The cerebral neuropathology of Type 2 diabetes (CNDM2) has not been positively defined. This review includes a description of CNDM2 research from before the ‘Pubmed Era’. Recent neuroimaging studies have focused on cerebrovascular and white matter pathology. These and prior studies about cerebrovascular histopathology in diabetes are reviewed. Evidence is also described for and against the link between CNDM2 and Alzheimer’s disease pathogenesis. To study this matter directly, we evaluated data from University of Kentucky Alzheimer’s Disease Center (UK ADC) patients recruited while non-demented and followed longitudinally. Of patients who had come to autopsy (N=234), 139 met inclusion criteria. These patients provided the basis for comparing the prevalence of pathological and clinical indices between well-characterized cases with (N=50) or without (N=89) the premortem diagnosis of diabetes. In diabetics, cerebrovascular pathology was more frequent and Alzheimer-type pathology was less frequent than in non-diabetics. Finally, a series of photomicrographs demonstrates histopathological features (including clinical–radiographical correlation) observed in brains of persons that died after a history of diabetes. These preliminary, correlative, and descriptive studies may help develop new hypotheses about CNDM2. We conclude that more work should be performed on human material in the context of CNDM2.

Posaconazole is a triazole with broad spectrum of activity against multiple fungi including members of the fungal order Mucorales. This activity has been shown both in clinical and in vitro studies, which are critically reviewed here. It has become very popular in prophylaxis in acute myelogenous leukemia (AML) induction and in the graft-versus-host disease (GVHD) settings after 2 recent prospective trials that showed advantage of posaconazole prophylaxis compared to fluconazole or itraconazole. In this report, 2 patients are presented, in whom, despite posaconazole prophylaxis, invasive and ultimately fatal Rhizopus pulmonary infections developed. These cases are similar to a previously reported case of Rhizopus infection in a stem cell transplant recipient who also received posaconazole, indicating a potential newly recognized pattern of breakthrough infections in patients receiving posaconazole prophylaxis.

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Ehlers-Danlos syndrome (EDS) type IV is a connective tissue disorder characterized by the inability to produce sufficient amounts of collagen or a defect in the structure of collagen. The most serious complications include a rupture of a viscus or vascular rupture with or without mural dissection. Death may result from internal hemorrhage. This report describes three cases of sudden and unexpected death caused by EDS type IV. Two cases involved hemothorax as a result of dissection of the subclavian artery and aorta, respectively. The third case represented spontaneous pulmonary rupture and hemorrhage. A detailed family history should be sought, and additional specimens collected to confirm the diagnosis, including skin fibroblasts for collagen testing and blood for DNA testing. The forensic pathologist should consider the possibility of EDS type IV upon discovery of spontaneous visceral or arterial rupture and should alert the family members of this hereditary and potentially fatal condition.

Fatal fat embolism is usually thought of as a sequel to long-bone fracture, although cases secondary to soft tissue injury and atraumatic conditions have been infrequently reported. In this case of a two-year-old child-abuse victim who sustained multiple blunt traumatic injuries without skeletal fractures, pulmonary and systemic (brain and kidney) fat emboli were identified. At autopsy, all thoracic and abdominal viscera were intact; cranial contents exhibited only diffuse symmetrical petechial hemorrhages of the white matter. Because of the severe and widespread nature of soft tissue hemorrhage, and the absence of a grossly discernible cause of death, fat embolism was suspected. Using a combination of frozen section with oil red O staining and formalin-fixed osmium stained tissues, the immediate cause of death was determined to be diffuse fat embolism. Review of the literature reveals a pathophysiologic basis for fat embolism in the absence of fracture, both as a consequence of an acute increase in local pressure at the site of trauma and an alteration of the emulsification of blood lipids during shock. In light of these findings, we present this case to remind the forensic science community to consider fat embolism as the cause of death in cases of blunt-force injury without fracture.

Replacement of the myocardium by fibrous and adipose tissue is well documented in the right ventricle, but has been rarely described in the left ventricle. We present two cases of extensive fibrofatty infiltration of the left ventricle without significant right ventricular involvement in young men whose presenting symptom was sudden death.

This is a report of a child who died at 20 months from what was clinically thought to be cardiomyopathy of unknown etiology. Barth syndrome, an X-linked mitochondrial cardioskeletal myopathy, was diagnosed by genetic testing at autopsy. Barth syndrome presents in infancy or childhood with cardiomyopathy, hypotonia, growth delays, and cyclic neutropenia. Other associated laboratory findings can include hypocholesterolemia, relative monocytosis, low prealbumin, low plasma carnitine, and lactic acidosis. The classic echocardiogram finding is left ventricular noncompaction, although not always present. Until recently, the most reliable biochemical finding has been 3-methylglutaconic aciduria. However, quantitative analysis must be specifically requested for results to be reliable. Recently, a confirmatory tetralinoleoyl cardiolipin high-pressure liquid chromotography-tandem mass spectrometry blood test has become available. Genetic testing is also confirmatory and details the underlying mutation. Diagnosis is often missed or delayed and early diagnosis improves survival. The purpose of this case report is to encourage physicians to include Barth syndrome in the differential for cardiomyopathy of uncertain etiology in males, especially in the presence of growth delays, hypotonia, neutropenia, and/or family history of pediatric male death of unknown etiology.

The width of cortical sulci in bipolar patients (n=19) and healthy controls (n=35) was examined using a novel automated technique involving magnetic resonance imaging. All sulci were wider for bipolar patients than for healthy controls. Bipolar-control differences were largest for the superior and intermediate frontal sulci, smallest for the occipital and cingulate sulci, and intermediate in magnitude for the other sulci (intraparietal, inferior frontal, and central sulci). The results were interpreted in terms of neurodegenerative-illness-related processes, which could produce cortical atrophy and result in wider sulci.