Sleep disorders are long-term sequelae of both bacterial and viral meningitis

Background: Many bacterial meningitis patients experience neurological or neuropsychological sequelae, predominantly deficits in short-term memory, learning, and attention. Neuropsychological symptoms after viral meningitis are observed less frequently. Sleep disturbance has been reported after both...

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Veröffentlicht in:Journal of neurology, neurosurgery and psychiatry neurosurgery and psychiatry, 2006-04, Vol.77 (4), p.554-558
Hauptverfasser: Schmidt, H, Cohrs, S, Heinemann, T, Goerdt, C, Djukic, M, Heimann, B, Wallesch, C-W, Nau, R
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Sprache:eng
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Zusammenfassung:Background: Many bacterial meningitis patients experience neurological or neuropsychological sequelae, predominantly deficits in short-term memory, learning, and attention. Neuropsychological symptoms after viral meningitis are observed less frequently. Sleep disturbance has been reported after both viral and bacterial meningitis. Objectives: To examine systematically the frequency and extent of sleep disturbance in meningitis patients. Methods: Eighty six viral or bacterial meningitis (onset of acute disease at least 1 year previously) patients were examined using two standardised questionnaires (Schlaffragebogen B and the Pittsburgh Sleep Quality Index, PSQI) in conjunction with a standardised neurological examination, and compared to a control group of 42 healthy age-matched volunteers. Results: Patients after both viral and bacterial meningitis described their sleep as reduced in quality and less restful than that of healthy control subjects; both patient groups had a pathological mean PSQI total score. Impaired sleep scores after meningitis were not correlated to either the Glasgow Coma Scale or the Glasgow Outcome Scale. Moreover, no relationship between residual neurological dysfunction or depressivity and sleep quality was observed. Conclusions: Impaired sleep is a long-term consequence of meningitis. Additional, so far undetermined, factors other than the severity of concomitant neurological deficits are responsible for the development of this sequela.
ISSN:0022-3050
1468-330X
DOI:10.1136/jnnp.2005.071142