No abstract

A rare case of provoked anal penetration of an 11-year-old boy by a male German shepherd dog was confirmed by the results of morphological, serological and molecular genetic investigations. These results were of great importance to refute the suspicion on two adults. Some serious doubts remained in the version of the course of the event as presented by the boy. Some weeks later when confronted by a psychologist, the boy admitted having deliberately stimulated the dog manually and caused the animal to penetrate him.

Experimental studies have shown that diffuse axonal injury is usually induced by positive or negative acceleration mechanisms. In order to determine the reliability of axonal injury (AI) as a marker of this type of traumatic insult, we compared cases of trauma-induced focal cortical hemorrhage without dural involvement (n = 67) with cases of trauma-induced subdural bleeding without cortical hemorrhage (n = 26). Both groups exhibited a wide range of post-traumatic survival times. The injuries in the first group were caused mainly by direct impact to the head, those in the second by acceleration/deceleration mechanisms. The investigations were based primarily on immunohistochemical demonstration of antibodies targeted to beta-amyloid precursor protein (beta-APP) in the pons as a marker of AI and the results were assessed semiquantitatively. No significant differences were found between the two groups. In both groups AI was detected in 80-100% of cases with survival times of more than 3 h and two thirds of all positive cases showed pronounced positivity. Additional comparison of cases of brain death due to mechanical trauma (n = 14) with cases of brain death due to non-mechanical trauma (n = 18) also disclosed no significant intergroup differences. Finally, investigations of the pons in cases of non-traumatic death due to cerebral hypoxia/ischemia (n = 51) demonstrated AI with the same frequency as in the other groups, although the expression tended to be less pronounced. Our results confirm that beta-APP expression in the pons is a reliable indicator of AI but does not discriminate between injuries caused by traumatic strain or shearing mechanisms and secondary damage due to cerebral hypoxia/ischemia or edema. In the large majority of cases with prolonged post-traumatic survival, it can therefore be assumed that AI in the pons is the consequence of primary and/or secondary events or a combination of both, as is common in non-missile head injury survived for more than 90-120 min. Therefore, positive differentiation of the type of biomechanical event based on this criterion alone is not possible.

No abstract

At the autopsy of a 25-year-old man who had died from combined morphine and cocaine intoxication, depositions of metallic mercury were incidentally found in the myocardium of the right ventricular septum and posterior wall. Deposits, toxicologically identified as mercury, were also found radiologically and histologically in the lungs. All these deposits were probably the result of intravenous injections of mercury many months previously, as is known to be done occasionally by addicts. Judging by the histological picture the greatest proportion of the mercury collected in the right ventricular cavity after injection, a smaller amount by embolization in the small pulmonary arteries. The mercury spheres which came to lie in the right ventricle then penetrated into the myocardium, moving outward and causing a chronic and partly transmural inflammatory response.