The spectrum of neuropathologic findings in deaths associated with seizure disorders

The pathologic and neuropathologic findings in 90 autopsied cases of death associated with a seizure disorder or complication thereof were reviewed. Most (69%) of the deceased individuals were between 21 and 40 years of age; two thirds were male. In 58% of patients, no cause of death other than seizure disorder was found. The ultimate cause of death in those patients was assumed to be a cardiac arrhythmia or respiratory arrest. Drowning accounted for 19% of deaths, and 17% of patients died of other contributory causes such as suicide, exposure, or atherosclerotic coronary vascular disease. Aspiration was found in the remaining 6%. Tongue lacerations or bite marks were observed in only one third of cases. The brain was normal in approximately two thirds of cases, with no focus for the origination of seizure found on neuropathologic examination. In the remainder of cases, a variety of lesions was found, with cavitary lesions, contusions, and dural lesions being the most common ones.     

Unsuspected meningoencephalitis in a case of assault by blunt force trauma

Reported is a case of an assault causing extensive blunt force injuries in which the clinical, radiologic, and postmortem findings were all consistent with death resulting from brain damage arising from the assault. The assailant was charged with murder. Subsequent full neuropathologic (including histologic) examination revealed the unsuspected finding of a widespread meningoencephalitis but no evidence of significant traumatic brain damage. The contributions of the infective process and of the trauma to death were felt to be unclear and a guilty plea to attempted murder was accepted. This case highlights the importance of a full neuropathologic examination, including histology, in cases of trauma to the head, even when the cause of death may initially appear obvious.     

Diagnosis of Hemorrhagic Stroke in an Exhumed Brain After Three Years of Burial in a Deep Grave

Abstract: We present the forensic neuropathologic analysis of an exhumed decomposed brain following long‐term interment in a 50‐year‐old white woman, who had been buried for 34 months. Next of kin authorized exhumation of the body for an autopsy to determine the cause of death. The embalmed body was anatomically intact and revealed decompositional changes with mold colonies. Internal viscera showed intact histomorphology. The brain revealed diffuse congestive swelling and extracellular edema with dissecting parenchymal hemorrhage and hematoma originating from the left putamen and thalamus and extending to the left lateral ventricle. Excitotoxic neuronal injury as well as penumbric parenchymal changes was noted. Cause of death was determined to be a hypertensive cerebral parenchymal hemorrhage. This case and our previously reported case are sentinel cases, which should encourage and guide the forensic neuropathologic work‐up and investigation of causes of death in spite of long‐term burial in deep graves.     

An Incidental Diffuse Midline Glioma Found at Autopsy

This case shows an unexpected midline glioma found at autopsy. Two siblings were riding on a single bicycle on the side of a road. The 13‐year‐old brother was seated and steering the bicycle, while the 14‐year‐old sister held onto the back. The bicycle veered left into traffic and was struck by a vehicle. The siblings were admitted to the local Level 1 trauma center, but both later succumbed to injuries. Autopsies were performed on the children, including brains for neuropathologic evaluation. The brother was found to have an infiltrating astrocytoma located in the left middle cerebellar peduncle, with extension to the pons and medulla. His hospital course included several imaging studies using CT and MRI modalities. However, this lesion was not identified until the postmortem neuropathologic examination. This rare case shows the continued need for postmortem autopsy and the current limitations of medical imaging.     

38例单纯型脑干损伤法医学尸检的回顾性研究

目的报道38例原发性单纯型脑干损伤致死案例法医学尸检所见的脑干损伤、致伤方式和致伤物等特点,并探讨在法医学鉴定中的意义。方法从208例脑干损伤死亡法医学尸检案例中,挑选出38例符合单纯型脑干损伤的案例,分析单纯型脑干损伤发生的案情、损伤的部位和类型等特点。结果38例中男性占绝大多数,农民明显多于其它人员;大多发生于纠纷斗殴中;头部拳击伤18例(47.4%);头皮挫伤19例(50.0%);头皮挫裂创9例(23.7%);未见头皮损伤7例(18.4%);受伤当时昏迷并很快死亡者34例(89.5%);其损伤为局灶性挫伤出血,有32例(84.2%)肉眼未能辨认出,镜检见小灶性出血:其中,桥脑18例(47.4%)、延脑10例(26.3%)、中脑4例(10.5%)、桥脑和延脑均有出血6例(15.8%)。结论原发性单纯型脑干损伤不仅存在,而且能致人死亡;应引起同行的重视。     

脑干轴索肿胀的半定量研究

目的 探讨轴索肿胀在鉴定脑干损伤中的意义。方法 取明确死于原发性脑干损伤(36例)和脑外疾病(28例)者共64例，分为损伤组(36例)和对照组(其中死于心血管疾病12例、非心血管疾病16例)，并将其死后24h和48h前、后做尸体解剖分为2组，通过对中脑、脑桥和延脑切片、镀银染色，在100倍光镜下采用显微测微器测量每片9条最粗的轴索横径，对所得数据作方差分析、t检验统计学处理。结果 损伤组与对照组(不包括心血管疾病死亡者)相比，中脑、延脑部的轴索肿胀程度有明显差异(P＜0.05)；死后48h内解剖的损伤组与对照组相比无差异(P＞0.05)，但超过48h解剖两组有明显差异(P＜0.05)。结论 中脑、延脑部轴索肿胀与外伤有明显的相关性。轴索肿胀对判断脑干损伤有意义。需排除心血管疾病致死。     

Unusual deaths associated with polyphagia

Perversion of appetite may be manifest in either qualitative (pica), quantitative (polyphagia), or combined derangements of eating. Ingested materials are capable of serving as dangerous physical agents through interference with normal cardiac and/or respiratory function. Since the mechanisms of injury are similar to those that might occur as a result of violence or serious natural disease, a thorough investigation of the history and circumstances immediately preceding the final event is warranted in addition to a complete autopsy. Three cases of asphyxia of unusual etiology are presented along with a rationale regarding the mechanisms believed to be involved. In case 1, sudden subdiaphragmatic viscus expansion with resultant lung volume displacement and impediment of venous return from the lower half of the body are believed to have been operative. In cases 2 and 3, both asphyxial loci are infraglottic. The common denominator in all of these fatalities is the physical impairment of vital air exchange as a complication of an abnormal eating pattern.     

Political Law Notes in Conclusion of the 39th Federal General Election held in Canada on 23 January 2006

Traditionally, the discovery of natural resources raises the hope of such a state to secure wealth and economic growth. However, history shows that in some developing countries, particularly the resource-rich, many citizens do not actually benefit from the resource revenues. This is due to factors such as mismanagement of the resource revenues, lack of transparency and accountability and corruption among others. All of these factors are characterised by what is known as the ‘resource curse’ phenomenon. This article examines the resource curse phenomenon with reference to Nigeria’s oil-rich Niger Delta region. It considers a potential legal instrument, which is the Impact and Benefit Agreement (IBA) that could be used to resolve some of the problems characterised by the resource curse phenomenon in the region. Using Canada as a reference point, the article demonstrates that the adoption of IBAs can be an alternative legal strategy for resolving the socio-economic and environmental symptoms of the resource curse in Nigeria’s oil-rich region.     

Forensic considerations in cases of neurofibromatosis--an overview

Neurofibromatosis types 1 and 2 are inherited neurocutaneous disorders characterized by a variety of manifestations that involve the circulatory system, the central and peripheral nervous systems, the skin, and the skeleton. Significant reduction in lifespan occurs in both conditions often related to complications of malignancy and hypertension. Individuals with these conditions may also be the subject of medicolegal autopsy investigation if sudden death occurs. Unexpected lethal events may be associated with intracranial neoplasia and hemorrhage or brainstem compression. Vasculopathy with fibrointimal proliferation may result in critical reduction in blood flow within the coronary or cerebral circulations, and aneurysmal dilatation may be associated with rupture and life-threatening hemorrhage. An autopsy approach to potential cases should include review of the history/hospital record, liaison with a clinical geneticist (to include family follow-up), a full external examination with careful documentation of skin lesions and nodules, measurement of the head circumference in children, photography, possible radiologic examination, a standard internal autopsy examination, documentation of the effects of previous surgery and/or chemo/radiotherapy, examination for specific tumors, specific examination and sampling of vasculature (renal, cerebral, and cardiac), formal neuropathologic examination of brain and spinal cord, possible examination of the eyeballs, examination of the gastrointestinal tract, histology to include tumors, vessels, gut, and bone marrow, toxicological testing for anticonvulsants, and sampling of blood and tissue for possible cytogenetic/molecular evaluation if required.     

原发性脑干损伤NF表达定量研究

目的探讨脑干神经丝蛋白的定量分析对短时间内死亡的原发性脑干损伤鉴定的法医学意义。方法14例原发性脑干损伤者的脑干标本（损伤组）和15例脑外疾病死亡者的脑干标本（对照组）,分别取中脑、脑桥及延脑组织,作NF广谱免疫组化染色,用OPTIMAS 6.0系统图像分析仪定量检测脑干的神经丝蛋白表达,所得数据进行统计学对比处理。结果中脑、脑桥、延脑的NF阳性表达率分别为75.84±23.62（对照组45.17±17.95）,65.94±14.61（对照组42.99±24.12）和83.30±26.66（对照组53.50±28.14）,损伤组与对照组的NF阳性物含量在中脑、脑桥及延脑等3个部位中均有显著差异,P〈0.001或〈0.01。结论定量分析人脑干神经丝蛋白的含量变化,超出常人数量对鉴定早期原发性脑干损伤有价值。     

Sarcoidosis and mechanisms of unexpected death

Sarcoidosis is a multisystem disease of uncertain etiology characterized by multifocal areas of discrete and confluent granulomatous inflammation that may rarely be responsible for sudden and unexpected death. Two cases are reported to demonstrate disparate pathological features in fatal cases, one involving cardiac sarcoidosis, and the other neurosarcoidosis with hypothalamic infiltration. Sarcoidosis in individuals dying suddenly may be completely unrelated to the death, contributory or causal. Cardiovascular causes of sudden death in sarcoidosis include arrhythmias associated with cardiomyopathy and ischemia, ventricular rupture, and cor pulmonale due to pulmonary hypertension; respiratory causes include hemorrhage and upper airway obstruction; central nervous system causes include arrhythmias from infiltration of autonomic centers, epilepsy, and obstructive hydrocephalus from brainstem involvement; and gastrointestinal deaths may be due to hemorrhage from esophageal varices associated with portal hypertension. The diagnosis relies on the demonstration of typical noncaseating granulomas and the exclusion of other infective and environmental diseases with similar histopathological findings.     

c-fos蛋白及其基因表达改变用于脑干损伤早期死后诊断的可行性研究

探讨人体脑干损伤后c fos蛋白及其基因表达的改变用于脑干损伤早期死后诊断的可行性。采用免疫组织化学和原位杂交技术 ,观察 16例人体脑干损伤后的c fos蛋白及其基因表达的改变。结果发现 :在正常脑干组织的不同部位 ,均有c fos蛋白和c fos mRNA阳性表达 ,且在各例脑干标本之间 ,表达的量及其分布不一致。脑损伤后 ,在脑干组织中也有c fos蛋白和c fos mRNA阳性表达 ,但与正常脑干组织相比无显著性差异。c fos蛋白和c fos mRNA的表达在各例脑干标本之间不一致 ,且在损伤后的改变无明显规律 ,不能用于脑干损伤早期的死后诊断。     

A frozen newborn infant: froth in the air-passage after thawing

We performed an autopsy on a frozen newborn infant who was found in a freezer at -18 degrees C. After thawing, froth emerged from the nostrils and was present in the trachea. Sometimes froth may be seen in the air-passage in cases of strangulation and drowning. In our case, however, there was neither proof of asphyxia due to strangulation nor drowning. The existence of the froth indicates that the infant was probably in a state of respiratory distress before death. Histologic findings of the lung showed that the infant did not suffer from respiratory disorders such as respiratory distress syndrome. Karyopyknosis and vacuolation of the keratinocytes, shrinkage of the hepatocytes, dilatation of the sinusoid, spaces between heart muscle fibers and deep staining of the nuclei and hemolysis were characteristic in our case. This case shows that froth persists in the internal air-passage for a long time as a result of freezing. Moreover, the froth in the air-passage, along with the findings of the lungs, demonstrates that the newborn infant was born alive.     

Forensic Case Reports Presenting Immersion Pulmonary Edema as a Differential Diagnosis in Fatal Diving Accidents

Immersion Pulmonary Edema (IPE) reduces the transport of gases over the respiratory membrane due to edema in the interstitium and respiratory zones. IPE has previously been described in both swimmers and divers, with a few known fatal cases. We have reviewed 42 SCUBA and snorkeling‐related drowning deaths, and through a thorough analysis of each case, including both diving physiology and forensic pathology, we present IPE as a differential diagnosis to drowning in four cases. Our findings propose that; absence of watery content in the stomach and conducting airways, and liquid filled lungs without hyperexpansion, may be compatible with IPE. We suggest that IPE should be considered in cases where witness testimony reveals; no obvious signs of aspiration and rapid respiratory deterioration despite continuous breathing through an appropriate air source. The diagnosis should be based on the overall impression, including both the autopsy findings and the circumstances regarding the accident.     

Lactic acid concentrations in vitreous humor: their use in asphyxial deaths in children

Lactic acid concentrations in brain tissue of humans have been shown to increase with an extended agonal period. Infants and children dying from various causes are undergoing different stress conditions terminally and the postulate of this study is that natural death cases and traumatic asphyxia cases are characterized by varying agonal periods, the former being somewhat prolonged with the latter being rather brief. One-hundred-and-two cases of infants and children were examined for vitreous humor lactic acid concentrations. They were divided into two major categories, Sudden Infant Death Syndrome (SIDS) and non-SIDS cases. SIDS was further divided into SIDS without additional findings and SIDS with secondary findings which contributed to death. The non-SIDS category included traumatic asphyxia cases as well as those dying from blunt trauma, known respiratory diseases, and other causes. Categorical mean values and standard deviations were calculated. The vitreous humor lactic acid mean value for traumatic asphyxia was significantly lower than the mean value for SIDS. Also the mean value for known respiratory diseases was statistically lower than the mean value for SIDS with secondary findings. These findings are probably suggestive of agonal time differences and may be a reflection of the various mechanisms of death.     

Study of the brainstem, particularly the arcuate nucleus, in sudden infant death syndrome (SIDS) and sudden intrauterine unexplained death (SIUD)

Complete examination of the brainstem involves transverse serial 5-microm sections made throughout the entire brainstem. The number of serial sections varies from 360 in sudden intrauterine unexplained death (SIUD) to 600 in term fetuses to over 1400 sections in sudden infant death syndrome (SIDS) victims. The procedure is not applicable in all histopathological laboratories, owing to the need for additional technical personnel. The simplified procedure allows a remarkable reduction of the number of sections. The brainstem is divided into 3 blocks. The first, cranial block, extends from the border between the medulla oblongata and pons up to the upper pole of the olivary nucleus. The second, intermediate block, corresponding to the submedian area of the inferior olivary nucleus, has as reference point the obex and extends 2 to 3 mm above and below the obex itself. The third, caudal block, includes the lower pole of the inferior olivary nucleus and the lower adjacent area of the medulla oblongata. Examinations of the brainstems from 106 SIDS victims, 30 controls, and 51 stillborns underlined a remarkable variability, particularly of the arcuate nucleus. The simplified examination of the brainstem makes it possible to evaluate the structures, examining 3 specific levels, defined by morphologic reference points.     

32例无心外原因猝死者传导系统病理学观察

在对32例无心外原因猝死者传导系统(CCS)组织学观察中,发现31例 CCS 有异常和病变,其中11例可致猝死。这些病变包括有急性炎症、出血、脂肪浸润和结内外神经病变,且与猝死有关。     

The neuropathology of heroin abuse

A broad spectrum of neuropathologic changes are encountered in the brains of heroin abusers. The main findings are due to infections, either due to bacterial spread from bacterial endocarditis, mycoses, or from HIV-1 infection. Other complications include hypoxic-ischemic changes with cerebral edema, ischemic neuronal damage and neuronal loss, which are assumed to occur under conditions of prolonged heroin-induced respiratory depression, stroke due to, for example, thromboembolism, vasculitis, septic emboli, hypotension, and positional vascular compression. Myelopathy is believed to be the result of an isolated vascular accident within the spinal cord due to an as yet unknown mechanism. A distinct entity, spongiform leukoencephalopathy, has been described mainly after inhalation of pre-heated heroin. A lipophilic toxin-induced process was considered to be due to contaminants and to be induced or enhanced by cerebral hypoxia, but a definite toxin could not be identified. At the cellular level, abnormalities in signal transduction systems and changes of various receptor densities have been reported. The exact etiology of the different neuropathological alterations associated with heroin abuse is still unclear, but may also be related to additional substances used as adulterants.     

Pseudo-subarachnoid hemorrhage of the head diagnosed by computerized axial tomography: a postmortem study of ten medical examiner cases

In this report, we describe ten cases of pseudo-subarachnoid hemorrhage on computer axial tomography (CT) scan of the head. A pseudo-subarachnoid hemorrhage is a false positive finding by CT of the head in which the scan is interpreted as being positive for a subarachnoid hemorrhage not substantiated by subsequent neuropathologic findings. This study is a retrospective review of postmortem cases brought into the Office of the Chief Medical Examiner for the State of Maryland over a three-year period (from 1997 to 2000). We compared the clinician's impression of the CT scan with the postmortem neuropathology. The clinical diagnosis of subarachnoid hemorrhage was based on misinterpretation of non-contrast CT scans of the head. In six of the ten cases, the reading was performed by a radiologist and in four cases by nonradiologist physicians (emergency room physician, neurologist, or neurosurgeon). All the patients survived between a few hours to a few days after being admitted to the hospital. For most of the cases (80%), the neuropathology showed hypoxic/ischemic encephalopathy. The most common cause of death (four out of ten cases) was narcotic intoxication. This report is submitted so that clinicians and pathologist become more familiar with this entity.     

Hypoglycemic brain damage

Hypoglycemia was long considered to kill neurons by depriving them of glucose. We now know that hypoglycemia kills neurons actively from without, rather than by starvation from within. Hypoglycemia only causes neuronal death when the EEG becomes flat. This usually occurs after glucose levels have fallen below 1 mM (18 mg/dl) for some period, depending on body glycogen reserves. At the time that abrupt brain energy failure occurs, the excitatory amino acid aspartate is massively released into the limited brain extracellular space and floods the excitatory amino acid receptors located on neuronal dendrites. Calcium fluxes occur and membrane breaks in the cell lead rapidly to neuronal necrosis. Significant neuronal necrosis occurs after 30 min of electrocerebral silence. Other neurochemical changes include energy depletion to roughly 25% of control, phospholipase and other enzyme activation, tissue alkalosis and a tendency for all cellular redox systems to shift towards oxidation. The neurochemistry of hypoglycemia thus differs markedly from ischemia. Hypoglycemia often differs from ischemia in its neuropathologic distribution, a phenomenon applicable in forensic practice. The border-zone distribution of global ischemia is not seen, necrosis of the dentate gyrus of the hippocampus can occur and a predilection for the superficial layers of the cortex is sometimes seen. Cerebellum and brainstem are universally spared in hypoglycemic brain damage. Hypoglycemia constitutes a unique metabolic brain insult.