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Differentiation between accessory sutures and fractures in the skull of an infant can be difficult. Apart from the regular sutures there is a multitude of variations that may be mistaken for a fracture line. Such variations include for instance the intraparietal suture between the two ossification centers of the parietal bone or the mendosal suture between the supraoccipital and interparietal bone of the occipital squama. The presented case refers to an approximately 20-month-old female child. During autopsy, a discontinuity in the right paramedian posterior cranial fossa parallel to the internal occipital crest with connection to the foramen magnum was observed. The macroscopic findings suggested a fracture line because of its course. However, neither a hemorrhage in the soft tissue nor callus formation was discernible. The discontinuity was preserved with the adjacent parts of the occipital bone for further histological examination. In the report of a cranial CT, which was carried out five days before the child's death, an accessory suture paramedially in the right posterior cranial fossa was described. When the clinical CT records were re-evaluated, a similar discontinuity at the corresponding position on the other side was detected, though of noticeably shorter length. Additionally, the preserved occipital bone fragment including the discontinuity was histologically processed. In the radiological literature, precise (radiological) criteria for differential diagnosis are indicated. A zigzag pattern with sclerotic borders and a bilateral and fairly symmetric occurrence indicate a suture, whereas a sharp lucency with non-sclerotic edges and a unilateral occurrence indicate a fracture. Taking all the findings into account, the depicted discontinuity was regarded as an accessory suture. This case demonstrates that differentiation between a fracture and an accessory suture may be difficult in the autopsy of a child and underlines the importance of a postmortem CT examination.

Cases of death related to simple routine outpatient surgery are repeatedly reported. Minimum standards of staff and medical equipment for postoperative surveillance are deliberately ignored for economic reasons. Using two case studies this article identifies classical types of medical malpractice and organizational fault. Recommendations for criminal investigation in this type of cases are outlined for the competent authorities.

Neuropathological studies may contribute to the discovery of central nervous system complications after heart surgery and thus help to reduce the incidence of postoperative neurological or cognitive disturbances. We examined the brains of 262 such patients operated for coronary bypass, valve replacement, or heart transplantation. Circulatory disturbances (macro- and microhemorrhages, infarcts, subarachnoid hemorrhages, and hypoxemic brain damage) were present in 128 cases (49%), as the cause of death in 33 cases (12.6%). The infarcts were caused by local arteriosclerosis of brain arteries, arterial emboli originating from the operative sites or myocardial infarctions, or by fat emboli, foreign body emboli or megakaryocytic capillary emboli in rare cases. Inflammatory disturbances were present in 17 cases and consisted of fungal or bacterial septicopyemic changes (12) or of glial nodules (5) as the substrate of a viral or autoimmunencephalitis (Bickerstaff). An incidental finding was Alzheimer's disease in 37 cases (14% of the material) of elderly patients, often associated with cerebral amyloid angiopathy but not as cause of death or cause of macroscopic brain hemorrhage. Since we have conducted an autopsy study, there is a limitation to transfer the documented changes to the total group of post-cardiac surgery patients with neurologic and cognitive deficits. Contrary to some previous reports, histologically overt microembolic phenomena do not seem to play a major role in our material. On the other hand, careful scrutiny revealed non-fatal white matter microhemorrhages of varying frequency in the different groups, especially after valve operations. These as well as the occasional glial nodules, after resorption and microscarring, could well be the cause of slight neurologic and cognitive impairments.

Objective: Are ontogenetic differences in the resistance of the brain towards ischemia reflected by differences in the postischemic disturbance of cerebral protein synthesis (PS) independently from energy metabolism (EM)?, Methods: We studied hippocampal slices from immature (E60) and mature (E60) fetal guinea pigs as well as from adult guinea pigs. Cerebral EM and PS were measured during and up to 24 h after ischemia., Results: After in vitro ischemia there was no inhibition in cerebral PS in immature fetuses, a transient inhibition in mature fetuses, and a permanent inhibition in adults. During and after in vitro ischemia cerebral EM was hardly disturbed in immature fetuses. No differences in cerebral EM could be observed between mature fetuses and adults., Conclusion: Ontogenetic differences in the resistance of the brain towards ischemia are reflected by differences in the postischemic disturbance of cerebral PS. The differences between mature fetuses and adults are independent from cerebral EM.

At necropsy of fatal cases due to craniocerebral trauma it is highly recommended that the intraosseous course of the internal carotid arteries are dissected, as detected injuries of these vessels may allow improved conclusions concerning the course of death. Suitable preparation techniques are presented. On the basis of the anatomical and physiological situation as well as pathophysiological considerations the acute lethal outcome of traumatic rupture of the intraosseous part of these arteries is not to be interpreted as death by hemorrhagic/hypovolemic shock but rather as lethal cerebral hypoxia subsequent to a rapidly developing insufficiency of the brain circulation.

We report an 11-year-old child who aspirated a toy balloon causing death by asphyxia. Children who chew balloons while running and who breathe deeply or laugh at the same time are under great risk. The saliva which smears the balloon makes it easier to slide into the airway. Therefore chewing of balloons by children must be avoided because of the danger of aspiration.

The histological localization and extent of ZNS-lesions caused by perinatal hypoxia has been examined in 83 cases. The neuropsychiatrical patterns of 71 in preschool and school age children after perinatal hypoxia were also investigated. Predominantly a brain stem damage with nerve cells lesions, hemorrhages and disturbance of neuroglia are found. In 1 fourth of the cases, nerve cell damage was localized in the medulla spinalis. Intramedullar hemorrhages can be observed in 10% of the cases. 41% of the cases showed subarachnoidal bleedings. Neuropsychiatrical examinations showed varying degrees of brain stem dysfunction in accordance with neurohistological findings. 1 third of the risk children demonstrated minimal brain dysfunction. In 10% an early rehabilitation of resulted in an amelioration of the ZNS-function. Special attention should be drawn to partial ZNS-disturbance-children. The problems of therapy are discussed.

The localization and extent of nerve cell damage caused by perinatal hypoxia has been examined in 83 cases. In 54% of the cases nerve cell damage was localized in the medulla oblongata, in 40% the thalamus and in one third the substantia grisea centralis was affected by nerve cell necroses. In contrast to the phylogenetically older structures of CNS, nerve cell lesions occurred in our material only in 30% in the cerebral cortex and in 18% of our observation the cerebellar cortex. The results show, that the brain stem is especially vulnerable to perinatal hypoxia, this is at variance with hitherto existing conceptions. In a fourth part of the material, nerve cell damage was found in the medulla spinalis, especially in the columna anterior, After prolonged hypoxia the neuron-glia index in the lamina tecti deviates by 0.0491 from that following peracute anoxia. This caused by loss of nerve cells in the brain stem due to perinatal continuous hypoxia.

Reye syndrome was observed in a 5 1/2-year-old girl after an appendectomy. It was accompanied by insulin-resistant hyperglycaemia. Central adaptation failure resulted in death on the fourth day of treatment. Post mortem and histological results showed phlegmonous pancreatitis of the excretory type, apart from the established manifestations of Reye syndrome (severe cerebral oedema, excessive hepatic steatosis, moderate fatty degeneration of renal tubuli). Neuropathology revealed exclusively signs of hypoxic damage. Pancreatitis, usually necrotising or haemorrhagic, is not infrequent in Reye's syndrome. Girls are predominantly affected and pancreatitis is associated with a tendency towards sometimes serious hyperglycaemia. The possibility of this complication should be considered in the treatment of Reye syndrome.

Long-term survival after carbon monoxide intoxication has been accepted for a long time as pathognomonic for elective cerebral tissue damage, especially in cases of isolated symmetrical necrosis of the globus pallidus. The results of old bilateral necrosis in the globus pallidus are described in a case of an acute heroin death after long-term drug abuse. The evaluation of such cerebral changes is discussed as they have to be interpreted as hypoxic or oligemic tissue damage. The different causes of symmetrical necrosis of the globus pallidus that are relevant for legal medicine are compiled and discussed.

From the autopsies of one year 47 brains (10 stillborns, 28 prematures and 9 newborns) were systematically examined for hypoxemic cerebral lesions. In contrast to literature findings in 75% of the cases not only veins but also arteries showed congestions and a cerebral edema due to disturbances of circulation and permeability, predominantly caused by hypoxia. Nearly half of the cases had primary leptomeningeal hemorrhages and hemorrhages in the germinal matrix tissue; stillborns had no hemorrhages in the germinal matrix. Encephalodystrophic foci were found in 17% of the cases examined. 41 of 47 brains showed single nerve cell damage with cytolysis and 8 ones a focal nerve cell decay, especially localized in the brain-stem. They were observed equally frequent in stillborne, newborns and prematures. The polyetiologic cerebral lesions point out that birth trauma does not play the dominating role in the etiology as hitherto supposed. Hypoxia gets an increasing importance. Frequently birth traumatic and hypoxemic cerebral lesions are associated.

The different aspects of brain death are discussed. It is pointed out that the diagnosis of poisoning as the cause of brain death can be checked by toxicological examination of brain tissue and of blood in the sinus of the dura mater, since the metabolism in the brain and sinus blood is markedly reduced while drugs and toxic substances continue to be broken down in the other organs. Particular importance attaches to this difference in the case of crimes of violence creating conditions that predispose to brain death when the significance of a further violent act, e.g. stabbing with resultant haemorrhage, has to be assessed. The simple vital reaction of bleeding does not of itself constitute proof in such a situation, unless it is possible to say with a good degree of certainty that brain death did not occur at the moment when the victim was stabbed. It may, however, be possible to state that brain death that could have been caused by violence has not yet occurred if complex vital reactions, such as inflammation of a wound, are seen.

4 deaths due to aspiration of a nasal pack with a similar sequence of events are reported to draw attention to the increased risk of nasal packing under general anaesthesia. The legal questions of anticipating the problems, avoidance of the incident, observance of the required degree of care and the distribution of the responsibility between the surgery and the anaesthetist are discussed.

A para III was found to have a constantly silent CTG. In two fetal blood analyses the pH was normal. During the first few hours post partum the infant had rapidly increasing neurologic disturbances with violent convulsions and coma. As early as on the first day of life the computer tomogram showed extensive, later persistent hypodense zones corresponding to severe asphyxial cerebral necrosis. Based an the course of CT changes it has to be assumed that the hypoxic crisis occurred some days prior to the onset of labor. Pathologic changes in the umbilical cord indicated that the cause could have been a transitory occlusion in utero. The computer tomogram enables cerebral insults to be dated more accurately. If prenatal hypoxia occurs repeatedly new methods of prevention must be sought.

The periodicity of paroxysmal wave complexes in EEG after acute cerebral anoxia with special reference to the dynamics of period duration (alteration of Zeitmass) is described in case 20 hours before isoelectric tracing. The completely asynchronous feature of paroxysmal events within certain limits of period duration in both hemispheres is a rare condition. Late and pure cortical electrogenesis is suggested. Short and long EEG- periods in similar and different pathological processes and functional states are compared with respect to topography of lesions. Subcortical interactions and extraneuronal influences upon periodicty are discussed. The parameters "complex wave and periodicity" in EEG and the dynamics respectively are a matter of serial investigations for better understanding pathophysiology and prognostic value.