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Query: UMLS:C0042384 (vasculitis)
 20,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The computed tomographic findings of three patients with cerebral syphilis, including cerebral gumma, which regressed completely under penicillin therapy, syphilitic angiitis with cerbral infarction, and syphilitic cerebral atrophy, are reported. CT is unable to provide specific diagnostic data for these conditions. The etiology can be clarified only by taking into consideration the clinical findings and course, the serological results, and the result of therapy.
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PMID:The value of computed tomography in cerebral syphilis. 53 Apr 30

The early manifestation of HIV infection of the brain, HIV encephalitis, is due to the invasion of HIV infected mono- and multinuclear macrophages into the brain tissue and cerebrospinal fluid. These cells are intensely PAS reactive, auto-fluorescent and express the macrophage antigen CD68. They clearly prefer the white matter of cerebral hemispheres, corpus callosum and internal capsule. Lymphocytic infiltrates and microglial nodules are additional, unspecific changes. HIV encephalopathy following HIV encephalitis is patho-anatomically characterized by brain tissue damage. Its clinical correlate is so-called AIDS dementia complex. It presumably is caused by neurocytotoxic and myelinotoxic factors released by activated macrophages and/or by shedding HIV retrovirus proteins. HIV encephalopathy includes leukoencephalopathy, diffuse poliodystrophy, disseminated basal ganglia damage and brain atrophy. In some cases, granulomatous angiitis may occur.
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PMID:[HIV encephalopathy]. 172 52

In an earlier study patients with symptoms of orbital venous vasculitis--that is, cases of characteristic orbital pain and pathologic orbital phlebograms--were found to have increased signs of cerebral atrophy compared with age-matched controls. One such patient with nine incidents of Tolosa-Hunt syndrome and advanced cerebral atrophy is reported, and his medical history and pathoanatomic studies are reported in detail. The cause of the atrophy was multiple small infarctions, which are suggested to be due to vasculitis. Other findings in this case support the hypothesis that the Tolosa-Hunt syndrome may be only one manifestation of a generalized vasculitis.
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PMID:Pathoanatomic studies in a case of Tolosa-Hunt syndrome. 335 81

A case is presented with early-onset polyarthritis involving both large and small joints, prolonged fever, skin rash, hepatosplenomegaly, persistent cerebro-spinal fluid pleocytosis, brain atrophy, macrocephaly with ventricular dilatation, a persistently open fontanelle, lymphadenopathy, subcutaneous nodules, developmental delay, failure to thrive, persistent hypochromic microcytic anemia, leukocytosis with shift to the left, early thrombocytopenia followed by thrombocytosis, high erythrocyte sedimentation rate, elevated immunoglobulin level, and vasculitis involving several organs. Thirteen cases have been previously reported under different names. A unified name is needed; we suggest "infantile-onset arthritis and multisystem inflammatory disease."
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PMID:Infantile-onset arthritis and multisystem inflammatory disease: "a new syndrome". 355 12

Of 102 patients with bacterial meningitis admitted to the Children's Hospital of Buenos Aires, 25 were selected for computed tomographic (CT) scans on the basis of altered consciousness for more than 96 hours after admission, persistent or recurrent seizures after 72 hours of antibiotic therapy, development of focal neurologic signs, increased intracranial pressure or prolonged fever. Scan findings included hydrocephalus, cerebritis, vasculitis, subdural effusion, cerebral atrophy, abscess, and ependymitis. Serial CT scans demonstrated the progression or regression of some complications. The CT scan was very useful in indicating the need for neurosurgical procedures.
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PMID:Computed tomography in purulent meningitis. 697 22

In this paper we report on a patient with obliterative retinal vasculitis which, within a few weeks, led to retinal necrosis with fibrous alterations of the central parts of the retina and annular retinal tears in the periphery. The clinical picture is interpreted as bilateral acute retinal necrosis, corresponding to earlier reports in the literature. Our patient differs from the case reports known to us so far in the purely obliterative-vascular progress form of retinal necrosis, the lack of uveal involvement, the presence of unilateral labyrinthine deafness (probably of vascular origin), and the demonstration of pronounced cerebral atrophy.
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PMID:Bilateral acute vascular retinal necrosis. 729 May 78

In order to evaluate the diagnostic and prognostic value of MRI in the very early stages of HIV infection, we have compared the results of postmortem brain MRI and neuropathological studies in 7 asymptomatic HIV seropositive individuals, 8 seronegative controls with similar cause of death and 6 patients who died of AIDS in the absence of focal cerebral changes (opportunistic infection or tumour). Cerebral atrophy was consistently evaluated by both techniques. Seropositive asymptomatic cases were significantly more atrophic than the seronegative controls and significantly less atrophic than AIDS patients. Small high signal intensity areas in the white matter and basal ganglia were not significantly more frequent in seropositives than in seronegatives. No corresponding lesion was found at neuropathological examination. Diffuse myelin pallor of the cerebral white matter on myelin preparation was somewhat more severe in seropositive asymptomatic cases than in seronegative controls and less than in AIDS cases. However, these differences were not statistically significant. No significant correlation could be found between neuropathological myelin pallor and diffuse signal abnormalities of the white matter on MRI. We conclude that brain abnormalities are present at the early asymptomatic stage of HIV infection. These include vasculitis with opening of the blood brain barrier and consequent myelin pallor and gliosis of the white matter, and moderate brain atrophy. However MRI correlates are discrete or non specific on post mortem examination, and some probably correspond to scars of transient vascular inflammation. It is very unlikely that MRI examination has any diagnostic or prognostic value at the early stages of the disease.
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PMID:[Early cerebral lesions in HIV infection. Postmortem radio-pathologic correlations in non-AIDS asymptomatic seropositive patients]. 747 29

Viliuisk encephalomyelitis (VEM) appears to be endemic disease, affecting native population in Yakutia (Yakut, Even, Evenk). The infectious nature of VEM is very likely, but not yet established with certainty. The mortality rate caused by VEM from 1950 to 1990 was 17.4 per 10000 of native population. The maximum morbidity can be seen in Viliui and Central zones of Yakutia. Women were affected one and a half times more than men. VEM is characterized by multiple micronecrotic foci with marked inflammatory reactions and gliosis in the brain tissue. The vascular component in VEM is manifested by vasculitis, plasmarhagies, obliteration of the capillary lumen with development of capillarofibrosis, progressive reduction of the microcirculatory bed, the deformation of walls in major vessels with atrophy of their muscular layer, in some cases--by hyaline thrombi. The data presented give no grounds to consider the vascular component as secondary, relating only to the brain atrophy.
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PMID:[New data on the epidemiology and morphology of Viliuisk encephalomyelitis]. 784 4

Sixteen patients (8 female, 8 male) with primary angiitis of the CNS (PACNS), were followed prospectively in a vasculitis clinic. Diagnosis was by angiography in patients without underlying disease. Median age at diagnosis was 36.5 years, and median duration of follow-up was 28 months. Onset was acute in 14 patients (88%), with 3.5 weeks (median) from onset symptoms to diagnosis. Three women developed symptoms within 3 weeks postpartum. The most frequent symptoms were severe headaches (12, 75%), stroke (6, 30%), transient ischaemic attack (TIA) (4, 28%), seizures (7, 44%), visual aberration (3, 19%), and cognitive impairment (5, 31%). Laboratory data included high ESR (2, 13%), leucocytosis (8, 80%), thrombocytosis (1, 6%), positive antinuclear antibody titre (3, 15%), and high levels of complement (5, 31%). Lumbar puncture was performed in 12 patients (75%). CSF analysis was abnormal in five patients (42%). EEG was abnormal in 5/9 patients. The major CT/MRI scan findings were cerebral haemorrhage (4, 25%), brain infarcts (5, 31%), brain atrophy (2, 13%) and non-specific lesions (2, 13%). Four patients had normal studies. All patients received corticosteroids (CS), and five were treated with oral cyclophosphamide. Two patients relapsed despite CS and cyclophosphamide therapy. All patients are alive, and at the last assessment, eight had a permanent neurological deficit, which included paresis (3, 19%), neurocognitive abnormalities (2, 13%), visual loss (2, 13%) and seizure activity (5, 31%). Our data suggest a non-progressive, non-fatal course in those PACNS patients diagnosed angiographically and treated with CS with or without cyclophosphamide.
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PMID:Primary angiitis of the CNS diagnosed by angiography. 804 67

Sixteen patients with chronic periorbital venous vasculitis without nerve involvement and 9 patients with active episodic cluster headache were studied as to cerebrospinal fluid (CSF) pressure. Eighty-one percent of the patients with chronic and 33% with episodic symptoms had pathologically increased CSF pressure. Magnetic resonance imaging of the brains in the chronic group showed empty sella in 60%, cerebral atrophy in 21% and white matter lesions with high signal intensity on T2 weighted sequences in 29%. Abnormal obesity was found in 31% of the patients with chronic periorbital venous vasculitis under 60 years of age. Venous vasculitis is suggested as a cause of intracranial hypertension, empty sella, and endocrinologic dysfunctions.
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PMID:Periorbital venous vasculitis, intracranial hypertension and empty sella. 816 74


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