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Biomedical subjects

J Ruutiainen

Publications and source records attributed to J Ruutiainen.

10 recordsLinked to original sources
PubMed1995

Attention related performance in two cognitively different subgroups of patients with multiple sclerosis.

To evaluate the underlying mechanisms of cognitive decline in multiple sclerosis, two clinically and demographically matched multiple sclerosis groups differing in cognitive status were assessed with attention related tasks. In addition to the attention tests recommended by the Cognitive Function Study Group of the American National Multiple Sclerosis Society, a test of sustained attention was used to evaluate the role of possible fatigue on cognitive performance. The cognitively mildly deteriorated group was slower than the cognitively preserved group and the controls on all tests of attention. The mildly deteriorated group did not, however, consistently differ from the other groups in the error scores of the attention tests. The preserved group exhibited slowness at the end of the visual vigilance test, but no deficits were found on the other attention related tests in this group. It is suggested that dissociable kinds of processing slowness are the origin of the deficits found on the attention tests in the two multiple sclerosis groups. Our preserved group exhibited signs of motor and fatigue related slowness, whereas the mildly deteriorated group also had extensive cognitive slowness. As sensitive indicators of cognitive slowness, attentional tests should be included in evaluation of the cognitive status of patients with multiple sclerosis.

Adult↗
PubMed1994

Automatic and controlled information processing in multiple sclerosis.

The purpose of this study was to evaluate the kind of slowing of information processing associated with multiple sclerosis and how this possible slowness is related to cognitive deterioration. We selected 45 patients with definitive multiple sclerosis diagnosis and 35 control subjects. Twenty-two patients had mild cognitive deterioration and 23 patients had preserved cognitive capacities, otherwise the groups were matched. Using computerized tests, we investigated three separate stages of information processing: automatic and controlled processing, and motor programming. The results indicate that patients with mild cognitive deterioration are slower than patients with preserved capacities or controls in every stage of processing measured in this study. Additionally, the preserved patients showed signs of mild slowing in automatic visual processing. These results show that, in multiple sclerosis patients, widespread information processing slowness is associated with multiple sclerosis-related cognitive deterioration. This study emphasizes the importance of studying subgroups rather than cognitively heterogeneous patient samples and, furthermore, the need to divide information processing into different stages is indicated.

Adult↗
PubMed1991

Treatment of acute exacerbations in early multiple sclerosis: cyclosporin A or prednisolone?

Twenty-six acute exacerbations in 26 patients with early definite multiple sclerosis (MS) were treated with oral cyclosporin-A (CyA) or oral prednisolone in a double-blind, controlled and randomized trial. The duration of the treatment was 6 weeks. All of the patients showed improvement during the treatment. There were no differences in outcome between patients on CyA (7.5 mg/kg) or prednisolone (decreasing doses from 0.8 mg/kg) during the 6 week treatment. However, the improvement of clinical signs 3 months after the treatment was slightly greater in the prednisolone group. The drugs did not have significant side-effects. There was no fluctuation in the CD4/CD8 ratio during the follow-up. The two treatment groups did not differ from each other in respect to the number of CD3 (T3), CD4 (T4), CD8 (T8), CD14 (monocytes), CD20 (B cells) or CD25 (interleukin-2 receptor positive cells). The number of active T cells with the interleukin-2 receptor was high in the beginning of the exacerbation but it decreased during the treatment. To conclude, the effects of CyA and prednisolone were comparable in the treatment of acute MS relapses.

Acute Disease↗
PubMed1986

Myelin basic protein antibodies in catatonic schizophrenia.

Myelin basic protein (MBP) antibodies were determined by solid-phase radioimmunoassay in the serum and cerebrospinal fluid of 10 patients with catatonia, 10 patients with other forms of schizophrenia, and 10 psychiatrically healthy controls. The mean counts per minute (cpm) value of serum anti-MBP antibody of the catatonia group was significantly higher than that of the patients with other forms of schizophrenic psychoses (p less than .05). No significant differences were observed among the cpm values of the CSF specimens from the three patient groups. The hypothesis of a central virus-induced immunologic aberration in catatonic schizophrenia is discussed.

Adult↗
PubMed1983

Antibodies in cerebrospinal fluid to white matter glycoproteins in multiple sclerosis patients.

Cerebrospinal fluid (CSF) specimens from 45 patients with multiple sclerosis (MS) and 45 age- and sex-matched controls with other neurological diseases (OND) were tested for antibodies to white matter (WM) membrane glycoprotein (GP) fractions prepared from MS and control WM membranes by lentil lectin chromatography. The binding of the CSF IgG to the 125I-labeled GP fractions was determined by immunoprecipitation using Protein A-Sepharose. CSF from patients with MS bound highly significantly more strongly to the GP fraction prepared from MS WM than did the OND CSF specimens (P less than 0.001). There was no such difference when control GP fraction was used as an antigen. No highly significant differences were observed when 20 paired serum specimens were tested. Electrophoresis of the immunoprecipitates showed that components with molecular weights (MWs) of 157,300, 135,600, 111,100, 93,000, 75,700, 63,300, 50,100, 24,300, 20,300 and 17,000 daltons were precipitated from the MS GP fraction by CSF specimens of both MS and OND groups, whereas components with MWs of 50,100, 24,300, 20,300 and 17,000 daltons were precipitated from the control GP fraction.

Adult↗
PubMed1981

Measurement of glial fibrillary acidic protein (GFAP) and anti-GFAP antibodies by solid-phase radioimmunoassays.

A solid-phase radioimmunoassay was developed for the detection of glial fibrillary acidic protein (GFAP) and GFAP-specific immunoglobulin G (IgG) antibodies. In antibody assays purified GFAP was absorbed onto polystyrene beads, followed by incubation in dilutions of serum. (125-I)-labelled human anti-IgG was used to quantify antibodies bound to solid-phase GFAP. GFAP in samples was measured by the inhibition of the binding of anti-GFAP antibody to solid-phase GFAP. The serum and CSF samples of 19 brain tumor, 40 multiple sclerosis and 66 control patients were assayed for anti-GFAP antibodies. The binding values in the serum and CSF samples of the brain tumor patient group were higher and the binding values in the CSF samples of the multiple sclerosis group lower than those of the control group. The differences were statistically significant.

Antibodies↗
PubMed1981

Myelin basic protein antibodies in the serum and CSF of multiple sclerosis and subacute sclerosing panencephalitis patients.

A solid-phase radioimmunoassay was developed for the detection of myelin basic protein antibodies of immunoglobulin G (IgG) class. Purified basic protein of myelin (MBP) was adsorbed onto polystyrene beads, followed by incubation in dilutions of serum or cerebrospinal fluid (CSF). 125I-labelled anti-human IgG was used to quantify antibodies bound to the solid-phase. The assay was optimized in tests with rabbit antibodies to MBP and with 125I-labelled anti-rabbit IgG. Serum and CSF specimens from 41 multiple sclerosis (MS), 16 subacute sclerosing panencephalitis (SSPE) and 58 control patients were tested for MBP antibodies. No statistically significant differences were found between MS and control patient groups, but the subgroup of acute MS patients had slightly elevated (P 0.02) antibody levels in their CSF specimens. The SSPE patients had markedly elevated levels (P 0.001) of antibodies to MBP in their CSF specimens.

Adsorption↗