Abstract
Cervical spondylotic myelopathy (CSM) is the most common spinal cord disorder and a major cause of disability in adults. Improvements following surgical decompression are limited and patients often remain severely disabled. Post mortem studies indicate that CSM is associated with profound axonal loss. However, our understanding of the pathophysiology of CSM remains limited.To investigate the hypothesis that axonal plasticity plays a role in the recovery following surgical decompression, we adopted a novel preclinical model of mild to moderate CSM. Spinal cord compression resulted in significant locomotor deterioration, increased expression of the axonal injury marker APP, and loss of serotonergic fibres. Surgical decompression partially reversed the deficits and attenuated APP expression. Decompression was also associated with axonal sprouting, reflected in the restoration of serotonergic fibres and an increase of GAP43 expression. The re-expression of synaptophysin indicated the restoration of functional synapses following decompression. Promoting axonal plasticity may therefore be a therapeutic strategy for promoting neurological recovery in CSM.Electronic supplementary materialThe online version of this article (doi:10.1186/s40478-016-0359-7) contains supplementary material, which is available to authorized users.
Highlights
Cervical Spondylotic Myelopathy (CSM) is the most common spinal cord disorder and one of the major causes of disability in adulthood [35]
We developed a novel rat model of mild to moderate CSM in which transient cervical spinal cord compression is induced by sublaminar insertion of a water-absorbing polyurethane elastomer
Chronic compression impaired motor function that was partly reversed by decompression A pre-clinical model of CSM was established by surgically inserting an expandable polymer in the dorsal cervical epidural space of C3/4
Summary
Cervical Spondylotic Myelopathy (CSM) is the most common spinal cord disorder and one of the major causes of disability in adulthood [35]. It is induced by degenerative changes occurring in the intervertebral discs triggering bony and ligamentous hypertrophy, which result in narrowing of the cervical canal. Tethering and compression cause injury of the spinal cord and increasing neurological deficits [2, 3]. Partial reversal of symptoms occurs after surgery over 3–12 months. This time frame implicates inherent regenerative or plastic changes within the spinal cord. Many patients remain disabled [29], and there are nonsurgical treatments available for improving outcome for CSM
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