dysfunction in adults worldwide. In this Review, the authors provide a comprehensive pathophysiological and clinical overview of the condition to equip physicians across broad disciplines with the knowledge needed for its diagnosis and management.

Malignant spinal cord compression (MSCC) is one of the most devastating complications of cancer. Patients often present with a history of progressive pain, paralysis, sensory loss, progressive spinal deformity, and loss of sphincter control. It is an emergency that requires rapid decision making on the part of several specialists, given the risk of permanent spinal cord injury or death. The goals of treatment in spinal metastases are pain control and improvement of neurological function in order to achieve better quality of life (QoL). The standard of care in most cases is rapid initiation of corticosteroids in combination with either surgical decompression in case of an operable candidate, followed by radiation therapy (RT) or RT alone. Surgery is associated with improved outcomes, but is not appropriate for many patients presenting with advanced symptoms of MSCC, such as paralysis, or those with a poor performance status, or cachexic state, as well as altered mental conditions, co-morbidities, surgical risks, and limited life expectancy. On the other hand, aggressive surgical treatment and post-operative RT is advocated for those with more favorable prognosis, or who are expected to have higher neurological recovery potential. Many candidates may require for combined anterior and posterior approaches to effectively deal with the compressive pathology and stabilize the spine. Most patients are presently treated by primary RT, given with the aim of improving function and symptom management. However, there is still debate regarding the most appropriate RT schedule. Rehabilitation can serve to relieve symptoms, QoL, enhance functional independence, and prevent further complications. Ambulatory status has been found to be an important prognostic factor for patients with MSCC.

Malignant spinal cord compression (MSCC) can lead to immediate neurological impairment. In order to preserve and, optimally, restore neurological functions, urgent treatment (usually, within 24 h) is necessary. Treatment options mainly consist of decompressive surgery (DS) and / or radiotherapy (RT) combined with steroids. Whereas historically, RT was the treatment of choice, DS has become standard of care, where applicable. Despite a variety of excellent studies, real world data of treatment in a large academic center is currently underrepresented. We performed a retrospective analysis of patients treated for MSCC in our department of radiotherapy between 1998 and 2018 ( n  = 131), evaluating treatment, achievement of clinically determined improvement of neurological functions as well as overall survival (OS) and treatment-related toxicity. Kaplan-Meier estimator was used for survival statistics, log rank test for survival time comparisons, univariable and multivariable Cox regression and logistic regression for assessing potential impacts of variables on survival and symptom relief. 42.7% of patients had DS before RT ( n  = 56), 57.3% ( n  = 75) received RT without DS. Symptom relief was achieved in 41.2% of all patients ( n  = 54, n  = 26 of those had DS before RT, p  = 0.12). RT completed as intended ( p  < 0.001) was statistically significant for symptom relief, wherein symptom relief ( p  < 0.001), completion of RT course as intended ( p  = 0.01) and more recent treatment dates ( p  = 0.002) were independent predictors for OS. We herein present a large cohort of patients treated for MSCC in our academic center, representing real world treatment data currently lacking in literature.

Intradural spinal cord compression impairs perfusion pressure and is putatively rate-limiting for recovery after traumatic spinal cord injury (tSCI). After cervical tSCI, even minimally improved tissue preservation may help promote neurological recovery. To assess the nature and extent of spinal cord swelling and compression post-acute cervical tSCI, we evaluated several baseline MRI parameters including BASIC score, intramedullary lesion (IML) length, maximal canal compromise (MCC), maximal spinal cord compression (MSCC), extent of cord compression (ECC), maximal swollen anteroposterior diameter adjacent to injury site (Dmax), and maximal cord swelling (MCS) in 169 consecutive patients across 2 centers. In patients with either primarily intradural or combined (MSCC ≤5% or >5%, respectively) cord compression, we examined the predictive value of clinical and imaging admission parameters on American Spinal Injury Association Impairment Scale (AIS) severity and conversion up to 1-year follow-up. 37 (21.9%) patients presented with primarily intradural while 132 (78.1%) had combined cord compression. MSCC, MCS, and Dmax values differed significantly between the two groups (p < 0.0001, < 0.01 and < 0.001, respectively). MSCC was associated with age, MCC and MCS at baseline, while MCS was associated with age, MSCC and Dmax, on multivariable analysis. Logistic regression analysis of areas under receiver operating characteristic curve (AUROC) confirmed ECC (AUC 0.678) and MCS (AUC 0.922) as good and excellent predictors, respectively of AIS-conversion at 1-year for intradural compression participants. Additionally, MCS was significantly more accurate in predicting AIS-conversion in intradural group and the probability of AIS-conversion significantly decreased with each 1% increase in MCS (p = 0.003; OR 0.949), for both compression subtypes. In conclusion, baseline measures of cord swelling predict AIS-conversion likelihood up to 1-year. The deleterious effects of intradural cord compression, either isolated or presenting with extradural compression, may benefit from supplemental decompression strategies in addition to current standard-of-care.

Compression of the spinal cord can result from trauma, cancer, epidural abscess, or epidural hematoma and can have a variety of clinical manifestations based on the anatomical level and completeness of the compression. Treatment approaches are outlined. Acute compression of the spinal cord is a devastating but treatable disorder. Diseases that cause acute spinal cord compression constitute a special category because they originate in the spinal column and narrow the spinal canal. This review addresses the disorders that account for most instances of acute spinal cord compression: trauma, tumor, epidural abscess, and epidural hematoma. The pathophysiological features and management of these disorders are similar to those of other acute and serious spinal conditions. The medical context of spinal cord compression determines the diagnosis and directs treatment. Traumatic cord compression is often self-evident. Cord compression in patients with . . .

Cervical spinal cord dysfunction can result from either traumatic or nontraumatic causes, including tumors, infections, and degenerative changes. In this article, we review the range of degenerative spinal disorders resulting in progressive cervical spinal cord compression and propose the adoption of a new term, degenerative cervical myelopathy (DCM). DCM comprises both osteoarthritic changes to the spine, including spondylosis, disk herniation, and facet arthropathy (collectively referred to as cervical spondylotic myelopathy), and ligamentous aberrations such as ossification of the posterior longitudinal ligament and hypertrophy of the ligamentum flavum. This review summarizes current knowledge of the pathophysiology of DCM and describes the cascade of events that occur after compression of the spinal cord, including ischemia, destruction of the blood–spinal cord barrier, demyelination, and neuronal apoptosis. Important features of the diagnosis of DCM are discussed in detail, and relevant clinical and imaging findings are highlighted. Furthermore, this review outlines valuable assessment tools for evaluating functional status and quality of life in these patients and summarizes the advantages and disadvantages of each. Other topics of this review include epidemiology, the prevalence of degenerative changes in the asymptomatic population, the natural history and rates of progression, risk factors of diagnosis (clinical, imaging and genetic), and management strategies. ABBREVIATIONS:CSM, cervical spondylotic myelopathyDCM, degenerative cervical myelopathyJOA, Japanese Orthopaedic AssociationmJOA, modified Japanese Orthopaedic AssociationOPLL, ossification of the posterior longitudinal ligamentSCI, spinal cord injury

Background Degenerative cervical myelopathy (DCM) is a poorly recognised form of spinal cord injury which arises when degenerative changes in the cervical spine injure the spinal cord. Timely surgical intervention is critical to preventing disability. Despite this, DCM is frequently undiagnosed, and may be misconstrued as normal ageing. For a disease associated with age, we hypothesised that the elderly may represent an underdiagnosed population. This study aimed to evaluate this hypothesis by comparing age-stratified estimates of DCM prevalence based on spinal cord compression (SCC) data with hospital-diagnosed prevalence in the UK. Methods We queried the UK Hospital Episode Statistics database for admissions with a primary diagnosis of DCM. Age-stratified incidence rates were calculated and extrapolated to prevalence by adjusting population-level life expectancy to the standardised mortality ratio of DCM. We compared these figures to estimates of DCM prevalence based on the published conversion rate of asymptomatic SCC to DCM. Results The mean prevalence of DCM across all age groups was 0.19% (0.17, 0.21), with a peak prevalence of 0.42% at age 50–54 years. This contrasts with estimates from SCC data which suggest a mean prevalence of 2.22% (0.436, 2.68) and a peak prevalence of 4.16% at age > 79 years. Conclusions To our knowledge, this is the first study to estimate the age-stratified prevalence of DCM and estimate underdiagnosis. There is a substantial difference between estimates of DCM prevalence derived from SCC data and UK hospital activity data. This is greatest amongst elderly populations, indicating a potential health inequality.

This report highlights an unusual case of a woman in her 70s who presented with diffuse idiopathic skeletal hyperostosis and an initial symptom of spinal cord compression and associated spinal degeneration. She presented with progressive thoracolumbar pain, bilateral lower limb weakness, and sensory deficits. Imaging showed continuous osteophytes in the anterior and lateral spine, multiple levels of intervertebral space narrowing, marked ligament ossification at T10/11, and severe spinal stenosis. Diffuse idiopathic skeletal hyperostosis was diagnosed and spinal cord compression was significantly reduced after laminectomy. Although diffuse idiopathic skeletal hyperostosis is relatively common in elderly patients, cases of spinal cord compression are still rare, and the combination of intervertebral space stenosis, and ossification of the ligamentum flavum may be misdiagnosed as degenerative spondylopathy. This case suggests the possibility of intervertebral stenosis and ossification of the thoracic ligamentum flavum coexisting with diffuse idiopathic skeletal hyperostosis, highlighting the importance of diagnostic imaging in the early stage of patient management.

BackgroundSpinal cord stimulation (SCS) is an efficacious treatment for various refractory chronic pain syndromes. Serious complications including spinal cord compression (SCC) are rare with 19 previous reports which are mainly attributed to fibrotic scar tissue formation at the distal end of the leads at the location of the contacts. We report a case of SCC following SCS implantation at the lead entry location secondary to a delayed progression of spinal canal stenosis.Case presentationA patient in her early 70s underwent SCS implantation with adequate therapeutic benefit for approximately 2 years before citing complaints of increasing lower back pain and lower extremity radicular pain. Lumbar spine X-rays excluded lead migration as a causative factor. An MRI of the lumbar spine obtained 30 months following SCS implantation demonstrated a marked interval progression of central canal stenosis secondary to facet and ligamentous hypertrophy manifesting in compression of the spinal cord at the lead entry location. An L1–L2 decompressive laminectomy with hardware removal resulted in the resolution of her symptoms. A literature search conducted with the PubMed database identified previously published cases of SCC following SCS implantation which highlighted the rarity of this complication.ConclusionOur case report urges physicians of SCS patients, noting a loss of therapeutic benefit with their device, to investigate new pathologies including SCC. Furthermore, our case highlights clinical symptoms and surgical treatments of SCC. Paddle leads are more commonly implicated in published cases of SCC than percutaneous leads. Lastly, MRI conditionality is critical to identifying cases of SCC.

Degenerative compressive myelopathy (DCM) is caused by cervical cord compression. The relationship between the magnitude and clinical findings of cervical cord compression has been described in the literature, but the details remain unclear. This study aimed to clarify the relationship between the magnitude and clinical symptoms of cervical cord compression in community-dwelling residents. The present study included 532 subjects. The subjective symptoms and the objective findings of one board-certified spine surgeon were assessed. The subjective symptoms were upper extremity pain and numbness, clumsy hand, fall in the past 1 year, and subjective gait disturbance. The objective findings were: Hoffmann, Trömner, and Wartenberg signs; Babinski's and Chaddock's signs; hyperreflexia of the patellar tendon and Achilles tendon reflexes; ankle clonus; Romberg and modified Romberg tests; grip and release test; finger escape sign; and grip strength. Using midsagittal T2-weighted magnetic resonance imaging, the anterior-posterior (AP) diameters (mm) of the spinal cord at the C2 midvertebral body level (DC2) and at each intervertebral disc level from C2/3 to C7/T1 (DC2/3-C7/T1) were measured. The spinal cord compression ratio (R) for each intervertebral disc level was defined and calculated as DC2/3-C7/T1 divided by DC2. The lowest R (LR) along C2/3 to C7/T1 of each individual was divided into 3 grades by the tertile method. The relationship between LR and clinical symptoms was investigated by trend analysis. The prevalence of subjective gait disturbance increased significantly with the severity of spinal cord compression (p = 0.002812), whereas the other clinical symptoms were not significantly related with the severity of spinal cord compression. The magnitude of cervical cord compression had no relationship with any of the neurologic findings. However, subjective gait disturbance might be a better indicator of the possibility of early stage cervical cord compression.