Serotonin Receptors in the Medulla Oblongata of the Human Fetus and Infant: The Analytic Approach of the International Safe Passage Study.

The Safe Passage Study is an international, prospective study of approximately 12 000 pregnancies to determine the effects of prenatal alcohol exposure (PAE) upon stillbirth and the sudden infant death syndrome (SIDS). A key objective of the study is to elucidate adverse effects of PAE upon binding to serotonin (5-HT) 1A receptors in brainstem homeostatic networks postulated to be abnormal in unexplained stillbirth and/or SIDS. We undertook a feasibility assessment of 5-HT1A receptor binding using autoradiography in the medulla oblongata (6 nuclei in 27 cases). 5-HT1A binding was compared to a reference dataset from the San Diego medical examiner's system. There was no adverse effect of postmortem interval ≤100 h. The distribution and quantitated values of 5-HT1A binding in Safe Passage Study cases were essentially identical to those in the reference dataset, and virtually identical between stillbirths and live born fetal cases in grossly non-macerated tissues. The pattern of binding was present at mid-gestation with dramatic changes in binding levels in the medullary 5-HT nuclei over the second half of gestation; there was a plateau at lower levels in the neonatal period and into infancy. This study demonstrates feasibility of 5-HT1A binding analysis in the medulla in the Safe Passage Study.

Clinicoradiologic response of neurologic tuberculous mass lesions in children treated with thalidomide.

Neurologic tuberculous pseudoabscesses that clinically progress despite conventional antituberculosis therapy may be responsive to adjuvant thalidomide, a potent tumor necrosis factor-α inhibitor. In this study, the addition of thalidomide provided substantial clinical benefit in the majority of patients, and magnetic resonance imaging evolution of lesions from early-stage "T2 bright" with edema to "T2 black" represented a marker of cure.

October 2001: 40-year-old Xhosa male with back pain and leg weakness.

A 40-year-old Xhosa male presented with progressive upper lumbar back pain and weakness At examination he was emaciated and had enlarged lymph nodes in the groin and axilla. Both lower limbs were severely atrophic and weak. Sensation to touch and pain was decreased below L3 bilaterally. MR of the spine showed a discrete, contrast-enhancing epidural mass. A T10-T12 laminectomy revealed an soft, vascular extradural tumor dorsal to the cord. The mass was loosely applied to the dura and easy to remove. The operative specimen consisted of a sausage-shaped (3.5 x 2.0 x 1.2 cm), thinly-encapsulated mass of reddish-brown tissue. The cut surface had a mottled, vaguely nodular, yellowish-brown appearance. Microscopic examination revealed sheets of hematopoeitic elements, including myeloid, red cell and megakaryocytic lines, the latter showing Factor 8-related positivity. The final diagnosis was extramedullary hematopoiesis (EMH). A bone marrow biopsy performed as a result of the diagnosis showed a myeloproliferative disease and polycythemia vera. EMH in the spinal epidural space is a rare but treatable cause of progressive paraparesis in patients with a variety of hematological disorders. Since 1956 there have been more than 50 reported cases, most of which occurred in association with thalassaemia. In spinal cord compression secondary to EMH, the lesions are commonly localized to the mid-lower thoracic region.

Alcohol-induced psychotic disorder: a comparative study on the clinical characteristics of patients with alcohol dependence and schizophrenia.

OBJECTIVE: Alcohol-induced psychotic disorder (AIPD) is a rare complication of excessive alcohol use for which limited comparative studies are available. The aim of this study was to prospectively investigate demographic and psychopathological characteristics in patients with AIPD, schizophrenia, and uncomplicated alcohol dependence. We postulated that AIPD is a discrete clinical entity that can be differentiated from schizophrenia and uncomplicated alcohol dependence by means of standardized clinical assessments. METHOD: Twenty-eight patients with AIPD, 21 with schizophrenia and 20 with uncomplicated alcohol dependence were assessed using psychiatric rating scales, including the positive and Negative Syndrome Scale. RESULTS: Patients with AIPD had a significantly lower educational level, later onset of psychosis, higher levels of depressive and anxiety symptoms, fewer negative and disorganized symptoms, better insight and judgment, and less functional impairment compared with patients with schizophrenia. CONCLUSION: The study provides further supportive evidence that AIPD can be clinically distinguished from schizophrenia.

Tuberculous cerebrovascular disease: a review.

Cerebrovascular complications of tuberculous meningitis are common, and may represent its most serious legacy. They present in clinically diverse ways, and continue to develop during the initial stages of treatment. Magnetic resonance imaging is the imaging modality of choice in detecting brain infarcts, typically revealing multiple or bilateral lesions in the territories of the middle cerebral artery perforating vessels. Vessel pathology appears to be a consequence of its immersion in the local inflammatory exudate. Infiltrative, proliferative and necrotising vessel pathologies have been described, but the relative contributions of each and of luminal thrombosis to brain damage remain unclear. There is some evidence that vasospasm may mediate strokes early in the course of the disease and proliferative intimal disease later strokes. Anti-tuberculous chemotherapy appears to be relatively ineffective in preventing vascular complications, perhaps suggesting an immune mechanism. However, a preventive role for corticosteroids remains to be proven. Study of the molecular pathogenesis of TBM vasculopathy is in its infancy. This review focuses in particular on pathogenetic aspects of tuberculous cerebrovascular disease, with a view to its future targeted prevention.

Tuberculous encephalopathy: a reappraisal.

Forty years ago Dastur and Udani described a form of diffuse cerebral damage in tuberculosis, which they called tuberculous encephalopathy. Their pathological and clinical observations led them to propose an immune pathogenesis. Although there have been no convincing independently reported series, the entity is now established in the tuberculosis literature. We review the literature on tuberculous encephalopathy, and suggest alternative aetiopathogenetic explanations for the appearances of the brain in these cases. We propose that tuberculosis is one of many infections which may be associated with a range of immune, drug-related, hypoxic-ischaemic and toxic diffuse brain pathologies.

Fatal human infection with rabies-related Duvenhage virus, South Africa.

Duvenhage virus was isolated from a patient who died of a rabies-like disease after being scratched by a bat early in 2006. This occurred approximately 80 km from the site where the only other known human infection with the virus had occurred 36 years earlier.