Myocarditis associated with Hashimoto's disease: a case report.

We report on a sudden cardiac death case involving a 40-year-old man with no known medical history. Forensic autopsy showed lymphocytic myocarditis associated with lymphocytic thyroiditis. In both the heart and the thyroid gland, the inflammatory foci often had a nodular pattern with a germinal centre. Virological and toxicological analyses were negative. Postmortem biochemistry showed a slight increase in TSH in combination with normal T3 and T4 blood levels suggesting hypothyroidism. High titres of antiperoxidase and antithyroglobulin antibodies with normal levels of TSH receptor antibodies, in addition to biological hypothyroidism and lymphocytic inflammation were consistent with the diagnosis of Hashimoto's thyroiditis. Immunohistochemical studies excluded a lymphoma and showed no evidence of viral myocarditis. In contrast to Grave's disease, Hashimoto's thyroiditis has never been reported in association with myocarditis as a cause of sudden death. We conclude that the cardiac immunological and histological pattern, similar to that found in the thyroid gland suggests an autoimmune myocarditis.

Skeletal remains presumed submerged in water for three years identified using PCR-STR analysis.

We describe the successful identification of the remains of a saponified body found in a dam by typing of nuclear DNA. Whereas DNA extracted from soft tissues yielded negative PCR results, DNA extracted from the bone by a slightly modified Qiagen procedure allowed the typing of sex (AMG locus) and of 10 additional STR loci. An identity document was found belonging to a man missing for 3 years and comparison of the results to the DNA profiles of his son and wife confirmed the identity. The longest delay reported until now for successful nuclear DNA genotyping after immersion in river water was 18 months. This case demonstrates a delay of up to 3 years.

Postmortem revelation of sickle cell disease following fatal episode of acute bronchial asthma.

A 19-year-old black male with previous history of mild bronchial asthma presented sudden dyspnea and died in a state of respiratory distress in spite of resuscitation attempts. Autopsy showed typical lesions of acute bronchial asthma in a context of long-standing asthma associated with a massive and disseminated intravascular sickling. Hemoglobin electrophoresis diagnosed heterozygous sickle cell disease. This rare case raises the problem of the accuracy of death certificate, especially the difficulties to distinguish postmortem lesions as the underlying cause of death or the contributory cause of death.

Symmetrical necrosis of the solitary tract nuclei as a contributory cause of death.

A 64-year-old man died in spite of surgery 4 days after attempting suicide. He first tried to hang himself with a rope and when the hanging did not succeed, he cut his throat with a knife. The autopsy showed four sutured cervical wounds with laryngeal wounds but without associated important vascular injury. The neuropathological study revealed two watershed-type haemorrhagic infarcts, involving the left occipital lobe and the left cerebellum. It also showed a symmetrical necrosis of solitary tract nuclei in the medullary tegmentum. Such a lesion is likely to result from sudden acute transient circulatory failure and might have played a role in the secondary autonomous cardiac and respiratory dysfunctions following a non-lethal trauma.

Presence and cellular distribution of HIV in the testes of seropositive subjects: an evaluation by in situ PCR hybridization.

Cellular distribution of HIV-1 proviral DNA has been studied, by in situ PCR hybridization, in the testes of infected men who died at various stages of the disease. In seropositive asymptomatic subjects, HIV-1 proviral DNA was present in the nuclei of germ cells at all stages of their differentiation. The presence of provirus did not induce germ cell damage, was associated with normal spermatogenesis, and was not accompanied by morphologic signs of immune response. The observed HIV hybridization pattern of germ cells suggests clonal infection. Mechanisms responsible for HIV penetration in testicular germ cells remain to be clarified; however, the possibility of a direct infection of the germ cells by cell-free virus is suggested. In the testes of AIDS-deceased men, histologic features of hypoplasia with arrested spermatogenesis were evident, and few infected spermatogonia and spermatocytes were observed. The whole of these data demonstrates that the testis is a site of early viral localization that fails to elicit an immunological response, and that HIV-seropositive men produce infected spermatozoa that are released in the genital tract.

[Central nervous system lesions in the early stages of HIV infection]. / Les lésions du système nerveux central au stade précoce de l'infection par le VIH.

Early HIV-1 invasion of the central nervous system has been demonstrated by many cerebrospinal fluid studies; however, most HIV-1 carriers remain neurologically unimpaired during the so-called "asymptomatic" period lasting from seroconversion to symptomatic AIDS. Therefore, very few neuropathological studies have been conducted in the early pre-AIDS stages, and the natural history of central nervous system changes in HIV-1 infection remains poorly understood. Examination of brains of asymptomatic HIV-1 positive individuals who died accidentally and of rare cases with acute fatal encephalopathy revealing HIV infection, and comparison with experimental simian immunodeficiency virus and feline immunodeficiency virus infections suggest that, invasion of the CNS by HIV-1 occurs at the time of primary infection and induces an immunological process in the central nervous system. This includes an inflammatory T-cell reaction with vasculitis and leptomeningitis, and immune activation of brain parenchyma with increased number of microglial cells, upregulation of major histocompatibility complex class II antigens and local production of cytokines. Myelin pallor and gliosis of the white matter are usually found and are likely to be the consequence of opening of the blood-brain barrier due to vasculitis; direct damage to oligodendrocytes by cytokines may also be involved. These white matter changes may explain, at least partly, the early cerebral atrophy observed, by magnetic resonance imaging, in asymptomatic HIV-1 carriers. In contrast, cortical damage seems to be a late event in the course of HIV-1 infection. There is no significant neuronal loss at the early stages of the disease, no accompanying increase in glial fibrillary acid protein staining in the cortex, and only exceptional neuronal apoptosis. Although HIV-1 proviral DNA may be demonstrated in a number of brains, viral replication remains very low during the asymptomatic stage of HIV-1 infection. This makes it likely that, although opening of the blood brain barrier may facilitate viral entry into the brain, specific immune responses including both neutralising antibodies and cytotoxic T-lymphocytes, continuously inhibit viral replication at this stage.

Kinetics of elimination and acute consequences of cerebral air embolism.

The pathophysiology of arterial air embolism inducing brain injuries remains unclear. Previous experiments demonstrated the usefulness of computed tomography (CT) in the detection of air emboli in canine brain. This canine study investigates CT's ability to detect small air bubbles and to determine the kinetics of air elimination from cerebral arteries and its relationship with clinical, electroencephalographic (EEG), and histological manifestations. CT detects small air embolism, and intracerebral air volume strongly correlates with injected air dose (r2 = 0.86, p = 2 x 10(-3)). Air clearance time significantly depends on intracerebral air volume (r2 = 0.86, p = 0.04) and on the number of bubbles (r2 = 0.71, p = 0.03), whereas half-life of air elimination does not. No relationship was found between injected air dose, air clearance time, intracerebral volume of air, and clinical, EEG, and histological findings. The data indicate that CT accurately detects small air bubbles in the early course of cerebral air embolism, that air elimination from cerebral arteries follows a first-order compartment model, and that early CT findings do not correlate with clinical, EEG, and histological manifestations.

Effects of mechanical ventilation with normobaric oxygen therapy on the rate of air removal from cerebral arteries.

OBJECTIVE: We conducted the current study to evaluate the removal rate of air embolism from cerebral arteries after spontaneous breathing at a low FIO2 in comparison with mechanical ventilation at an FIO2 of 1.0. DESIGN: Randomized, experimental trial. SETTING: Neuroimaging department at a veterinary school hospital laboratory. SUBJECTS: Nine anesthetized beagles undergoing mechanical ventilation with previous normal cranial computed tomography (CT) scan. INTERVENTIONS: In each dog, after a control scan, air was infused at a constant flow rate, via a catheter inserted into the internal carotid artery. CT scan was repeated until typical bubbles appeared. Immediately after, the animals were randomly assigned to breathe room air (group A), or to be mechanically ventilated at an FIO2 of 1.0 (group B). CT scan was again repeated every minute until the removal of all bubbles. We compared the volume of air infused per kg of body and brain weights, the lowest density among bubbles (Hounsfield units), the duration of radiologic findings, and the ratio of volume/duration (mL/kg/min) between the two groups, using the Mann-Whitney test. RESULTS: The volume of air infused per kg of body and brain weights and density were not significantly different between the two groups. The duration of radiologic findings was shorter (p < .02) in group B (7.0 +/- 4.7) than in group A (20.4 +/- 3.8), and the air removal rate from cerebral arteries (expressed as volume/duration of radiologic findings) was dramatically improved (p < .02) in group B (0.159 +/- 0.042) in comparison with group A (0.046 +/- 0.016). CONCLUSIONS: These results suggest that the removal rate of air from cerebral arteries is dramatically increased by mechanical ventilation at an FIO2 of 1.0. Consequently, the time of cerebral ischemia may be decreased, but the result does not account for the effects of each factor separately. Further studies are required to evaluate the clinical benefits of high FIO2 administration and of mechanical ventilation separately. However, the prompt application of mechanical ventilation with an FIO2 of 1.0 may be recommended when air embolism is suspected.

[Intramedullary localization of a primary cerebral lymphoma in AIDS]. / Localisation intramédullaire d'un lymphome cérébral primitif au cours du SIDA.

A 36 years-old male with AIDS, presented with left hemiparesis revealing a right parietal tumour. Stereotactic biopsy demonstrated a malignant non-Hodgkin's lymphoma. His condition partially improved following radiotherapy and chemotherapy. Three months later he was re-admitted with progressive bilateral root pain and urinary incontinence resulting in paraplegia with sensory loss below T10. He died one month later from generalized sepsis. Neuropathology confirmed an immunoblastic B-cell malignant non-Hodgkin's lymphoma in the white matter of the right parietal lobe and revealed a centrospinal localisation of the lymphoma in the thoracic cord at T10. There was no visceral localisation of the tumour. Secondary spread to the spinal cord of malignant non Hodgkin's lymphomas, usually causes meningo-myelo-radiculitis. Intraspinal deposits of primary cerebral lymphomas are uncommon and have never been previously described in AIDS, to our knowledge. Their pathogenesis is unclear. In our case, neuropathological findings are consistent with diffusion of the primary tumour to leptomeninges and secondary infiltration of the spinal cord along the perivascular spaces.

Early brain changes in HIV infection: neuropathological study of 11 HIV seropositive, non-AIDS cases.

We examined 11 brains of human immunodeficiency virus (HIV) seropositive cases who died from unnatural causes (10 intravenous drug abusers who died from heroin overdose and 1 homosexual dead from a gunshot injury); 10 brains of HIV seronegative heroin addicts who died from overdose and 1 seronegative drug abuser who died from gunshot injury served as controls. Complete postmortem examination did not show evidence of acquired immune deficiency syndrome (AIDS) or AIDS related complex. Terminal changes including nerve cell ischemia, edema and diffuse vascular congestion were observed in all cases. Perivascular pigment deposition with macrophages was a constant finding in drug addicts and was probably related to chronic intravenous injection. In contrast, cerebral vasculitis was significantly more frequent and marked in HIV seropositive cases and was often associated with lymphocytic meningitis. Granular ependymitis, myelin pallor with reactive astrocytosis and microglial proliferation were also more frequent and more severe in HIV seropositive cases. Immunocytochemistry was negative for HIV antigens. Our study further supports the view that early central nervous system changes occur in HIV infection.

Suicidal stab wounds of the throat.

Suicide by stabbing one's throat remains very rare and very few cases have been reported in the forensic literature. In such cases, the important distinction is between suicide and homicide. The direction of stab wounds, their depth, site and number have particular importance in helping to recognize suicide. Suicide when attempted by transfixion of the neck in middle aged and elderly adults often reveals a definite resolution to kill oneself.

MR imaging of acute spinal cord injury: results of an experimental study in dogs.

A weight-drop model was used to induce 16 acute lesions of varying severity in the spinal cords of eight mongrel dogs. The subsequent 3- to 7-hr postinjury MR images (0.5 T) were assessed. T1-weighted images contributed little information. Injection of gadolinium tetra-azacyclododecane tetraacetic acid did not result in significant enhancement. T2-weighted sequences offered precise detection and delineation of the lesions, displaying fusiform hyperintense signal abnormalities that corresponded to both edema and hemorrhage. In low-impact injuries, abnormalities were small and centrally located, sparing the periphery of the spinal cord. In these cases hemorrhage was minimal and limited to the center of the lesion. In severe-impact injuries, MR showed widespread longitudinal extension with involvement of the periphery of the spinal cord. In the most severe injuries, a central heterogeneous signal component was frequently observed opposite the site of impact because of important hemorrhage within the cord. Overall, hyperintense areas correlated closely with lesion severity, as demonstrated by pathologic findings. T2-weighted MR images obtained at 0.5 T were found to be reliable in the evaluation of acute spinal cord trauma.

Age estimation from quantitation of features of "chest plate" X-rays.

This study presents a method for estimating the age at death from the quantitation of roentgenologic features of X-ray films of chest plates obtained during routine autopsies. Multiple linear regression analysis allows estimation of coefficients of regression of features on known age-at-death individuals. The regression equation can be used in turn for age estimation of an unknown age-at-death individual. The accuracy of age estimation is about +/- 8.4 years (standard error) which is in the range of previously published macroscopic methods, though the present method is much faster and simpler.