Experimental intracranial pressure gradients in the human skull.

Cerebral concussion, post-traumatic unconsciousness with associated vasomotor, cardiac, and respiratory changes, has been the subject of conjecture and investigation for many years. The mechanism by which this state is produced is not entirely clear, but many authors agree that the final common pathway of concussion must implicate the brain-stem, reticular formation, and medulla. The production of unconsciousness with associated cardiovascular and respiratory changes may result from the application of increased intracranial pressure over many time scales. A slowly expanding tumour or subdural haematoma will produce these changes over days to weeks. A rapidly expanding epidural haematoma will produce the syndrome in hours. Cerebral concussion produces similar changes, brought about rapidly by the great magnitude of acceleration and deformation of the skull resulting from impact. There seems little reason to doubt that all forms produce unconsciousness and vital function changes through a final common path, i.e., the reticular formation and medulla. Evidence continues to accumulate that the effect of a sudden increase in intracranial pressure at the time of an impact is related to the patho-physiology of concussion, and may be due to acceleration or deceleration forces or to deformations of the skull during impact. Presumably, a combination of these two effects occurs in most head injury, both experimental and clinical. Since 1944, we have advocated the presence of a pressure gradient across the intracranial space following trauma (Gurdjian and Lissner, 1944). Many authors (Braquehaye, 1895; Chipault and Braquehaye, 1895; Goggio, 1941; Gurdjian and Lissner, 1944; Gross, 1958; Sellier and Unterharnscheidt, 1963; Lindgren, 1964; Roberts, Hodgson, and Thomas, 1966) have observed an increase in intracranial pressure on the side of the impact while the intracranial pressure of the opposite pole is decreased. Goggio and Unterharnscheidt have