Immune dysfunction after spinal cord injury - A review of autonomic and neuroendocrine mechanisms.

Infections impair neurological outcome and increase mortality after spinal cord injury (SCI). Emerging data show that pathogens more easily infect individuals with SCI because SCI disrupts neural and humoral control of immune cells, culminating with the development of "SCI-induced immune deficiency syndrome" (SCI-IDS). Here, we review data that implicate autonomic dysfunction and impaired neuroendocrine signaling as key determinants of SCI-IDS. Although it is widely appreciated that mature leukocyte dysfunction is a canonical feature of SCI-IDS, new data indicate that SCI impairs the development and mobilization of immune cell precursors in bone marrow. Thus, this review will also explore how the post-injury acquisition of a "bone marrow failure syndrome" may be the earliest manifestation of SCI-IDS.