Bennet Omalu

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.

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.

Isolated eosinophilic coronary arteritis (IECA) has been reported as a cause of sudden unexpected death and has recently been recognized as a newly emerging vasculitic disease. We identified eight case reports and two case series of sudden death due to IECA in the medical literature and we present two new cases of sudden death due to IECA. Our cases further support the proposition that IECA may be a newly emerging distinct vasculitis, which can go undiagnosed and present with sudden death. At autopsy IECA presents with isolated non-necrotizing predominantly eosinophilic inflammation of the coronary arteries without vasculitis in any other organ or blood vessel. The mean age of death of our two cases and the previously reported cases of IECA is 47 years, comprising 13 females and 3 males with a range of 34-64 years. All cases died suddenly and unexpectedly. Past medical history of recurrent chest pain was documented in 63% of cases. The patho-etiology of IECA may involve an aberrant immune response or hypersensitivity reaction. Elucidation of the pathology of IECA may be translated into definitive diagnostic, interventional, and preventive modalities, which will further reduce the person years of life lost to heart disease.

BACKGROUND:. We define chronic traumatic encephalopathy (CTE) as a progressive neurodegenerative syndrome caused by single, episodic, or repetitive blun

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 a case of chronic traumatic encephalopathy (CTE) in a retired National Football League (NFL) Player with autopsy findings, apolipoprotein E genotype, and brain tissue evidence of chronic brain damage. This 44-year-old retired NFL player manifested a premortem history of cognitive and neuropsychiatric impairment, which included in part, chronic depression, suicide attempts, insomnia, paranoia, and impaired memory before he finally committed suicide. A full autopsy was performed with Polymerase Chain Reaction-based analyses of his blood to determine the apolipoprotein genotype. Histochemical and immunohistochemical analyses were performed on topographical gross sections of the brain. Autopsy confirmed a fatal gunshot wound of the head. The apolipoprotein E genotype was E3/E3 and the brain tissue revealed diffuse cerebral taupathy (Neurofibrillary Tangles and Neuritic Threads). This will be the third case of CTE in a national football player, which has been reported in the medical literature. Omalu et al., reported the first two cases in 2005 and 2006. This case series manifested similar premortem history of neuropsychiatric impairment with autopsy evidence of cerebral taupathy without any neuritic amyloidopathy. For a definitive diagnosis of CTE to be made, and for medicolegal purposes, a full autopsy must be performed with histochemical and immunohistochemical analyses of the brain to identify the presence of Neurofibrillary Tangles (NFTs) and Neuritic Threads (NTs). Further longitudinal prospective studies are required to confirm the common denominators and epidemiology of CTE in professional American football players, which have been identified by this case series.