Abstract
Spinal cord injury often results into severe neurological deficits. Currently, there is no treatment available which can reverse the damage. Cell transplantation is a novel treatment strategy which has shown promising results in animal models of spinal cord injury. We administered fifty six chronic cervical spinal cord injury patients with autologous bone marrow mononuclear cells, intrathecally. As a part of the protocol, all the patients also underwent rehabilitation along with cell transplantation. On a mean follow up of 2 years ± 1 month, symptoms such as trunk stability, sitting balance, trunk muscle strength, upper limb strength, standing balance, deep touch sensation, bladder sensation, spasticity and walking balance demonstrated improvements. On performing McNemars test, a significant association was found between the improvements in these symptoms and the intervention. The improvement in Functional Independence Measure (FIM) scores was statistically significant using Wilcoxon Signed Rank test. A detailed analysis of factors such as age, cause of injury, chronicity of injury and rehabilitation before the intervention was performed. Here, we also compare this chronic cervical SCI group with chronic thoracolumbar SCI patients of our previous study. Though functional improvements were observed at greater extent in chronic thoracolumbar SCI group, the results in chronic cervical SCI group were also significant. Cell transplantation may promote neurofunctional recovery and improve the quality of life of the patients with chronic cervical spinal cord injury.
Highlights
An injury to spinal cord often results into a severe neurological deficit
The protocol of the study was approved by The Institutional Committee for Stem Cell Research and Therapy (IC-SCRT) in accordance to the Indian Council of Medical Research (ICMR) guidelines. 56 cases of cervical spinal cord injury (SCI) were included in the study
The underlying pathophysiology of spinal cord injury majorly includes a primary mechanical insult followed by a secondary cascade which includes ischemia, free radical formation, death of oligodendrocytes, release of myelin associated inhibitory molecules, glial scar formation, etc which may inhibit the regeneration of axons [14]
Summary
An injury to spinal cord often results into a severe neurological deficit. The spinal cord is either completely disrupted or at times there is contusion, compression or penetration of the spinal cord which can lead into necrosis, axonal loss, glial scarring, etc [1]. The demyelination of axons may lead to a permanent loss of sensorimotor functions [2]. The recovery after spinal cord injury (SCI) is restricted as intrinsic neurogenesis and replacement of disrupted myelin rarely occurs in the CNS. The spontaneous reestablishment of neural connectivity is difficult [3]. The scar consists of axonal growth inhibitors which further limits the repair process [4]
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