Journal of the neurological sciences
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Myelin basic protein (MBP) and proteolipid protein (PLP) were purified from non-MS human brain and used in solid phase radioimmunoassays to detect their specific antibodies in cerebrospinal fluid (CSF) of optic neuritis and clinically definite multiple sclerosis (MS) patients. In 53 optic neuritis patients free anti-MBP was elevated in 47 and in 6 of these 47 patients bound anti-MBP was also increased. The remaining 6 patients with undetectable anti-MBP had increased levels of anti-PLP in their CSF. ⋯ Of 87 MS patients in remission, 15 had modestly elevated anti-MBP and none had detectable anti-PLP. Considering the total of 370 clinically definite MS patients with active and inactive disease, 77% had increased CSF anti-MBP and 1% had increased CSF anti-PLP. These findings are suggesting 2 immunochemically distinct forms of MS: a common form with autoantibodies directed against MBP and a more rare form associated with anti-PLP.
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The etiology of Parkinson's disease is mainly unknown. Immune abnormalities have been reported, including the occurrence of autoantibodies against neuronal structures and abnormal T cell functions. gamma delta+ T cells represent a recently recognized T cell subpopulation which is considered to play a role in immune responses in infections and autoimmunity. We examined by three-colour flow cytometry the proportions of gamma delta+ T cells in blood and cerebrospinal fluid (CSF) from patients with Parkinson's disease. ⋯ No differences between gamma delta+ T cells in CSF compared to blood were demonstrable in the individual patient groups. CD25 was not expressed on gamma delta+ T cells in blood of the majority of cases, but 50% of patients with Parkinson's disease and 30% with OND and tension headache had CD25+ gamma delta+ T cells in CSF arguing for a preferential activation of gamma delta+ T cells in the CSF compartment. Whether the elevated gamma delta+ T cell population in Parkinson's disease reflects previously unrecognized inflammation or may occur also in non-inflammatory disorders remains to be elucidated.
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To elucidate the possible role of vitamin C in the risk for developing Parkinson's disease (PD), we compared serum levels of ascorbic acid (vitamin C), measured by a fluorometric method, of 63 PD patients using their spouses as the control group. The serum levels of vitamin C did not differ significantly between the groups (47.13 +/- 0.89 micrograms/ml for PD and 47.60 +/- 0.60 micrograms/ml for controls). ⋯ Serum levels of vitamin C did not correlate with age, age at onset and duration of the disease, scores of the Unified PD Rating Scale or the Hoehn and Yahr staging in the PD group. These results suggest that serum vitamin C concentrations are apparently unrelated to the risk of developing PD.
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Case Reports
An immunologic abnormality common to Bickerstaff's brain stem encephalitis and Fisher's syndrome.
The nosological position of Bickerstaff's brain stem encephalitis (BBE) has yet to be established, and its etiology is not clear. Because anti-GQ1b antibody frequently occurs in patients with Fisher's syndrome (FS) and there are clinical similarities between FS and BBE, we investigated anti-ganglioside antibodies in sera from 3 BBE patients who had transient long tract signs in addition to acute ophthalmoplegia and cerebellar-like ataxia in order to clarify the etiology and nosological position of BBE. ⋯ In contrast, no anti-GQ1b antibody was found in sera from patients with other neurologic diseases which were able to produce transient brain stem disturbance: multiple sclerosis, neuro-Behçet's disease, brain stem infarction, herpes simplex virus encephalitis, and Wernicke's encephalopathy. The finding that BBE and FS shared common autoantibody suggests that autoimmune mechanism common to FS is likely in BBE, and that both conditions represent a distinct disease with a wide spectrum of symptoms that include ophthalmoplegia and ataxia.