1,721,033 research outputs found
Neurosarcoidosis - Clinical description of 7 cases with a proposal for a new diagnostic strategy
No full textAbstract
OBJECTIVE:
Chronic involvement of the nervous system is relatively rare in sarcoidosis. We describe 7 cases that fulfil Zajicek's criteria for neurosarcoidosis (NS) and propose some modifications to such criteria.
MATERIALS AND METHODS:
The patients were admitted for various neurological syndromes: 2 cases presented with chronic lymphocytic meningitis, 4 with spinal cord symptoms, one case was initially confused with multiple sclerosis. Serological tests, immunological screening, cerebrospinal fluid (CSF) analysis, bacteriological and viral testing were performed in all patients. Spinal and cerebral MRI, gallium scan, bronchoscopy with biopsy and bronchoalveolar-lavage fluid analysis, high-resolution computed tomography (HRCT) of the chest, biopsy of the lungs, skin, mediastinal lymph-node and meninges, were useful in diagnosing NS.
RESULTS AND DISCUSSION:
Laboratory tests showed serum inflammatory abnormalities, but were negative for infectious diseases, while CSF showed inflammatory signs in all patients. MRI revealed meningeal enhancement or hypertrophic pachymeningeal lesions in 4 patients, white matter abnormalities and mass lesions in 2 patients, and a spinal mass lesion in 1 patient. Gallium scan, HRCT, bronchoscopy were positive in most cases. Patients were treated with steroid and immunosuppressive therapy, with improvement in six cases. One patient died from infectious complications.
CONCLUSION:
A definite diagnosis of NS requires demonstration of non-caseating granulomas affecting nervous tissues. In most cases, histological evidence of systemic disease (probable NS) is sufficient in the presence of compatible alterations in the CNS. In our patients the bronchoalveolarlavage fluid analysis, gallium scan, and chest HRCT were important for diagnosis, while serum ACE was always normal and chest radiographs were not suggestive of sarcoidosis
IMMUNOHISTOCHEMICAL STUDY OF LEWYS BODIES AND NEUROFIBRILLARY TANGLES WITH A MONOCLONAL-ANTIBODY AGAINST PHOSPHORYLATED EPITOPES OF NEUROFILAMENTS IN DIFFERENT CLINICAL CONDITIONS
No full textGlutamic acid decarboxylase autoantibodies and neurological disorders
No full textGlutamic acid decarboxylase (GAD) is the enzyme that catalyses the production of GABA, a major neurotransmitter of the central nervous system. Antibodies to GAD (GAD-Ab) were first recognised in a patient affected by stiff-person syndrome; subsequently they were reported in a large number of cases with type 1 diabetes. Recently GAD-Ab have been described in a number of patients affected by chronic cerebellar ataxia, drug-resistant epilepsy and myoclonus. These cases usually harbour other autoantibodies or are affected by organ-specific autoimmune diseases. The role of GAD-Ab is still unclear; the lack of experimental models makes it difficult to investigate their potential pathogenetic role. However two mechanisms have been suggested: the reduction by GAD-Ab of GABA synthesis in nerve terminals or the interference with exocytosis of GABA
Isoelectric focusing combined with anion-echange chromatography for investigation of normal and monoclonal immunoglobulins.
No full textRelationship between accumulation of beta-APP and neuropsychological abnormalities in HIV encephalitis
No full text
Cerebellar ataxia associated with anti-glutamic acid decarboxylase autoantibodies
No full textRecent reports describe the detection of high titres of antibodies to glutamic acid decarboxylase (GAD-Ab) in the serum and cerebrospinal fluid. (CSF) of patients with cerebellar ataxia. Most of these cases are females with Polyglandular Autoimmune Disorder who develop a chronic cerebellar syndrome. The CSF profile is in keeping with an autoimmune disorder and intrathecal GAD-Ab synthesis has been demonstrated. The ataxia could reverse after immunomodulatory treatments suggesting a possible pathogenetic role for GAD-Ab
Long-term trial of Levamisole on A-T: effect on the immunological and clinical parameters.
No full text- …
