[Physiopathology of non-traumatic subarachnoid hemorrhage: loss of consciousness]

The mechanisms underlying the loss of consciousness following the SAH can be only hypothesized at present time. The more convincing hypothesis appears to be the role of a cerebral circulatory insufficiency. Such an hypothesis stems from the following chain of events: 1) immediate increase of the intracranial pressure; 2) simultaneous constriction of the arteries of the poligone of Willis (early vasospasm); 3) decrease of the cerebral perfusion pressure; 4) cerebral ischemia. Different cerebral regions can be affected by the ischemia according to the prevalent location of the SAH, as for instance brain stem or telencephalon; consequently, different pathophysiological modalities can be responsible for the consciousness impairment. The entity of the SAH and of the consequent events responsible for the cerebral ischemia, influence the severity and reversibility of the loss of consciousness.