[Sleep problems among the elderly--what is done and what should be done?].
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Biomedical subjects
Publications and source records attributed to G O Fossan.
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Eighty-five seamen exposed to a variety of organic solvents and hydrocarbon compounds during their work on chemical tankers were compared with 59 unexposed seamen. Visual memory, auditory memory and visual abstraction were examined 14 days or more after the last solvent exposure. Multivariate analyses were performed to control the effects of confounding factors such as age, alcohol consumption, smoking, cerebral concussions and educational level. Significant correlations were found between increasing solvent exposure and poor results in tests of auditory memory and visual abstraction. These results indicate adverse psychological effects caused by chronic organic solvent exposure.
A seaman with symptoms and signs from the nervous system was examined. He had symptoms and signs of affection of his mental status, cerebellum and peripheral nerves. He had been working on tankers for 31 years, and had regularly been exposed to different organic solvents during loading, unloading and cleaning of the tanks. As no other disease was present in this patient, the existence of a chronic organic solvent intoxication syndrome was suggested.
A cross-sectional study of 85 long-term solvent exposed seamen working on chemical tankers compared to 59 unexposed seamen. Symptoms from the nervous system, clinical neurological findings and neurographic measurements were studied. The examinations were performed at least 2 weeks after the last solvent exposure. A stepwise multiple regression analysis was used to evaluate the dose-response relationship between the registered data on one hand and solvent exposure, employment on chemical tankers, age, alcohol and chloroquine phosphate consumption on the other. A significant correlation was found between increasing solvent exposure and reduced sensory nerve conduction velocities, as well as between increasing solvent exposure and prolonged distal latencies of motor nerves, and between increasing exposure and reduction of action potential amplitudes of sensory nerves. No correlation was found between solvent exposure and symptoms from the nervous system or clinical neurological findings.
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Thirty-four patients (20 female and 14 male) were admitted to a neurological department between 1974 and 1983 with intracranial meningioma. The mean age was 56.9 years. The patient material was divided in two groups, one with dementia (11 patients) and one without (23 patients). The most frequent symptom leading to admission was mental deterioration in the dementia group and epileptic seizures in the other group. The location of the tumours was similar in both groups. In all patients with dementia a combination of history, neurological examination and electroencephalogram clearly indicated a focal brain lesion.
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Cerebrospinal fluid and blood were examined for immunologic factors before and after metrizamide myelography in 13 patients who underwent lumbar myelography and seven patients who underwent thoracic myelography. Clinical symptoms were also recorded. The results were consistent with a toxic reaction to the contrast medium, rather than an immunologic one.
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In successive lumbar samples of cerebrospinal fluid (CSF), each consisting of 5 ml, immunoglobulin G (IgG) and total protein were determined. Variation was studied by comparing the values in the initial sample with values in succeeding samples. In 13 out of 17 patients, IgG was reduced in sample 2. There was no reduction in the following samples. The concentration of IgG in sample 2 was below 50% of the concentration in sample 1 in 2 patients and below 70% in 9 patients. IgG was also reduced if the concentration in each sample was given as percent of the total protein concentration. The total protein concentration was not significantly reduced during collection of 25 ml of CSF. IgG was increased in sample 2 in 3 out of the 4 patients with neurological diseases since childhood. In 1 patient there was a considerable rise in the total protein concentration after collection of the first 5 ml, without a corresponding rise of IgG concentration. In clinical practice, the portion to which the CSF sample belongs should be noted, and comparison of values from various patients should be made between equivalent samples.
Concentrations of IgG and titres of IgG antibodies to rabbit erythrocytes were studied in serum and cerebrospinal fluid (CSF) from 21 phenytoin-treated patients; 11 of these had reduced serum IgA. The CSF IgG concentration was not reduced in any patient. A reduction of CSF IgG has been found earlier in phenytoin-treated patients, when other antisera to IgG were used for the determination of IgG concentration. The present findings therefore indicate that an alteration of the composition or quality of the CSF IgG is present in phenytoin-treated patients. 1 patient had a phenytoin-induced low serum concentration of IgG and IgA. In this patient the ratios CSF:serum were normal both for IgG concentration and for IgG antibodies to rabbit erythrocytes.
Titres in CSF of natural IgG antibodies (AB) to rabbit erythrocytes (RRBC) correlated well with titres in serum in normal individuals, indication a passive transfer of the Ab. The ratio of CSF Ab to serum Ab mostly found was 1:400. The ratios of total IgG were slightly lower than the ratios of Ab to RRBC in normal individuals and in the majority of the diseases, except in multiple sclerosis and in subacute sclerosing panencephalitis (SSPE) where the ratios of total IgG were markedly elevated, indicating production of IgG in the central nervous system. In SSPE the ratio of measles Ab was even more elevated, suggesting that these antibodies contribute to the local IgG production. The ratios of Ab to RRBC in the two diseases were not elevated, or only slightly elevated. In normal and pathological CSF and in the Ab to RRBC all subclasses of IgG were found. In conclusion, the Ab to RRBC are considered convenient markers of serum IgG in the CSF.
Rabbits immunized subcutaneously with a mixture of normal human serum, Freund's complete adjuvant and a soluble diphenylhydantoin preparation, produced antibodies that differed qualitatively and quantitatively from the controls, as revealed by immunoelectrophoresis and passive haemagglutination. Antibodies in human IgG were greatly increased, whereas antibodies to human albumin were not influenced, and antibodies to some alpha- and beta-globulins were reduced.
Rabbits treated with phenytoin in various ways, were immunized with human serum or with sheep erythrocytes. The antibody response in rabbits injected with the antigen mixed with phenytoin differed distinctly from the response obtained in animals having received the antigen alone or mixed with diluent. The effect of phenytoin on the antibody response depended on the nature of the antigen. The response to some antigens was suppressed, to some potentiated, and to some potentiated in the early phase and then suppressed. The effect comprised both IgM and IgG responses. Skin hypersensitivity tests did not reveal any effect on the cellular immune response. These findings may explain why particularly IgA is affected in patients taking phenytoin by the oral route, and why either reduction or elevation of IgA may occur.