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The Secretary of the United States Department of Veterans Affairs (VA) Honorable Robert McDonald recently pledged to donate his brain for chronic traumatic encephalopathy (CTE) research. Citing exposures to football, rugby, boxing, and paratrooper escapades as an army ranger, Secretary McDonald suggested that his brain could add to the body of knowledge on the effect of repeated concussions. In the meantime, work is under way to make the connections between the CTE postmortem diagnosis and the clinical findings while people are alive. Such knowledge is expected to positively impact medical management for people at risk and inform necessary policies, preventive actions, and health equity issues. (Am J Public Health. Published online ahead of print June 16, 2016: e1-e2. doi:10.2105/AJPH.2016.303293). Language: en

Quantitative analysis in business decision making and operations management has evolved into an independent but non-exclusive alternative to qualitative analysis. We are the first to commoditise the autopsy and establish it as the fundamental cost base/object for a medical examiner's office. We apply the multiplicative seasonal forecasting method for the determination of autopsy demand and the optimal quantitative operations management of a medical examiner's office. Five-year historical data and archives were reviewed at the Allegheny County Medical Examiner's Office, Pennsylvania. The numbers of daily and monthly autopsies performed were collected. Seasonal factors were derived for two seasonal series: days of the week and months of the year. Monday had the lowest seasonal factor of 0.94 and Saturday had the highest of 1.08. October had the lowest seasonal factor of 0.94 and January had the highest at 1.10. Human and other resources may be optimally task-assigned and scheduled based on differential seasonal series forecasting of autopsy demand. Conferences and vacations may also be scheduled on the days and months with lower seasonal factors. Forecasting methods are increasingly becoming an operations management tool in the health and death investigation industries.

We present the second reported case of autopsy-confirmed chronic traumatic encephalopathy in a retired professional football player, with neuropathological features that differ from those of the first reported case. These differing pathological features underscore the need for further empirical elucidation of the pathoetiology and pathological cascades of long-term neurodegenerative sequelae of professional football.A psychological autopsy was performed with the next-of-kin and wife. Medical and hospital records were reviewed. A complete autopsy was accompanied by a comprehensive forensic neuropathological examination. Restriction fragment length polymorphism analysis was performed to determine apolipoprotein-E genotype.Pertinent premortem history included a 14-year span of play in organized football starting from the age of 18 years. The subject was diagnosed with severe major depressive disorder without psychotic features after retirement, attempted suicide multiple times and finally committed suicide 12 years after retirement by ingestion of ethylene glycol. Autopsy revealed cardiomegaly, mild to moderate coronary artery disease, and evidence of acute ethylene glycol overdose. The brain showed no atrophy, a cavum septi pellucidi was present, and the substantia nigra showed mild pallor. The hippocampus and cerebellum were not atrophic. Amyloid plaques, cerebral amyloid angiopathy, and Lewy bodies were completely absent. Sparse to frequent tau-positive neurofibrillary tangles and neuropil threads were present in all regions of the brain. Tufted and thorn astrocytes, as well as astrocytic plaques, were absent. The apolipoprotein-E genotype was E3/E4.Our first and second cases both had long careers without multiple recorded concussions. Both manifested Major Depressive Disorder after retirement. Amyloid plaques were present in the first case and completely absent in the second case. Both cases exhibited neurofibrillary tangles, neuropil threads, and coronary atherosclerotic disease. Apolipoprotein-E4 genotypes were different. Reasons for the contrasting features in these two cases are not clear. Further studies are needed to identify and define the neuropathological cascades of chronic traumatic encephalopathy in football players, which may form the basis for prophylaxis and therapeutics.

After 20 months of interment in a deep grave, the decomposed body of the 81-year old testator of a will was exhumed to sustain the burden of proof that he lacked testamentary capacity when the will was rewritten two days prior to his death. The brain was mushy and pulverized with complete disappearance of the brainstem, cerebellum and subcortical ganglia. Small foci of relatively intact dorsal frontal neocortex were identified. Sections from these foci were stained with hematoxylin and eosin, bielchowsky silver stain and immunostains for beta amyloid peptide (betaA4), tau and alpha-synuclein. Despite severe autolysis and decomposition, the bielchowsky stain and the betaA4 immunostains showed preserved frequent neuritic amyloid plaques with very few residual neurofibrillary tangles. Cerebral Amyloid Angiopathy was present. At the present time this case represents the first documented and reported case of direct tissue diagnosis of Alzheimer's Disease pathology in a decomposed brain following long term burial in a deep grave.

Context: Complementary alternative medicine therapies based on the use of cesium chloride preparations for the treatment of cancer and radiation poisoning, have generated therapeutic interest; but oral or intravenous administration of cesium chloride (CsCl) to cancer patients as an alternative mode of cancer therapy have not been approved by the U.S. Food and Drug Administration (FDA). Objective: Cesium (Cs) levels from human tissue were measured to determine exposure to an alternative medical treatment. Cesium levels are reported from two patients who were administered cesium chloride in conjunction with aloe vera as part of an alternative cancer treatment. Design: The samples were analyzed by graphite furnace atomic absorption spectrometry with Zeeman background correction. As a reference, Cs was also determined in brain, liver, kidney, and whole blood from control case materials retrieved from the National Tissue Repository of the Armed Forces Institute of Pathology. Results: High levels of cesium were found in brain, liver, kidney, bile, gastric content, and whole blood collected at autopsy as compared to reference levels. The administration of cesium chloride resulted in blood levels a factor of 1100 higher than normal. The highest Cs concentrations were found in the liver (1029 µg/g, dry wt), followed by the kidney (815 µg/g, dry wt) and brain (219 µg/g, dry wt). Conclusion: The high accumulation in the liver suggests that hepatotoxicity from Cs might be an initial presenting symptom in Cs-poisoning cases. This is the first report describing two cases with high Cs levels in human tissues.

Infectious aneurysms are potentially deadly sequelae of multiple etiologies, typically associated with subacute bacterial endocarditis (SBE). Since these aneurysms tend to be distal, there are no consistent landmarks by which to localize them, in contrast to more typical aneurysms that occur on the circle of Willis or proximal, large cerebral vessel bifurcations. In addition, they tend to be extremely friable and may be obscured by blood if intracranial hemorrhage (ICH) has already occurred. These factors make clipping these aneurysms technically difficult, and searching for easily ruptured aneurysms without standard landmarks adds risk to the procedure. In this report, we describe the case of a 9-year-old boy with SBE and subsequent ICH secondary to a mycotic aneurysm. This aneurysm was localized to within millimeters by the MRI protocol described herein. The aneurysm was excised and the patient recovered without incident. Thus, MRI/MRA-guided frameless stereotaxy may be useful for localizing distal mycotic aneurysms, improving patient outcome by decreasing morbidity and mortality.

Following his discovery of chronic traumatic encephalopathy (CTE) in football players in 2002, Dr. Bennet Omalu hypothesized that posttraumatic stress disorder (PTSD) in military veterans may belong to the CTE spectrum of diseases. The CTE surveillance at the Brain Injury Research Institute was therefore expanded to include deceased military veterans diagnosed with PTSD. The authors report the case of a 27-year-old United States Marine Corps (USMC) Iraqi war veteran, an amphibious assault vehicle crewman, who committed suicide by hanging after two deployments to Fallujah and Ramadi. He experienced combat and was exposed to mortar blasts and improvised explosive device blasts less than 50 m away. Following his second deployment he developed a progressive history of cognitive impairment, impaired memory, behavioral and mood disorders, and alcohol abuse. Neuropsychiatric assessment revealed a diagnosis of PTSD with hyperarousal (irritability and insomnia) and numbing. He committed suicide approximately 8 months after his honorable discharge from the USMC. His brain at autopsy appeared grossly unremarkable except for congestive brain swelling. There was no atrophy or remote focal traumatic brain injury such as contusional necrosis or hemorrhage. Histochemical and immunohistochemical brain tissue analysis revealed CTE changes comprising multifocal, neocortical, and subcortical neurofibrillary tangles and neuritic threads (ranging from none, to sparse, to frequent) with the skip phenomenon, accentuated in the depths of sulci and in the frontal cortex. The subcortical white matter showed mild rarefaction, sparse perivascular and neuropil infiltration by histiocytes, and mild fibrillary astrogliosis. Apolipoprotein E genotype was 3/4. The authors report this case as a sentinel case of CTE in an Iraqi war veteran diagnosed with PTSD to possibly stimulate new lines of thought and research in the possible pathoetiology and pathogenesis of PTSD in military veterans as part of the CTE spectrum of diseases, and as chronic sequelae and outcomes of repetitive traumatic brain injuries.

BACKGROUND: We define chronic traumatic encephalopathy (CTE) as a progressive neurodegenerative syndrome caused by single, episodic, or repetitive blunt force impacts to the head and transfer of acceleration-deceleration forces to the brain. OBJECTIVE: We present emerging histomorphologic phenotypes of CTE that we identified in our cohort of CTE cases with apolipoprotein E genotyping and causes and manners of death. METHODS: Autopsy brain tissue of 14 professional athletes and 3 high school football players was examined after unexpected deaths. Histochemical and immunohistochemical tissue staining was performed with apolipoprotein E genotyping. RESULTS: Ten of 14 professional athletes (71%) were positive for CTE: 7 of 8 football players, 2 of 4 wrestlers, and 1 boxer. One of 3 high school players manifested incipient CTE. The age range of those with CTE was 18 to 52 years; they were all male athletes. In all cases of CTE, Alzheimer-type cerebral cortical atrophy was absent; negligible to mild neocortical neuronal dropout was present. The fundamental neuropathologic feature of CTE was the topographic distribution of sparse, moderate, and frequent band-shaped, flame-shaped, small and large globose neurofibrillary tangles and neuritic threads in the cerebral cortex, subcortical nuclei/basal ganglia, hippocampus, and brainstem nuclei. Sparse to frequent diffuse amyloid plaques may accompany tauopathy and was seen in only 2 CTE cases. No α-synucleinopathy was present. All 7 CTE-positive professional athletes with known apolipoprotein E genotypes had at least 1 E3 allele comprising 5 E3/E3 (71%) and 2 E3/E4 (29%). Alcohol- and drug-related deaths, suicides, and accidental deaths were overrepresented in our CTE cohort. CONCLUSION: The emerging histomorphologic features of our CTE cohort may specify histologic criteria for CTE diagnosis, may identify emerging histologic variants of CTE and may facilitate more objective surveillance and accurate identification of sentinel CTE cases. Language: en

We present in this case report the tissue substrates and forensic evidence for chronic traumatic encephalopathy (CTE) in a professional American wrestler with Apolipoprotein E (apoE) genotyping. Professional wrestling is a contact-sport, with an integral risk for players to sustain repeated concussions over their careers. This case provides the first autopsy evidence of neuropathological abnormalities that accompany CTE in professional American wrestlers. A complete autopsy was performed on a 40-year-old Caucasian male, after he died unexpectedly by suicidal hanging after he had killed his wife and son. The brain showed no atrophy and no recent or remote contusions or necrosis. There was a mild to moderate neocortical neuronal dropout without any amyloid plaques. There were diffuse, sparse to frequent tau-immunoreactive Neurofibrillary Tangles and Neuropil Threads in the neocortex, subcortical ganglia, and brainstem nuclei including the substantia nigra consistent with CTE. The apoE genotype was determined to be E3/E3. Other autopsy findings included cardiomegaly, left ventricular hypertrophy, and bilateral atrioventricular dilatation; toxicologic analyses showed alprazolam and hydrocodone in the blood, and evidence of exogenous testosterone in the urine. Longitudinal studies of professional contact-sport athletes are needed to identify the differentiating characteristics of athletes who develop CTE and devise strategies for intervention.

We present 5 cases of professional American contact sport athletes who committed parasuicides and suicides aged 50, 45, 44, 36, and 40 years old. Full forensic autopsies and immunohistochemical analyses of the brains revealed chronic traumatic encephalopathy (CTE). The brains appeared grossly normal at autopsy without gross evidence of remote traumatic injuries or neurodegenerative disease. Brain immunohistochemical analyses revealed widespread cerebral taupathy in the form of neurofibrillary tangles and neuritic threads without neuritic amyloid plaques. CTE refers to chronic cognitive and neuropsychiatric symptoms of chronic neurodegeneration following a single episode of severe traumatic brain injury or repeated episodes of mild traumatic brain injury. CTE can only be definitively diagnosed by direct tissue examination. Without full autopsies and immunohistochemical brain analyses these cases would never have been identified. Forensic pathologists will play a vital and central role in the emerging disease surveillance of CTE in professional American athletes, in the identification of CTE cases, and in the establishment of the epidemiology of CTE, with the goal of eventually developing preventive and interventional therapeutic protocols for CTE outcomes.

A study of elderly homicide victims brought to a Pennsylvania medical examiner's office reveals interesting findings about cause of death. Language: en

From 2003 to 2005, deaths of 3 individuals as a result of cardiac arrest caused by hypocalcemia during chelation therapy were reported to the Centers for Disease Control and Prevention. Two were children, both of whom were treated with edetate disodium. At the time of this writing, the adult case was still under investigation. No previous cases of death resulting from hypocalcemia during chelation have been reported. From our experience and review of the literature, we suggest that health care providers who are unfamiliar with chelation consult an expert before undertaking treatment and that hospital formularies evaluate whether stocking edetate disodium is necessary, given the risk for hypocalcemia and the availability of less toxic alternatives.

The process of swallowing or inserting illegal packets of drugs for the purpose of evading law enforcement officers carries risks other than criminal charges. It can be fatal. Individuals engaged in such activities are called "Body Packers" or "Mules". The most frequent cause of the death among body packers is acute drug intoxication due to rupture of the package(s) within the gastrointestinal tract. We present the first documented case of a body packer that died from cocaine intoxication following the rupture of packets of cocaine in Western Pennsylvania.

In the 1970s, J. H. Adams and other researchers at the Institute of Neurological Sciences, Glasgow, Scotland introduced a grading system for the quantification and analysis of contusions of the brain. They derived a brain contusion index based on regional surface distribution and parenchymal depth of contusions of the brain. Following a subsequent modification of this scheme in the 1980s, they recommended evolving modifications that will fit a variety of possible applications. Having tested the applicability of this grading system for the forensic/medico-legal autopsy, we have encountered some applied anatomic limitations and have derived a modification that addresses these limitations in reference to the forensic/medico-legal autopsy.We recommend a two-tier system based on the Adams' system, which quantifies contusions of the brain by the gyral spread of contusions and by the parenchymal depth of penetration of contusions with a re-definition of the lobar distinctions and classifications of the brain. Gyral spread is assigned a grading scheme of 0-3 and the parenchymal depth of contusions is assigned a grading scheme of 0-4. A lobar contusion score is derived by multiplying the two assigned grades. A total brain contusion index is derived by summating all the lobar contusion scores. This reproducible grading system can be applied to routine bench forensic neuropathology reporting, court room illustrations and in comparative research analysis of brain trauma subjects.

We present the results of the autopsy of a retired professional football player that revealed neuropathological changes consistent with long-term repetitive concussive brain injury. This case draws attention to the need for further studies in the cohort of retired National Football League players to elucidate the neuropathological sequelae of repeated mild traumatic brain injury in professional football.The patient's premortem medical history included symptoms of cognitive impairment, a mood disorder, and parkinsonian symptoms. There was no family history of Alzheimer's disease or any other head trauma outside football. A complete autopsy with a comprehensive neuropathological examination was performed on the retired National Football League player approximately 12 years after retirement. He died suddenly as a result of coronary atherosclerotic disease. Studies included determination of apolipoprotein E genotype.Autopsy confirmed the presence of coronary atherosclerotic disease with dilated cardiomyopathy. The brain demonstrated no cortical atrophy, cortical contusion, hemorrhage, or infarcts. The substantia nigra revealed mild pallor with mild dropout of pigmented neurons. There was mild neuronal dropout in the frontal, parietal, and temporal neocortex. Chronic traumatic encephalopathy was evident with many diffuse amyloid plaques as well as sparse neurofibrillary tangles and tau-positive neuritic threads in neocortical areas. There were no neurofibrillary tangles or neuropil threads in the hippocampus or entorhinal cortex. Lewy bodies were absent. The apolipoprotein E genotype was E3/E3.This case highlights potential long-term neurodegenerative outcomes in retired professional National Football League players subjected to repeated mild traumatic brain injury. The prevalence and pathoetiological mechanisms of these possible adverse long-term outcomes and their relation to duration of years of playing football have not been sufficiently studied. We recommend comprehensive clinical and forensic approaches to understand and further elucidate this emergent professional sport hazard.

Obesity has attained epidemic proportions in the United States, with more than 50% of adults classified as overweight or obese. If untreated, morbidly obese patients have a 1 in 7 chance of reaching normal life expectancy. The surgical treatment of obesity has emerged as the most effective treatment modality in long-term weight control and has become increasingly popular, with attendant postoperative complications and death. We performed a cross-sectional, coroner based, 2-year retrospective review of archival case records for decedents who died following bariatric surgery for the treatment of obesity to identify underlying causes of death and forensic characteristics of this cohort. Fifteen (0.5%) out of 3097 archival cases died following bariatric surgery, with approximately 73% of decedents dying within 6 months of surgery. The underlying causes of death in 80% of decedents were natural comorbidities of obesity, with cardiovascular diseases (33%) being the most frequent causes of death, followed by gastrointestinal diseases (20%), acute pulmonary thromboembolism (13%), and acute bacterial pneumonia (13%). The majority of decedents were white females who remained morbidly obese after bariatric surgery. Only 2 decedents died of direct inadvertent/ accidental surgical complications.

The February COM. A 53-year-old obese man presented with new onset seizures and an MRI scan revealed a large cystic and necrotic heterogeneously enhancing left frontal mass. Craniotomy revealed a firm subdural tumor on the cortical surface that was delivered en-bloc preserving the pial planes and stripping it from the falx cerebri. The tumor consisted of multiple irregular fragments of white-tan rubbery tissue admixed with globules of bosselated, white-tan rubbery tissue and a fragment of bone. Sections of the tumor revealed mature hyaline cartilage with no atypia of the chondrocytes. There was focal mineralization and endochondral ossification. A diagnosis of intracranial mesenchymal osteochondroma was made. Osteochondroma, a benign cartilaginous neoplasm comprised of mature hyaline cartilage with focal ossification, is the most common benign bone tumor. Extraskeletal (mesenchymal) osteochondromas are known to originate from non-skeletal or non-cartilaginous tissue. Intracranial osteochondromas are uncommon, typically arising from the base of the skull. Only about 15% of intracranial osteochondromas arise supratentorially, from the dura, usually in a parafalcine frontoparietal location and some have been a component of Maffucci's syndrome and Ollier disease. Intracranial osteochondromas can occur at any age with a predilection for younger individuals. Intracranial mesenchymal osteochondromas exhibit a benign clinical course. Typically, the histomorphology resembles mature hyaline cartilage without anaplastic proliferation of chondrocytes or nuclear atypia, with a lobular arrangement of clusters of lacunae containing single chondrocytes. Transition to osteochondrosarcoma has rarely been documented.

We report two cases of sudden unexpected death in two unrelated African American female infants, 2 months and 4 months old. Both infants were attended to by the same babysitter in the same apartment and died 39 days apart in the same bed and in the same bedroom. The autopsy of the first infant revealed sudden unexplained death in an infant. Toxicologic analysis for carbon monoxide (CO) was not performed because it was not suspected. When the second infant died, investigation into the ambient air quality within the apartment revealed high levels of CO emanating from a poorly ventilated and defective hot water heater, which was located across a hallway from the bedroom where the two babies died. CO saturation levels in the postmortem blood samples of the two babies were elevated and were similar (13% and 14%). Nicotine and cotinine were not detected in the blood sample of the two infants. Cherry-red livor mortis was absent. Acute CO intoxication was determined to be the underlying cause of these two unexpected deaths. These two cases underscore the need to integrate ambient air analysis and postmortem CO analysis as routine components of the comprehensive death investigation of infants who die suddenly and unexpectedly.