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Axonal Degeneration and Demyelination Following Traumatic Spinal Cord Injury; A Systematic Review and Meta-analysis.

07:00 EST 3rd February 2019 | BioPortfolio

Summary of "Axonal Degeneration and Demyelination Following Traumatic Spinal Cord Injury; A Systematic Review and Meta-analysis."

The pathophysiology of spinal cord injury (SCI) related processes of axonal degeneration and demyelination are poorly understood. The present systematic review and meta-analysis were performed such to establish quantitative results of animal studies regarding the role of injury severity, SCI models and level of injury on the pathophysiology of axon and myelin sheath degeneration. 39 related articles were included in the analysis. The compiled data showed that the total number of axons, number of myelinated axons, myelin sheath thickness, axonal conduction velocity, and internode length steadily decreased as time elapsed from the injury (P<0.0001). The rate of axonal retrograde degeneration was affected by SCI model and severity of the injury. Axonal degeneration was higher in injuries of the thoracic region. The SCI model and the site of the injury also affected axonal retrograde degeneration. The number of myelinated axons in the caudal region of the injury was significantly higher than the lesion site and the rostral region. The findings of the present meta-analysis show that the pathophysiology of axons and myelin sheath differ in various phases of SCI and are affected by multiple factors related to the injury.

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This article was published in the following journal.

Name: Journal of chemical neuroanatomy
ISSN: 1873-6300
Pages:

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A syndrome associated with traumatic injury to the cervical or upper thoracic regions of the spinal cord characterized by weakness in the arms with relative sparing of the legs and variable sensory loss. This condition is associated with ischemia, hemorrhage, or necrosis involving the central portions of the spinal cord. Corticospinal fibers destined for the legs are spared due to their more external location in the spinal cord. This clinical pattern may emerge during recovery from spinal shock. Deficits may be transient or permanent.

Pathologic conditions which feature SPINAL CORD damage or dysfunction, including disorders involving the meninges and perimeningeal spaces surrounding the spinal cord. Traumatic injuries, vascular diseases, infections, and inflammatory/autoimmune processes may affect the spinal cord.

Repair of the damaged neuron function after SPINAL CORD INJURY or SPINAL CORD DISEASES.

A group of disorders marked by progressive degeneration of motor neurons in the spinal cord resulting in weakness and muscular atrophy, usually without evidence of injury to the corticospinal tracts. Diseases in this category include Werdnig-Hoffmann disease and later onset SPINAL MUSCULAR ATROPHIES OF CHILDHOOD, most of which are hereditary. (Adams et al., Principles of Neurology, 6th ed, p1089)

Longitudinal cavities in the spinal cord, most often in the cervical region, which may extend for multiple spinal levels. The cavities are lined by dense, gliogenous tissue and may be associated with SPINAL CORD NEOPLASMS; spinal cord traumatic injuries; and vascular malformations. Syringomyelia is marked clinically by pain and PARESTHESIA, muscular atrophy of the hands, and analgesia with thermoanesthesia of the hands and arms, but with the tactile sense preserved (sensory dissociation). Lower extremity spasticity and incontinence may also develop. (From Adams et al., Principles of Neurology, 6th ed, p1269)

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