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Background Meningiomas are the single most common brain tumor. The incidence of these tumors increases with age; different studies have shown that meningiomas usually appear after the age of 50. These tumors are more common in women than in men, and women are twice as likely to suffer from the condition. Surgery is the primary form of treatment, which can be curative with complete resection. If the tumor is unresectable or other treatments such as surgery and radiotherapy have failed, hormonal therapy or chemotherapy may be considered. There is limited information about the clinical, demographic, and histopathological characteristics of these tumors in the population of Bogota, Colombia. Objective To evaluate the expression of progesterone receptors in patients over 18 years old who have been diagnosed with meningiomas in a high-complexity hospital in Bogota, Colombia, and to describe the demographic and histopathological characteristics of these patients. Methods This is a descriptive and retrospective case series. Patients with meningioma who underwent surgical resection at a high-complexity hospital in Bogota, Colombia, from 2016 to 2019 were retrospectively identified and studied. Demographic variables, such as age and gender, were extracted from the clinical chart. Indirect immunoperoxidase staining was carried out for the progesterone receptor (PR) and Ki67. PR is analyzed as positive and negative, and the Ki67 proliferation index was determined. Results Thirty-two meningiomas from patients who underwent surgery were available for analysis. Twenty-five (78.1%) were positive for PR, 71.8% were females, and 93% were World Health Organization (WHO) grade I. Meningothelial (28%), fibrous (25%), and transitional (25%) meningiomas were the most frequent subtypes, correspondingly. The Ki67 mean value was 1.14 (0.11-10.71). Conclusion Our case series showed a greater frequency of meningiomas in women, with a high PR expression and a low Ki67 proliferation rate. These data correlate with literature worldwide.

To determine the cause of death (as a result of neurologic or nonneurologic complications or accidents) in patients with multiple sclerosis (MS), we reviewed the autopsies of 50 subjects with MS from the Office of the Chief Medical Examiner of Maryland (OCME) between 1982 and 2004. The series included 32 females and 18 males (mean age, 45.8 years; range, 25-69 years) and the causes of death were classified into 3 categories: (A) neurologic complication directly related to MS; (B) nonneurologic complications or other medical causes; and (C) accidents, etc. Of the 50 cases, in 43 there was a history of MS, but in 7 subjects there was not, and the diagnosis was established by neuropathologic examination. In Group A, 21 (42%) cases, deaths were directly related to a neurologic complication; in Group B, 14 (28%) cases were related to the following nonneurologic and medical causes: ASCVD 9 (18%), metabolic disorder 1 (2%), pulmonary embolism 3 (6%), and bronchopneumonia 1 (2%); and in Group C, 15 (30%) cases, deaths were due to trauma, 9 (18%); intoxication, 5 (10%); and thermal injury, 1 (2%). Thus, among the 50 subjects, in 26, deaths occurred naturally; and in 24, from accidents, homicides, suicides, or undetermined causes. Pathologically, the majority of cases showed either chronic inactive (66.7%) or chronic active (15.6%) demyelinating lesions, mainly in the cerebral hemispheres. In some cases, it appears that demyelinating lesions, involving brain regions that regulate cardiorespiratory activity, could be considered as the immediate cause of death, but a large proportion appears to be due to other causes such as accidents and trauma. Thus, it seems likely that taking specific precautions could prevent some deaths in MS.

To better understand the pathogenesis of brain dysfunction in Gaucher disease (GD), we studied brain pathology in seven subjects with type 1 GD (four also exhibited parkinsonism and dementia), three with type 2 GD and four with type 3 GD. Unique pathologic patterns of disease involving the hippocampal CA2-4 regions and layer 4b of the calcarine cortex were identiWed. While these Wndings were common to all three GD phenotypes, the extent of the changes varied depending on the severity of disease. Cerebral cortical layers 3 and 5, hippocampal CA2-4, and layer 4b were involved in all GD patients. Neuronal loss predominated in both type 2 and type 3 patients with progressive myoclonic encephalopathy, whereas patients classiWed as type 1 GD had only astrogliosis. Adjacent regions and lamina, including hippocampal CA1 and calcarine lamina 4a and 4c were spared of pathology, highlighting the speciWcity of the vulnerability of selective neurons. Elevated glucocerebrosidase expression by immunohistochemistry was found in CA2-4. Hippocampal 45 Ca 2+ uptake autoradiography in rat brain was performed demonstrating that hippocampal CA2-4 neurons, rather than CA1 neurons, were calcium-induced calcium release sensitive (CICR-sensitive). These Wndings match recent biochemical studies linking elevated glucosylceramide levels to sensitization of CA2-4 RyaR receptors and 300% potentiation of neuronal CICR sensitivity. In two patients with type 1 GD and parkinsonism, numerous synuclein positive inclusions, similar to brainstem-type Lewy bodies found in Parkinson disease, were also found hippocampal CA2-4 neurons. These Wndings argue for a common cytotoxic mechanism linking aberrant glucocerebrosidase activity, neuronal cytotoxicity, and cytotoxic Lewy body formation in GD. Published by Elsevier Inc.

Neurocysticercosis (NCC) is a common central nervous system (CNS) infection caused byTaenia soliummetacestodes. Despite the well-documented importance of the granulomatous response in the pathogenesis of this infection, there is limited information about the types of cells and cytokines involved. In fact, there has been limited characterization of human brain granulomas with any infectious agent. In the present study a detailed histological and immunohistochemical analysis of the immune response was performed on eight craniotomy specimens where a granuloma surrounded eachT. soliummetacestode. The results indicated that in all the specimens there was a dying parasite surrounded by a mature granuloma with associated fibrosis, angiogenesis, and an inflammatory infiltrate. The most abundant cell types were plasma cells, B and T lymphocytes, macrophages, and mast cells. Th1 cytokines were prevalent and included gamma interferon, interleukin-18 (IL-18), and the immunosuppressive, fibrosis-promoting cytokine transforming growth factor β. The Th2 cytokines IL-4, IL-13, and IL-10 were also present. These observations indicate that a chronic immune response is elicited in the CNS environment with multiple cell types that together secrete inflammatory and anti-inflammatory cytokines. In addition, both collagen type I and type III deposits were evident and could contribute to irreversible nervous tissue damage in NCC patients.