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A Murine Model of Cervical Spinal Cord Injury to Study Post-lesional Respiratory Neuroplasticity
Published on: May 28, 2014
Rewiring the Lung-CNS Axis After Spinal Cord Injury
HaiRong Wu1, Xiaolong Li1, Wenjun Zhao1
1Wuxi Affiliated Hospital of Nanjing University of Chinese Medicine., Wuxi, 214071, People's Republic of China.
None:
Spinal cord injury (SCI) is a catastrophic disorder of the central nervous system, most commonly resulting from traumatic events such as motor vehicle collisions or falls, but it can also arise from non-traumatic causes including neoplastic, infectious, or degenerative diseases. Respiratory complications are among the most frequent and life-threatening sequelae of SCI. In the acute phase, up to 80% of patients experience respiratory dysfunction, including pneumonia, atelectasis, and respiratory failure. These issues are particularly pronounced in individuals with high cervical injuries, where diaphragmatic and intercostal muscle paralysis impairs effective ventilation and clearance of secretions, substantially increasing the risk of infection. Emerging evidence underscores the bidirectional interplay between pulmonary pathology and central nervous system injury. SCI-induced autonomic dysfunction alters immune regulation, heightening susceptibility to pulmonary infections. Conversely, pulmonary complications can amplify systemic inflammatory responses, which may exacerbate neurological deterioration. Understanding the complex interactions between respiratory complications and SCI pathophysiology is essential for improving patient outcomes. This review therefore focuses on elucidating the mechanisms of pulmonary complications post-SCI and exploring therapeutic strategies to mitigate their impact on neurological recovery.

