The SCIentinel study - prospective multicenter study to define the spinal cord injury-induced immune depression syndrome (SCI-IDS) - study protocol and interim feasibility data

Marcel A Kopp, Claudia Druschel, Christian Meisel, Thomas Liebscher, Erik Prilipp, Ralf Watzlawick, Paolo Cinelli, Andreas Niedeggen, Klaus-Dieter Schaser, Guido A Wanner, Armin Curt, Gertraut Lindemann, Natalia Nugaeva, Michael G Fehlings, Peter Vajkoczy, Mario Cabraja, Julius Dengler, Wolfgang Ertel, Axel Ekkernkamp, Peter Martus, Hans-Dieter Volk, Nadine Unterwalder, Uwe Kölsch, Benedikt Brommer, Rick C Hellmann, Ramin R Ossami Saidy, Ines Laginha, Harald Prüss, Vieri Failli, Ulrich Dirnagl, Jan M Schwab

Infections are the leading cause of death in the acute phase following spinal cord injury and qualify as independent risk factor for poor neurological outcome ("disease modifying factor"). The enhanced susceptibility for infections is not stringently explained by the increased risk of aspiration in tetraplegic patients, neurogenic bladder dysfunction, or by high-dose methylprednisolone treatment. Experimental and clinical pilot data suggest that spinal cord injury disrupts the balanced interplay between the central nervous system and the immune system. The primary hypothesis is that the Spinal Cord Injury-induced Immune Depression Syndrome (SCI-IDS) is 'neurogenic' including deactivation of adaptive and innate immunity with decreased HLA-DR expression on monocytes as a key surrogate parameter. Secondary hypotheses are that the Immune Depression Syndrome is i) injury level- and ii) severity-dependent, iii) triggers transient lymphopenia, and iv) causes qualitative functional leukocyte deficits, which may endure the post-acute phase after spinal cord injury.