Schematic diagram showing the current understanding of the role of complement activation in the pathophysiology associated with traumatic spinal cord injury (SCI). Mechanical damage to the spinal cord causes neuronal cell death and disruption of the blood-spinal cord barrier (BSB). This primary damage triggers a potent inflammatory response and initiates complement activation. Although complement activation may aid the clearance of cellular debris through opsonisation, it is also known to potentiate injury beyond the site of trauma through e.g. the opsonins C1q, C3b and MAC, which can promote clearance of only mildly compromised cells and thus contribute to secondary demyelination and apoptosis. Known functions of complement in the pathology of SCI are shown in italics; a green font colour indicates a putative reparative role, whereas a red font points towards an injurious role, 1, 2, 3, 4, 5, 6, 7[4, 94].