gms | German Medical Science

Respiratory insufficiency still contributes to increased mortality and morbidity following human spinal cord injury. Experimental high cervical complete or partial hemisections are currently available but a model of cervical contusion is lacking probably because of high mortality due to injury of the descending bulbospinal respiratory pathways commanding the phrenic motoneurons. The present work reports a new cervical spinal cord contusion model inducing a persistent ipsilateral diaphragmatic paralysis.

The cervical spinal cord of adult Sprague-Dawley rats was exposed and a spinal “1 mm³ - dorsal gap” was performed at the left C2 level. At this level a metallic impactor was used to compress unilaterally the spinal cord. A 20 g-weight was dropped from a 100 mm height along the impactor and the compression was maintained during 30 minutes.

Electrophysiology showed a complete ipsilateral diaphragmatic paralysis and a silent corresponding phrenic activity. Such a respiratory deficit started just after the compression and was still persistent 7 days later. Morphology showed damaged ventro-lateral columns. The “dorsal gap” appeared necessary 1) to prevent mechanical absorption of the spinal shock by the dorsal columns, 2) to target the impact drop at the ventro-lateral white matter, which included the descending respiratory pathways.

Our model of C2 lateralized contusion leads to a persistent ipsilateral respiratory deficit. This model presents the interest to injure the descending cervical respiratory pathways by multiple lesions similar to those encountered in human traumatic pathology (streching, crushing, ischemic compression, demyelination). From this model of unilateral respiratory deficit, different experimental therapeutic strategies (local spinal cord hypothermia, glial cell transplantation, neuroprotrective substances…) will be tested to improve functional recovery after cervical spinal cord trauma.