Globus Pallidus Necrosis Unrelated to Carbon Monoxide Poisoning: Retrospective Analysis of 27 Cases of Basal Ganglia Necrosis

Bilateral globus pallidus necrosis is said to be characteristic of carbon monoxide (CO) poisoning. However, there has been no scientific test of this hypothesis. To examine the assertion that globus pallidus necrosis is typical of CO poisoning, this study examined autopsy cases from the King County Medical Examiner's Office (KCMEO) between 1994 and 2013. Twenty-seven cases with bilateral basal ganglia lesions were identified and examined for associated or causative disease or injury with the following results: 10 cases of drug overdose, seven heart disease, three asphyxia, two chronic ethanolism, two Huntington-like disorder, and one case each of remote trauma, rheumatic heart disease, and cerebral artery gas embolism. Additionally, review of all known cases at KCMEO of CO poisoning found no evidence of globus pallidus or basal ganglia necrosis. Thus, this study provides no support for the assertion that globus pallidus necrosis is characteristic of CO poisoning.     

Evaluation of human brain damage in fire fatality by quantification of basic fibroblast growth factor (bFGF), glial fibrillary acidic protein (GFAP) and single-stranded DNA (ssDNA) immunoreactivities

Burns and inhalation of toxic gases, including carbon monoxide (CO) and cyanide, which are produced by combustion, are major factors involved in fire death. The present study immunohistochemically investigated basic fibroblast growth factor (bFGF), glial fibrillary acidic protein (GFAP) and single-stranded DNA (ssDNA) in the brains of fire fatalities (n=49) to examine the differences between fatal burns and CO intoxication, compared with those in cardiac deaths (n=24) and mechanical asphyxiation cases (n=23). In acute fire fatality, neuronal ssDNA immunopositivity in the cerebral cortex of the parietal lobe was high in both fatal burns and fatal CO intoxication, but that of the pallidum was higher for CO intoxication than for burns. The number of neurons was decreased in prolonged fire deaths, irrespective of the severity of burns or CO intoxication, but glias were increased in cases of fatal burns. Prolonged deaths due to burns had a higher glial bFGF immunopositivity in the cortex and white matter, higher and lower glial GFAP immunopositivity in the cortex and white matter, respectively, and a low neuronal ssDNA immunopositivity in the cerebral cortex and hippocampus. In prolonged deaths due to CO intoxication, however, glial bFGF and GFAP immunopositivities were low at each site, but neuronal ssDNA immunopositivity showed a higher value. These observations suggest increased cerebral neuronal ssDNA immunopositivity to be a finding of vitality in acute fire death, and a neuronal loss accompanied by active glial responses after severe burns, and a neuronal loss and progressive apoptosis without glial responses after CO intoxication to be characteristic in prolonged death.     

Carbon Monoxide Poisoning and Death in a Large Enclosed Ventilated Area

A 55‐year‐old man with a medical history of tobacco use suddenly collapsed while power washing an empty indoor pool in a hotel. The decedent was transported to the local hospital where he was pronounced. A postmortem examination revealed atherosclerotic heart disease and bilateral pulmonary edema and congestion. A postmortem blood carbon monoxide (CO) level was 27% saturation, and a CO performed on hospital admission blood was 49% saturation. CO poisoning is a common cause of toxicological morbidity and mortality in the United States. The circumstances most often occur in an enclosed environment and may be intentional or unintentional. CO poisoning has been reported in open, well‐ventilated spaces, but rarely results in death. A warning label was present on the engine clearly stating the dangers of CO emission. However, there was a false sense of security due to the large size of the pool room and the presence of industrial blowers that were being used for ventilation.     

Histomorphometric characteristic of human brain in acute alcoholic intoxication

Different brain sections were studied in 20 subjects, who died of ethanol intoxication and in 14 subjects who died of injuries of the heart and main vessels, in order to detect histological changes in the brain and for the purpose of defining spatial and quantitative ratios between cerebral tissue structures in alcoholic intoxication. Different histological, stereometric and morphometric tools were made use of. It was demonstrated that, in alcoholic intoxication, there occur severe disorders of the circulation with affection of vessels in the brain; there are also dystrophic and necrotic changes in neurocytes, glial cells and white substance. The square of neurons shrinks due to death of some of them in the cortex of hemispheres, thalamus and cerebellum. As for the medulla, they are more resistant, there, to ethanol. The diameter of capillaries in the studied brain sections diminishes due to a reduced tonus of cerebral arteries; the quantity of such vessels increases within a standard area, which is conditioned by the compensatory opening of reserve capillaries. All this can be important in dealing with issues of thanatogenesis and of forensic medical diagnosis in death of alcoholic intoxication.     

Pseudolaminar necrosis in cyanide intoxication: a neuropathology case report

We describe the gross and microscopic neuropathological changes in the brain of a 17-year-old male who died 4 days after being poisoned with cyanide. Previous reports indicate that following cyanide intoxication, the brain develops diffuse hypoxic/ischemic changes, predominantly of the basal ganglia. The case we describe here had similar features but in addition showed striking laminar necrosis of the cerebral cortex. This finding in cyanide poisoning has been previously demonstrated by neuroimaging, but not pathologically.     

Subarachnoid Hemorrhage and Carbon Monoxide Exposure: Accidental Association or Fatal Link?

This case study reports a fatal subarachnoid hemorrhage (SAH) with concomitant accidental carbon monoxide (CO) exposure in 32‐year‐old man. Autopsy results indicated an antemortem aspiration of smoke, and a massive SAH was identified as the cause of death. Intriguingly, the carboxyhemoglobin level was 30%, suggesting that CO could have played a specific role. Intracranial hemorrhages following CO exposure in brain areas and tissues such as the basal ganglia, globus pallidus, or white matter are rare, but well characterized, whereas SAH related to CO exposure has not been previously described. In this case report, the possible role of CO, either as a primary cause or as a facilitating factor, in the pathogenesis of SAH is discussed. In particular, we propose the hypothesis that the excessive vasodilating effects produced by CO on the cerebral endothelium results in consequential loss of microvascular integrity.     

Acute and subacute fetal CO-poisoning

The main principles of placental CO exchange in cases of CO intoxications of pregnant women are shown. Fetal COHb lags behind maternal COHb by several hours depending on the exposure pattern. During CO elimination the fetal COHb levels again lag behind the mother's. A case of a lethal CO intoxication of a pregnant woman, mens IX, with exposure time of 10-12 h and COHb of 75% for the mother and 46% for the fetus allows to make conclusions about process of intoxication and about different times of death for mother and fetus. In highly acute lethal intoxications of the mother COHb in fetal blood is low or negative. A vital danger of the fetus is not probable when mother survived a short CO exposure.     

A Case of Nonfatal Intoxication Associated with the Recreational use of Diphenidine

Diphenidine is a dissociative drug that shows several psychotropic effects including euphoria, shifts in perception of reality, hallucinations, and transient anterograde amnesia. In this study, a case of acute intoxication occurring after diphenidine intake is reported. A 30‐year‐old Caucasian male was hospitalized after he was found in a confused and agitated state and unable to communicate. The physical examination displayed tachycardia, miotic pupils, and increased both body temperature and respiratory rate. After a liquid–liquid extraction procedure, GC/MS analysis revealed the presence of diphenidine in plasma and urine at concentrations of 308 and 631 ng/mL, respectively. Methylphenidate and diclazepam were also detected in the plasma. The clinical progress of the patient was favorable, and his symptoms were cured with a symptomatic treatment. The combined circumstantial elements and toxicological results of the case reported revealed the occurrence of an acute intoxication ascribable to the recreational abuse of diphenidine.     

Single-stranded DNA as an immunohistochemical marker of neuronal damage in human brain: an analysis of autopsy material with regard to the cause of death

Single-stranded DNA (ssDNA) is a marker of apoptosis and programmed cell death, which appears prior to DNA fragmentation during delayed neuronal death. The present study investigated the immunohistochemical distribution of ssDNA in the brain to investigate apoptotic neuronal damage with regard to the cause of death in medicolegal autopsy cases (n=305). Neuronal immunopositivity for ssDNA was globally detected in the brain, independent of the age, gender of subjects and postmortem interval, and depended on the cause of death. Higher positivity was typically found in the pallidum for delayed brain injury death and fatal carbon monoxide intoxication, and in the cerebral cortex, pallidum and substantia nigra for drug intoxication. For mechanical asphyxiation, a high positivity was detected in the cerebral cortex and pallidum, while the positivity was low in the substantia nigra. The neuronal ssDNA increased during the survival period within about 24h at each site, depending on the type of brain injury, and in the substantia nigra for other blunt injuries. The neuronal positivity was usually lower for drowning and acute ischemic disease. Topographical analysis of ssDNA-positive neurons may contribute to investigating the cause of brain damage and survival period after a fatal insult.     

Morphofunctional interaction of adrenal zones in acute lethal carbon monoxide poisoning in people with alcoholic intoxication

Morphological examination of human epinephroses at acute lethal poisoning with carbon monoxide against a background of alcoholic intoxication was done. Acute lethal poisoning with carbon monoxide decreases effect of alcoholic intoxication upon morphofunctional state of epinephroses and disorders characteristics of interzonal interaction. Interaction between zones of one epinephros recedes but interaction between both glands increases.     

Electroretinogram and Histopathologic Changes of the Retina after Methanol Intoxication

In order to study the functional and structural alterations of the retina in SD rat model after methanol intoxication,35 rats were divided randomly into five groups administrated with saline,3-day high dose,7-day high dose,3-day low dose and 7-day low dose methanol separately.The retinal function of each group was assessed by flash electroretinogram(F-ERG) 3 and 7 days after methanol poisoning.The microstructure and ultrastructure of the retina were observed at the same time.The high-dose methanol intoxication induced irreversible retinal functional and structural damages 3 days after poisoning,which included prolonged latency and reduced amplitude of the Max-reaction of F-ERG.These injuries were aggravated 7 days after poisoning.Meanwhile,the latency and amplitude of the Cone-reaction of F-ERG were also affected 3 days after poisoning,but there were no further worsening tendency 7 days after poisoning.The retinal histological analysis showed cellular edema,heteromorphy and disarrangement,tissular loosen of the inner nuclear layer and photoreceptors layer.The mitochondrial damage began at the photoreceptors layer and developed further into the inner nuclear layer.The low-dose methanol intoxication only caused transient damage of the retina.Our results showed that the function and structure of the photoreceptor and inner nuclear layer were the primary target of methanol intoxication and that the rod cells were more sensitive to methanol intoxication than the cone cells.The mitochondrial damage developed from outer layer to inner layer of the retina.     

An apple a day does not always keep the doctor away...

The authors describe a case of suicide in the workplace. A 45-year-old man employed by a fruit and vegetable packing company was found dead in a room containing a modified atmosphere for the packaging of fruits and vegetables. The rescue team measured the carbon monoxide (CO) concentration of the ambient air with a digital CO tester and found a level higher than 600 particles per million. Analysis of an arterial blood sample taken with an airtight syringe revealed the absence of CO but high levels of carbon dioxide (CO(2)). Autopsy revealed no significant injury and police investigators found a handwritten note of intent, describing a recent personal crisis. The authors concluded that the cause of death was suicide by asphyxiation secondary to CO(2) intoxication and notably oxygen (O(2)) depletion. This manner of suicide is rare and most cases previously described in the literature were accidental intoxications. To the best of our knowledge, this is the first case of suicide by CO(2) intoxication and O(2) depletion in a room with a modified atmosphere.     

Forensic medical diagnostics of chronic alcoholic intoxication based on histological changes in the soft tissues of oral cavity and salivary glands

Histological studies of oral cavity mucosa and salivary glands in subjects with chronic alcoholic intoxication revealed changes at the surface of the tongue and in the glandular tissues. Specific features of chronic alcoholic intoxication include acinar and ductal hyperplasia, reduction of the adipose tissue mass in salivary gland stroma, predominance of T-lymphocytes in hard palate minor salivary glands and B-lymphocytes in the stroma of labial minor salivary gland, the absence of plasma cells in the stroma of hard palate minor salivary glands and labial mucosa. Leukoplakia, dysplasia, and hyperplasia of the basal epithelial layer of oral cavity mucosa are considered to be the signs of long-term (over 12 months) alcohol consumption.     

Olanzapine‐Induced Fatal Ketoacidosis with Pneumomediastinum and Subcutaneous Emphysema

We report a case of fatal olanzapine‐induced ketoacidosis in which pneumomediastinum (PM) and subcutaneous emphysema (SE) were detected on postmortem computed tomographic (CT) images. A man in his forties was found in a state of cardiopulmonary arrest with profuse perspiration, and 50 empty capsules of olanzapine (10 mg) and flunitrazepam (1 mg) were found in his room. The major findings of postmortem CT prior to autopsy were PM and SE from the lower half of the face to the height of the first rib. The results of autopsy, biochemical tests, and toxicological analyses indicated the cause of death to be fatal ketoacidosis induced by olanzapine intoxication. No injuries, medical interventions, or particular diseases were evident, suggesting that PM and SE were caused by ketoacidosis. Our findings indicated that toxicological analyses should be performed when PM and SE are detected on CT images.     

Fatal outcome of poisoning with ethylene glycol

After an act of violence, a delinquent swallowed about 250 ml ethylene glycol (EG) - probably to commit suicide before being arrested. During an interrogation by the police he appeared to be inebriated. A blood sample taken at this time did not contain ethanol but 5.1 g/l EG, as revealed by the analytical results. Only after a second examination was he taken to an intensive care unit in a hospital in spite of signs of pronounced intoxication after 12 h at the first examination. The patient died 30 h after taking EG without being effectively treated. The correct diagnosis, initiated by information from the poison control center, was made too late. At autopsy, findings were indicative of stage II of EG poisoning with a body burden of still 40-60 g EG. The mean rate of degradation in the blood was approximately 0.15 g/l per hour.     

Accidental poisonings involving carbon monoxide, heating systems, and confined spaces

Eleven incidents of carbon monoxide (CO) intoxication resulting in sixteen fatalities are reported. All of the cases involved heating systems as either the source or the means of distributing the CO. Blood samples were analyzed for ethanol and CO. Elevated blood CO saturations were found in 14 of the 16 victims while none of the victims had a blood ethanol concentration greater than 0.10% (w/v).     

Sexual Behavioral Disinhibition Associated with Nucleus Lentiformis Lesion: A Forensic Neuroscience Perspective Through a Case

Organic brain disturbances particularly related to frontal cortex structures and subcortical areas including the basal ganglia may play a role in behavioral disinhibition disorders. Kluver–Bucy syndrome (KBS), which is one of the better knowns of these syndromes, includes hyperorality, visual agnosia, and hypersexuality, has been reported to occur after temporal lobe and amygdala lesions; however, several patients who had focal lesions in areas other than the temporal cortex and amygdala have been reported to present partial KBS symptoms. Nucleus lentiformis refers to a large portion of the basal ganglia including the putamen and globus pallidus, and specific structures within this broad area are known to be important for reward and value-based decision making. To date, KBS symptoms including hypersexual behavior associated with nucleus lentiformis lesions have never been reported. Here, we present a 38-year-old male patient who developed increased sexual interest and hyperorality after infarctions in the right lenticular nucleus and right occipitotemporal region and committed a first-degree sexual assault. He was sent to our institution for the assessment of criminal responsibility to the index sexual crime. According to a comprehensive and thorough forensic psychiatric evaluation, he was diagnosed as having an organic personality disorder with partial KBS symptoms. To the best of our knowledge, this is the first reported case of deviant sexual behavior and hyperorality developing after nucleus lentiformis infarction. We aimed to discuss possible neurobiologic explanations of late-onset deviant sexual behavior, which resulted in sexual criminal behavior following a cerebrovascular infarction.     

Diesel fumes do kill: a case of fatal carbon monoxide poisoning directly attributed to diesel fuel exhaust with a 10-year retrospective case and literature review*

While it is known that diesel fuel combustion engines produce much lower concentrations of carbon monoxide (CO) than gasoline engines, these emissions could certainly generate lethal ambient concentrations given a sufficient amount of time in an enclosed space and under suitable environmental conditions. The authors report a case of CO poisoning which was initially referred for autopsy as a presumed natural death of a truck driver found in the secure cab of a running diesel tractor trailer truck. Completion of the preliminary investigation ascribed death to complications of ischemic heart disease (IHD), pending toxicological analysis that included quantification of CO. When the toxicology results showed lethal blood COHbg, the cause of death was re-certified as CO intoxication secondary to inhalation of (diesel) vehicular exhaust fumes. Because of the unique source of fatal CO intoxication in this case, the contributory IHD and the possible contaminants in the putrefied blood, a 10-year retrospective review was conducted on all nonfire related CO deaths autopsied (n = 94) at the Office of the Chief Medical Examiner in Louisville, KY from 1994 to 2003. For validation of the COHbg detection method used by the Kentucky Office of Forensic Toxicology (KYOFT), blood samples from these cases along with controls were submitted to three laboratories using various analytical methods yielding no statistically significant differences. Lastly, an extensive literature review produced no scientifically reported cases of fatal CO poisoning attributed to diesel fuel exhaust.     

毒鼠强诱导细胞DNA损伤的彗星电泳检测

目的　研究毒鼠强对小鼠淋巴细胞和脑细胞DNA的损伤作用。方法　分离健康小鼠的淋巴细胞和脑细胞 ,以彗星电泳的方法测定不同浓度毒鼠强处理后的细胞DNA损伤。结果　 1/2 0～ 1/2LD50 剂量组的毒鼠强均可引起淋巴细胞和脑细胞不同程度的DNA损伤 ,与对照组呈极显著性差异 (P <0 0 0 1)。结论　毒鼠强引起细胞DNA断裂损伤 ,并呈现明显的剂量 -效应关系。     

New findings concerning the pathogenesis of acute carbon monoxide (CO) poisoning

The pathomechanism of carbon monoxide (CO) poisoning was studied by means of cardiopathological and neuropathological investigations in experimental CO intoxication. It has been shown that besides CO-hemoglobin association, the binding of CO to cytochromes is a significant factor. The latter is thought to be responsible for the cytotoxic phenomena. Combined ultrastructural and cytochemical studies have enabled differentiation between toxic, hypoxic, and mixed alternations.