Degenerative cervical myelopathy — update and future directions

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Abstract

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.

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Cellular inflammatory response after spinal cord injury in Sprague-Dawley and Lewis rats.

B T Stokes, P Wei, P. Popovich (1997)

The distribution of microglia, macrophages, T-lymphocytes, and astrocytes was characterized throughout a spinal contusion lesion in Sprague-Dawley and Lewis rats by using immunohistochemistry. The morphology, spatial localization, and activation state of these inflammatory cells were described both qualitatively and quantitatively at 12 hours, 3, 7, 14, and 28 days after injury. By use of OX42 and ED1 antibodies, peak microglial activation was observed within the lesion epicenter of both rat strains between three and seven days post-injury preceding the bulk of monocyte influx and macrophage activation (seven days). Rostral and caudal to the injury site, microglial activation plateaued between two and four weeks post-injury in the dorsal and lateral funiculi as indicated by morphological transformation and the de-novo expression of major histocompatibility class II (MHC II) molecules. Similar to the timing of microglial reactions, T-lymphocytes maximally infiltrated the lesion epicenter between three and seven days post-injury. Reactive astrocytes, while present in the acute lesion, were more prominent at later survival times (7-28 days). These cells were interspersed with activated microglia but appeared to surround and enclose tissue sites occupied by reactive microglia and phagocytic macrophages. Thus, trauma-induced central nervous system (CNS) inflammation, regardless of strain, occurs rapidly at the site of injury and involves the activation of resident and recruited immune cells. In regions rostral or caudal to the epicenter, prolonged activation of inflammatory cells occurs preferentially in white matter and primarily consists of activated microglia and astrocytes. Differences were observed in the magnitude and duration of macrophage activation between Sprague-Dawley (SD) and Lewis (LEW) rats throughout the lesion. Increased expression of complement type 3 receptors (OX42) and macrophage-activation antigens (ED1) persisted for longer times in LEW rats while expression of MHC class II molecules was attenuated in LEW compared to SD rats at all times examined. Variations in the onset and duration of T-lymphocyte infiltration also were observed between strains with twice as many T-cells present in the lesion epicenter of Lewis rats by 3 days post-injury. These strain-specific findings potentially represent differences in corticosteroid regulation of immunity and may help predict a range of functional neurologic consequences affected by neuroimmune interactions.

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Concurrent related validity of the GAITRite walkway system for quantification of the spatial and temporal parameters of gait.

Belinda Bilney, Meg Morris, Kate E. Webster (2003)

The GAITRite is a portable gait analysis tool for automated measurement of spatiotemporal gait parameters. Although frequently used for clinical and research purposes, the concurrent validity of GAITRite has not been validated against a criterion measure. The aim of this experiment was to investigate the concurrent validity and test retest reliability of the GAITRite carpet walkway system for quantification of spatial and temporal parameters of the footstep pattern. Twenty-five healthy adults aged 21-71 years (mean 40.5 years, S.D. 17.2) performed three walk trials at self-selected pace, three at fast pace and three at slow pace. For each trial, data were simultaneously collected from the GAITRite and a Clinical Stride Analyzer, which has established reliability and validity. At preferred, slow and fast walking pace there were very high correlations between the two measurement systems for gait speed (ICC (2,1)=0.99), stride length (ICC (2,1)=0.99) and cadence (ICC (2,1)=0.99). Correlations between the electronic carpet and the stride analyser were moderate to high for single limb support (SLS) time (ICC (2,1)=0.69-0.91) and weak for the proportion of the gait cycle spent in double limb support (ICC (2,1)=0.44-0.57). The reliability of repeated measures for the GAITRite was good at preferred and fast speed for speed (ICC (3,1)=0.93-0.94), cadence (ICC (3,1)=0.92-0.94), stride length (ICC (3,1)=0.97), single support (ICC (3,1)=0.85-0.93) and the proportion of the gait cycle spent in double limb support (ICC (3,1)=0.89-0.92). The repeatability of the GAITRite measures were more variable at slow speed (ICC (3,1)=0.76-0.91). These results indicate that the GAITRite system has strong concurrent validity and test retest reliability, in addition to being a portable, simple clinical tool for the objective assessment of gait.