1/6. 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 = vessel (Clic here for more details about this article) |
2/6. syringomyelia as a complication of tuberculous meningitis.Tuberculous meningitis may rarely be followed by the development of syringomyelia despite appropriate chemotherapy. In the present paper, we report a case of tuberculous meningitis in a 23-year-old Vietnamese male complicated by a rapidly progressive myelopathy due to granulomatous arachnoiditis which culminated in the development of a syrinx. The relevant literature is reviewed. The present case supports the hypothesis that vasculitic thrombosis of spinal cord vessels leading to ischemic myelomalacia is the mechanism causing postinflammatory syringomyelia.- - - - - - - - - - ranking = 0.25keywords = vessel (Clic here for more details about this article) |
3/6. Cysticercal chronic basal arachnoiditis with infarcts, mimicking tuberculous pathology in endemic areas.neurocysticercosis (NCC) is the most common of the parasitic diseases affecting the CNS, with protean clinical manifestations. stroke as a complication of NCC occurs in a very small percentage of cases, mostly involving small perforating vessels while major intracranial vessel involvement is extremely rare. The present report involves two autopsied cases of chronic cysticercal basal arachnoiditis causing large arterial territory infarcts and, in the second case, a hypothalamic mass. They were diagnosed and managed, clinically and by neuroimaging, as stroke and neurotuberculosis, respectively. The diagnosis was established only at autopsy, which revealed NCC causing basal arachnoiditis, major vessel vasculitis and infarcts. Histologically, case 1 showed degenerating racemose cysticercal cyst within the thick basal exudate. In the second case, remnants of the degenerated cysticercal cyst in the form of hooklets and calcareous corpuscles were identified within the giant cell inciting a granulomatous response to form a hypothalamic mass lesion mimicking tuberculoma. The present case report highlights the importance of considering the non-tuberculous etiologies of chronic basal arachnoiditis like NCC before initiating therapy especially in countries endemic to both NCC and tuberculosis, like india.- - - - - - - - - - ranking = 0.75keywords = vessel (Clic here for more details about this article) |
4/6. Internuclear ophthalmoplegia in tuberculous meningitis. A report of two cases.Internuclear ophthalmoplegia (INO) is characteristic of lesions of the medial longitudinal fasciculus and usually indicates primary brain stem pathology. Here we describe 2 cases of tuberculous meningitis (TBM) in which INO was a prominent presenting sign. The mechanism of INO in TBM is presumed to be ischemia secondary to involvement of small basilar vessels supplying the MLF in the inflammatory process. In both cases the INO resolved on antituberculous therapy suggesting that the cause of the ischemia is reversible. INO in a patient with meningitis must suggest a basal process probably TBM.- - - - - - - - - - ranking = 0.25keywords = vessel (Clic here for more details about this article) |
5/6. Radiologic evaluation of tuberculous meningitis.Five cases of primary tuberculous meningitis are presented. In three cases of acute meningeal process, the classic computed tomographic (CT) scan findings of basal meningeal enhancement, hydrocephalus and arteritis on angiography were found. These radiologic findings suggested the diagnosis, and antituberculosis treatment was therefore instituted at an early stage of the disease. In the remaining two cases with late complication of tuberculous meningitis, hydrocephalus and basal vessel arteritis were present. The importance of correlation of the clinical and radiographic findings is discussed.- - - - - - - - - - ranking = 0.25keywords = vessel (Clic here for more details about this article) |
6/6. pathology and pathogenetic mechanisms in neurotuberculosis.The mechanisms and the changes described herein typically begin with a dense basal meningeal exudate often resulting from a "Rich focus" along the basal surface of the cerebrum or ventricular ependyma. In the interpeduncular fossa, when the exudate is copious, among other structures the proximal parts of the optic nerves and of the internal carotid arteries are seen surrounded and compressed by the exudate. This exudate is made up of small and large mononuclear cells, including epithelioid cells, which also act as macrophages and may fuse to form Langhans' giant cells. Further extension of this exudate along small proliferating blood vessels into the brain substance constitutes a border zone encephalitis with the development of focal and diffuse ischemic brain changes due to vasculitis. Entrapment and occasional arteritic occlusion of larger arteries, such as the middle cerebral in the Sylvian fissures, results in infarction. Blockage of the basal subarachnoid cisterns around the midbrain and pons by the dense basal exudate or narrowing of aqueduct and third ventricle by a small tuberculoma causes consequent hydrocephalus. Development of many or one large focal granuloma (i.e., tuberculoma) occurs in the cerebrum, cerebellum, and/or brain stem. Similar pathogenetic mechanisms produce tuberculous spinal meningitis myeloradiculopathy that may be secondary to or occur before cranial tuberculous meningitis. More extensive damage to the white matter may occur together with the infrequent onset of perivascular demyelination on the basis of a hypersensitivity reaction to tuberculoprotein (i.e., "allergic tuberculous encephalopathy"). Finally, there may be a part played by NO in the production of the vascular and perivascular inflammatory central nervous system changes and a role for the the potential beneficial action of corticosteroids, especially in cases of tuberculous encephalopathy.- - - - - - - - - - ranking = 0.25keywords = vessel (Clic here for more details about this article) |