Ruptures of parasagittal bridging veins in killed victims (passengers) of motorvehicle accidents

Experimental data and clinical as well as postmortem experiences have indic ated that subdural hematomas are less frequent in acceleration injuries in traffic accidents compared to falls or assaults. The present report demonst rates that this does not hold true in the same way for bridging vein ruptur es (one of the predominant causes for subdural bleedings). Ruptures of thes e vessels without subdural bleeding (SDB) are only seldom mentioned in the literature. However, if no SDB is present, no one will look for these struc tures. In our institute a systematic analysis of the bridging veins in all cases of lethal blunt head injury is made: prior to the careful morphologic al preparation we investigate these vessels by radiographic imaging after f illing with contrast medium. 6 car passengers (age between 4 and 31 years) which suffered a lethal head injury were examined in the last year. 2 victi ms had impressed fractures with cerebral compression injuries. In 1 case th e base of the skull was broken and in 3 cases no skull fracture was present ; no serious focal brain injury had occured in these 4 cases,but 3 victims had signs of diffuse brain injury. In 5 cases a direct impact of the head a gainst the interior of the car was obvious. In 5 cases ruptures of several bridging veins could be demonstrated. In one case (survival for 3 days) a m inor SDB (20 ml) was present and the ruptures had been closed by thrombosis ; another victim died at the scene. The other 3 victims survived between 4 and 15 hours without developing SDB and without closing of the ruptures by thrombosis. This combination is surprising and shows that our knowledge con cerning the relationship between bridging vein ruptures and SDB is restrict ed. The frequency of bridging vein lesions in severe head injuries is likel y underestimated in the clinical as well as in the postmortem literature. A rapid increase of intracranial pressure after the accident resulting in a collapse of the cerebral circulation is probably responsible for the absenc e of the SDB in the presented cases.