High cervical lateral spinal cord injury results in long-term ipsilateral hemidiaphragm paralysis.

Although axon regeneration is limited in the central nervous system, partial lesions of the spinal cord induce neuroplasticity processes that can lead to spontaneous functional improvement. To determine whether such compensatory mechanisms occur in the respiratory system, we analyzed the incidence of partial injury of the cervical spinal cord on diaphragm activity in adult rats. We show that a section of the lateral area of the C2 cervical spinal cord induces complete phrenic nerve inactivation and ipsilateral hemidiaphragm paralysis, whereas medial or dorsolateral sections had only a moderate effect on respiratory activity. In the case of lateral hemisection, activity of the ipsilateral phrenic nerve was partially restored after a lapse of 3 months. No spontaneous diaphragm recovery was observed, however, even after a lapse of several months in the case of hemisection or lateral section. Ipsilateral hemidiaphragm activity could however be restored after transection of the contralateral phrenic nerve, by activation of the "crossed phrenic phenomenon" (involving activation of previously latent respiratory contralateral pathways crossing the midline). These data suggest that the respiratory system develops important long-term plasticity processes at the level of phrenic motoneuron innervation. However, they do not by themselves allow substantial diaphragm recovery, underscoring the continued need for developing repair strategies. These studies also validates the use of the respiratory system as a model to evaluate the functional incidence of repair strategies not only after hemisection but also after more limited sectioning restricted to the lateral side of the cervical cord.