Mechanical and pathophysiological aspects of acute spinal cord trauma

Experimental spinal cord trauma is studied with the purpose of better understanding and of finding better treatments for clinically occurring spinal cord trauma. In recent years major new insights have occurred in the pathophysiology of spinal cord trauma. A large amount of research has been carried out in experimental spinal cord trauma. It has mainly focused on vascular aspects of pathophysiology and on treatment. No generally accepted, very successful therapy for clinical use has emerged from this data. In addition, quite a few therapies which have been postulated to work have not yet been tested clinically. Finally the experimental models that have been used vary tremendously and standardisation is need ed. In this standardised model the influence of variables should be clear. The main pathophysiological phenomena that occur are rupture of cell membranes and microvessels. Microvessel rupture leads to free radical formation to thrombocyte aggregation and vessel obstruction. Cell oxygenation becomes impaired and eventually cell death occurs. This can be observed especially in the spinal cord grey matter. Cell membrane rupture leads to Ca 2+ ‐influx, neurotoxic firing with glutamate release and the activation of the arachidonic acid cascade. This results in production of thromboxanes, prostaglandins and prostacyclins. These actuate thrombocyte aggregation serotonin release, vasoconstriction and oedem and lead to cell anoxia and cell death. All processes are completed within 24 hours after which regeneration takes place.