Detection of diphenhydramine in autolytic brain tissue in poison-induced brain death syndrome

A case of accidental monointoxication caused by diphenhydramine is reported. Having taken 12 dragées of Neo-Emedyl (50 mg diphenhydramine), an 18-month-old girl showed the following symptoms: generalized erythema, dyspnoea, vomiting, hyperpyrexia, tremor, convulsions, coma, respiratory arrest and absence of reflexes. Computed tomography (CT) suggested a massive cerebral oedema. Her electroencephalogram was abnormally diffused at first; later on, it flattened significantly and became isoelectric between the 14th day and the final stoppage of circulation (after 5 weeks). Autopsy revealed total necrosis of the brain, with the venous cerebral blood vessels being thrombosed (the morphological basis for dissociated cerebral death). In autolysed brain tissue, diphenhydramine was detected at a concentration of 30 ng/g by GC/MS (gas chromatography, mass spectrometry); the concentration of the substance was less than 10 ng/g in the liver. The relatively high concentration in the brain was due to the previous blocking of the circulation. Cerebral death syndrome caused by intoxication offers the chance of detecting measurable amounts of the unchanged drug in autolysed brain tissue.     

Sudden death resulting from epidermoid cyst of the brain

Epidermoid cysts of the brain are rare tumor-like lesions, most often of maldevelopmental origin. They are benign in nature, causing symptoms depending on their localization. Surgical resection leads to excellent results. A case is reported of a 68-year-old-man who died suddenly and unexpectedly. Postmortem examination revealed signs of central dysregulation and a bifrontal epidermoid cyst. To the authors' knowledge, death resulting from epidermoid cyst of the brain has not been reported so far.     

A critique on the concept of "brain death"

Since the concept of "brain death" was introduced in medical terminology, enough evidence has come to light to show that the concept is based on an unclear and incoherent theory. The "brain death" concept suffers by internal inconsistencies in both the tests-criterion and the criterion-definition relationships. It is also evident that there are residual vegetative functions in "brain dead" patients. Since the content of consciousness is inaccessible in these patients who are in a profound coma, the diagnosis of "brain death" is based on an unproved hypothesis. A critical evaluation of the role and the limitations of the confirmatory tests in the diagnosis of "brain death" is attempted. Finally it is pointed out that a holistic approach to the problem of "brain death" in humans should necessarily include the inspection of the content of consciousness.     

Complex brain malformation as a rare cause of neonatal death

A dead female neonate was brought to a children's hospital by the mother. The MRI scan suggested a malformation of the brain. Because of the other circumstances of the case (the mother left the hospital unauthorizedly), a forensic autopsy was ordered, in the course of which the brain was removed while the head was totally immersed in water. This method, which was introduced by Prahlow et al., helps to obtain intact brain specimens without interfering with the necessary medicolegal preparations to determine whether the child was born alive. Neuropathological examinations classified the cerebral malformation as (lethal) lissencephaly. Further investigations showed that the mother had lived in Germany without a residence permit.     

自愿适用脑死亡标准的法律设计

自愿适用脑死亡标准是指根据完全民事行为能力人的真实意思表示,尊重其意愿,对其适用脑死亡标准作为死亡判断标准。自愿适用脑死亡标准具有自愿性、科学性和复杂性。预立自愿适用脑死亡标准意思表示制度对自愿适用脑死亡标准有一定的制度意义。     

脑死亡脑外器官病理变化的实验性研究

选用34只家猫研究脑死亡后脑外器官（心、肺、肝、肾）的病理学变化。经任内持续加压造成脑死亡模型,根据人工维持心跳和呼吸的时间分3组。结果脑死亡后出现：（1）缺血性心肌病变,心内膜下出血,心肌局灶性坏死及线粒体、微丝破坏;（2）肺淤血,水肿,间质炎症;（3）肝小叶中央带、中间带缺血性病变;（4）肾近曲小管缺血性病变。     

Acallosal brain in sudden infant death syndrome (SIDS).

A definitive explanation of "crib" or "cot" death remains unknown. An unusual incidental autopsy finding of agenesis of the corpus callosum in a case presenting as "near miss" sudden infant death syndrome (SIDS) is discussed. Hitherto, only a single case associated with SIDS has been reported in the literature. The condition may be easily missed outside the interest in neuropathology.     

Sevoflurane concentrations in blood, brain, and lung after sevoflurane-induced death

Sevoflurane concentrations in blood, brain, and lung were measured in an individual apparently dying from sevoflurane inhalation. Sevoflurane is a volatile nonflammable fluorinated methyl isopropyl ether inhaled anesthetic, chemically related to desflurane and isoflurane. The incidence of abuse of sevoflurane is lower than that of other drugs of abuse possibly due to its inaccessibility to the general public and less pleasurable and addicting effects. The dead subject was an anesthetist found prone in bed holding an empty bottle of sevoflurane (Ultane). Serum, urine, and liver were screened for numerous drugs and metabolites using enzyme immunoassays and gas chromatography-mass spectrometry. Analysis did not reveal presence of any drug, including ethanol, other than sevoflurane. Sevoflurane was determined by headspace gas chromatography and revealed concentrations of 15 microg/mL in blood and 130 mg/kg in brain and lung. Autopsy revealed pulmonary edema and frothing in the lung, pathological findings associated with death by sevoflurane or hypoxia. The cause of death was ruled as sevoflurane toxicity and the manner of death as accident.     

Early and late meningeal reaction to trauma after long-term brain death.

We examined histologically the meninges adherent to traumatic lesions of a patient with brain death sustained for 101 days and observed both early and late reactions of wound healing at the same site of the dura mater. Some parts of the dura mater were thick and histological examinations revealed formation of new vessels and fibrosis with strong positive reaction for iron and fat staining. We also observed fresh haemorrhage and some cell infiltration in the dura and fresh haemorrhage in a small piece of necrotic brain tissue adhered to the dura mater, while other areas of the brain tissue were completely necrotic, enabling the sites of head injury to be localised. These observations suggested that the blood flow in the dura mater fluctuates due to a change of microenvironment, which probably causes repeated secondary petechial haemorrhages in the dura and its adherent necrotic brain tissue, even 101 days after brain death.     

Autopsy at 2 months after death: brain is satisfactorily preserved for neuropathology

Disclosure of neurological disorders by neuropathological examination may be one important aim of forensic autopsies. There are insufficient data on human brain tissue preservation after prolonged postmortem periods. Here, we describe neuropathological findings in a brain of a 77-year-old woman that was fixed at autopsy 2 months after death. The body had been stored in a cooling chamber at 3 degrees C temperature. Gross inspection of the brain was satisfactorily possible. Histomorphology was excellently preserved. Many histochemical and immunohistochemical stains allowed satisfactory neuropathological evaluation of brain tissue and the diagnosis of Alzheimer's disease. Nevertheless, some immunohistochemical stainings repeatedly yielded negative or suboptimal results. We conclude that neuropathological examination of human brain tissue extracted from the skull and fixed after prolonged body storage in a cool environment is feasible for forensic diagnosis of neurological disorders even several months after death. However, in such cases the significance of negative immunohistochemical staining results must be interpreted with caution.     

Sudden death in a 35-year-old man with occult malformation of the brain and aseptic meningitis

A 35-year-old man was found dead by his wife. He was reported to have had symptoms of a common cold the week preceding his death. The medicolegal autopsy yielded signs of central dysregulation (ectasia of the urinary bladder and rectum, dystelectasis of the lungs) together with marked brain edema and fresh bite marks on the tongue. The cause of death was presumed to be lethal epileptic seizure. Neuropathologic examination revealed neuronal nodular heterotopia as well as discrete lymphocytic meningitis (aseptic meningitis). The death was most probably caused by the combination of the meningitis with the occult malformation, leading to a lowered seizure threshold and subsequent lethal seizure. The morphologic findings of this case are presented, and the probable mechanisms of death are discussed.