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      Epilepsy and Obstructive Sleep Apnea

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          Abstract

          A few publications documented the coexistence of epilepsy and obstructive sleep apnea (OSA). The extent, nature, and clinical relevance of this association remain poorly understood. We retrospectively reviewed the database of our sleep center to identify patients with both sleep apnea and epilepsy. Characteristics of epilepsy, sleep history, presence of excessive daytime sleepiness [Epworth Sleepiness Scale (ESS)] and polysomnographic data were assessed. The effect of continuous positive airway pressure (CPAP) on seizure reduction was prospectively analyzed after a median interval of 26 months (range: 2–116 months) from the diagnosis of OSA. OSA was found in 29 epilepsy patients (25 men and 4 women) with a median age of 56 years (range: 37–79). The median apnea hypopnea index was 33 (range: 10–85), the oxygen desaturation index was 12 (range 0–92), and 52% of the patients had an ESS score >10. In 27 patients, epilepsy appeared 1 month to 44 years prior to the diagnosis of OSA. In 21 patients, the appearance of OSA symptoms coincided with a clear increase in seizure frequency or the first appearance of a status epilepticus. Treatment with CPAP was continued with good compliance in 12 patients and led to a significant reduction of both ESS scores and seizure frequency in 4 patients. Our data suggest the importance of considering diagnosis and treatment of OSA in epilepsy patients with poor seizure control and/or reappearance of seizures after a seizure-free interval.

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          Most cited references 14

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          Obstructive sleep apnea.

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            Obstructive sleep apnea in epilepsy patients: the Sleep Apnea scale of the Sleep Disorders Questionnaire (SA-SDQ) is a useful screening instrument for obstructive sleep apnea in a disease-specific population.

            To determine useful cutoffs on the Sleep Apnea scale of the Sleep Disorders Questionnaire (SA-SDQ) in an epilepsy population. Epilepsy and obstructive sleep apnea (OSA) frequently coexist, and treating OSA in epilepsy patients may reduce seizure frequency and improve daytime sleepiness. The SA-SDQ, a 12-item validated measure of sleep-related breathing disorders, may be a useful tool to screen epilepsy patients for OSA, although appropriate cutoff points have not been established in this population. Previously suggested SA-SDQ cutoff points for OSA in a non-epilepsy population were 32 for women and 36 for men. One hundred twenty-five subjects with epilepsy undergoing polysomnography completed a survey about their sleep, including the 12-item SA-SDQ scale. Receiver-operating characteristics curves were constructed to determine optimal sensitivity and specificity. Sixty-nine of the 125 subjects (45%) had apnea-hypopnea indices greater than five, indicating OSA. The area under the curve was 0.744 for men and 0.788 for women. For men, an SA-SDQ score of 29 provided a sensitivity of 75% and a specificity of 65%. For women, an SA-SDQ score of 26 provided a sensitivity of 80% and a specificity of 67%. The SA-SDQ is a useful screening instrument for OSA in an epilepsy population. Our results indicate that the previously suggested cutoffs for OSA (36 for men and 32 for women) may be too high for this specific population. We suggest screening cutoffs of 29 for men and 26 for women.
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              Evaluation of sleepiness in epilepsy.

              Excessive daytime sleepiness often complicates the clinical picture of epilepsy, facilitating the occurrence of seizures and aggravating cognitive disabilities and/or behavioral problems. Thus it further adversely affects social and working activities of epileptic subjects. Both unstructured and structured clinical reports documented a not negligible proportion of epilepsy patients suffering from excessive daytime sleepiness. Studies based on neurophysiological testing such as Multiple Sleep Latency Test or Maintenance Wakefulness Test revealed a degree of daytime sleepiness tendency in epilepsy patients greater than that they subjectively estimate. Antiepileptic drugs play a remarkable role in determining drowsiness in epilepsy patients and they are generally viewed as the only cause of sleepiness in these patients. However excessive daytime sleepiness has been documented in epilepsy patients before starting any drug treatment or after its discontinuation. Both clinical and neurophysiological studies have clearly documented the possible role of seizure occurrence and of co-morbidity as determinants of excessive daytime sleepiness in epilepsy patients. Nocturnal sleep fragmentation and daytime sleepiness have been reported in temporal lobe and frontal lobe epilepsy, namely nocturnal frontal lobe epilepsy. Some recent reports have stressed that obstructive sleep apnea and periodic limb movements during sleep can significantly account for sleepiness complaints in epilepsy patients; most of the antiepileptic drugs can worsen obstructive sleep apnea. To date the evaluation of daytime sleepiness of epilepsy patients in clinical practice has been based mainly or exclusively on clinical reports. To improve our understanding of this symptom in epilepsy patients, the use of standardized sleepiness scales should be encouraged. Patients with persistent daytime sleepiness without a clear cause-and-effect relationship with antiepiletic drugs treatment or in whom a coincident sleep pathology is suspected, should be investigated by means of neurophysiological testing such as Multiple Sleep Latency Test or Maintenance Wakefulness Test.
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                Author and article information

                Journal
                ENE
                Eur Neurol
                10.1159/issn.0014-3022
                European Neurology
                S. Karger AG
                0014-3022
                1421-9913
                2006
                May 2006
                10 March 2006
                : 55
                : 2
                : 74-79
                Affiliations
                aDepartments of Neurology and Pneumology, University Hospital Bern, Bern, and bDepartment of Neurology, University Hospital Zürich, Zürich, Switzerland
                Article
                92306 Eur Neurol 2006;55:74–79
                10.1159/000092306
                16567944
                © 2006 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Tables: 2, References: 22, Pages: 6
                Categories
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