1/7. Vascular changes in tuberculous meningoencephalitis.Our report refers two cases of tuberculous encephalomeningitis which differ in the course and pathological changes. In case 1 blood vessels showed features of peri, endo-, or panvasculites. In some vessels endothelium proliferation leading to the stenosis or obliteration of the vascular lumen was observed. necrosis was an effect of vessels occlusion. In case 2 many fewer vessel were involved in onflammation process. Vascular changes were also less extensive and were observed more rarely. Tuberculous infection often caused less tissue lesions than vascular changes. Different pathological changes probably depend on the type and virulence of Myobacterium tuberculosis and on the host immune response to the infection.- - - - - - - - - - ranking = 1keywords = blood vessel (Clic here for more details about this article) |
2/7. Fatal encephalitis due to nipah virus among pig-farmers in malaysia.BACKGROUND: Between February and April, 1999, an outbreak of viral encephalitis occurred among pig-farmers in malaysia. We report findings for the first three patients who died. methods: Samples of tissue were taken at necropsy. Blood and cerebrospinal-fluid (CSF) samples taken before death were cultured for viruses, and tested for antibodies to viruses. FINDINGS: The three pig-farmers presented with fever, headache, and altered level of consciousness. myoclonus was present in two patients. There were signs of brainstem dysfunction with hypertension and tachycardia. Rapid deterioration led to irreversible hypotension and death. A virus causing syncytial formation of vero cells was cultured from the CSF of two patients after 5 days; the virus stained positively with antibodies against hendra virus by indirect immunofluorescence. IgM capture ELISA showed that all three patients had IgM antibodies in CSF against Hendra viral antigens. Necropsy showed widespread microinfarction in the central nervous system and other organs resulting from vasculitis-induced thrombosis. There was no clinical evidence of pulmonary involvement. inclusion bodies likely to be of viral origin were noted in neurons near vasculitic blood vessels. INTERPRETATION: The causative agent was a previously undescribed paramyxovirus related to the hendra virus. Close contact with infected pigs may be the source of the viral transmission. Clinically and epidemiologically the infection is distinct from infection by the hendra virus. We propose that this Hendra-like virus was the cause of the outbreak of encephalitis in malaysia.- - - - - - - - - - ranking = 1keywords = blood vessel (Clic here for more details about this article) |
3/7. Pathological and virological assessment of acute HTLV-I-associated myelopathy complicated with encephalopathy and systemic inflammation.HTLV-I-associated myelopathy, also known as tropical spastic paraparesis (HAM/TSP), is a chronic inflammatory disease of the spinal cord. Acute cases are uncommon. We report the case of a 41-year-old woman with acute HAM/TSP complicated with encephalitis, an intense inflammatory reaction of the nervous system and lymphocytic infiltration of skeletal muscles, liver, salivary, adrenal and pituitary glands. The immunohistochemical studies of the lymphocytes surrounding blood vessels showed both B- and t-lymphocytes, in similar proportion, with both CD4- and CD8-positive cells. In addition, many perivascular and scattered macrophages were observed. adult T-cell leukemia/lymphoma (ATL) was ruled out. The marrow aspirate was normal. Serial cerebrospinal fluid (CSF) analysis showed presence of htlv-i antibodies, but without intrathecal synthesis of specific antibodies. Determination of HTLV-I viral loads demonstrated increased levels in the CSF relative to the peripheral blood and may be associated with widespread inflammation. The pathological and immunological findings may help understand the role of immune-reactive cells in the pathogenesis of HTLV-I-associated myelopathy.- - - - - - - - - - ranking = 1keywords = blood vessel (Clic here for more details about this article) |
4/7. The patterns of varicella zoster virus encephalitis.Varicella zoster virus (VZV) encephalitis has become increasingly prevalent in the era of acquired immunodeficiency syndrome (AIDS), and a widening spectrum of pathological lesions has defined the disease in these and other severely immunosuppressed patients. VZV produces three distinct morphological patterns of brain damage. VZV can cause bland or hemorrhagic infarctions secondary to a large or medium vessel vasculopathy. Deep white matter, ovoid mixed necrotic, and demyelinative lesions occur as a consequence of small vessel vasculopathy, with demyelination dependent on the degree of additional oligodendrocyte infection. Distinctive Cowdry A intra-nuclear viral inclusions are rare in either large or small blood vessels or near infarctions, but are commonly found in glial cells at the edge of the smaller ovoid, demyelinative lesions. Ependymal and periventricular necrosis occurs as a result of vasculopathy of subependymal vessels and secondary infection of ependymal and other glial cells in the periventricular region. To clarify these patterns of VZV encephalitis and shed light on their pathogenesis, the authors have examined all cases of VZV encephalitis seen at our institution since 1984. Additionally, the authors review the extensive literature in an attempt to classify the patterns of VZV encephalitis into (1) large/ medium vessel vasculopathy with bland or hemorrhagic infarctions, (2) small vessel vasculopathy with mixed ischemic/demyelinative lesions, and (3) ventriculitis/periventriculitis. Although one of these three patterns often predominates clinically and radiographically, careful histological examination at autopsy shows mixed features in many cases.- - - - - - - - - - ranking = 1keywords = blood vessel (Clic here for more details about this article) |
5/7. Imaging findings in rabies.A 10 year old Vietnamese girl presented with clinical features of an acute encephalitic process. A cerebral angiogram performed to rule out vasculitis showed narrowing at the supraclinoid internal carotid and terminal basilar arteries. A diagnosis of rabies was established at autopsy. Although the major blood vessels and basal meninges were normal it was possible that transient arterial spasm induced by the viral infection was responsible for the angiographic appearance. Other imaging findings in our patient are described with a brief review of the literature. This is only the second case of rabies reported in australia. rabies is a rare disease in the Australian community. Recently one patient with atypical clinical presentation was confirmed to have the disease only at autopsy. In the clinical work-up, various radiological examinations were performed and a range of interesting features were encountered including an abnormal cerebral angiogram. The purpose of this paper is to report on these unusual features and to review those documented in the literature.- - - - - - - - - - ranking = 1keywords = blood vessel (Clic here for more details about this article) |
6/7. Clinical and radiological variability of influenza-related encephalopathy or encephalitis.BACKGROUND: Influenza-related encephalopathy or encephalitis is not rare in children. However, it is not well understood why the brain lesion develops from influenza infection. The purpose of this study was to clarify its pathogenesis by analyzing the clinical and neuroradiological findings in patients having influenza-related brain lesions. methods: The clinical findings in 10 children with influenza-related brain lesions were analyzed. Eight patients had findings consistent with the diagnosis of acute encephalopathy and two had postinfectious focal encephalitis. RESULTS: The results from magnetic resonance imaging (MRI) or computed tomography were divided into five categories: normal (category 1); diffuse involvement of the cerebral cortex (category 2); diffuse brain edema (category 3); symmetrical involvement of the thalamus (category 4); and postinfectious focal encephalitis (category 5). patients in categories 2-4 had symmetrical or diffuse brain lesions without leukocytosis in their cerebrospinal fluid, and there were no inflammatory reactions in the brains of two autopsied patients. Furthermore, serum concentrations of GOT were high in all, and disseminated intervascular coagulation was present in 4 of 5. CONCLUSIONS: These findings suggested that the pathogenesis of the brain lesions in these cases was toxic or metabolic damage due to multisystemic organ diseases induced by the influenza virus. The MRI findings in patients in category 2 suggested diffuse cortical cell necrosis. On the other hand, the thalamic lesions in category 4 patients reflected hyperpermeability of the blood vessels followed by severe edema with or without microhemorrhages. The pathogenesis of lesions of category 5 included allergic angitis of a self-limiting nature. These findings indicated that the pathogenesis of brain damage induced by influenza infection was very variable.- - - - - - - - - - ranking = 1keywords = blood vessel (Clic here for more details about this article) |
7/7. Profound cerebrospinal fluid pleocytosis and Froin's Syndrome secondary to widespread necrotizing vasculitis in an hiv-positive patient with varicella zoster virus encephalomyelitis.Demonstration of the direct involvement of cranial blood vessels by varicella zoster virus (VZV) is facilitated by immunohistochemistry (IHC), in situ hybridization (ISH) and polymerase chain reaction (PCR) techniques. The extent to which an inflammatory vasculitis serves as the pathogenic mechanism for VZV encephalomyelitis (VZVE) is still, however, debated. Most VZVE patients are immunocompromised and show little inflammation, either pre-mortem in cerebrospinal fluid (CSF) or at autopsy. We describe an hiv-positive patient with a moderately depressed CD4 count (304) who presented with massively elevated CSF protein (1800 mg/dl), bloody CSF and pleocytosis (1300 white blood cells (WBC)/mm3). His CSF was positive for VZV dna by PCR. He was treated with acyclovir and foscarnet, but died. At autopsy, an unusually widespread, inflammatory, transmural vasculitis caused by VZV affected meningeal vessels at virtually all brain stem and spinal cord levels, causing multiple subpial hemorrhages and necrosis. Virus dna in multiple areas of brain, brainstem and spinal cord was readily revealed by PCR, but not by the presence of viral inclusions, IHC or ISH. This case, with a clinically confusing presentation for VZVE, illustrates the extensive, albeit infrequent, degree of necrotizing vasculitis and CSF abnormalities that VZV is capable of producing. Antiviral therapy may have inhibited VZV genome replication and subsequent antigen production, resulting in negative ISH and IHC studies, but generated increased VZV genomic fragments that were detectable by the more sensitive PCR technique.- - - - - - - - - - ranking = 1keywords = blood vessel (Clic here for more details about this article) |