The influence of carbamazepine on sleep-EEG and the clonidine test in healthy subjects: Results of a preliminary study

Gann, Horst; Riemann, Dieter; Hohagen, Fritz; Müller, Wernér E.G.; Berger, Thomas

doi:10.1016/0006-3223(94)90027-2

Cited by 41 publications

(23 citation statements)

References 16 publications

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“…However, few investigators have examined the role of AEDs in sleep. In particular, despite its widespread clinical use, very few studies have been made of the effects of carbamazepine (CBZ) on nocturnal sleep, in either animals or humans (2,7,(19)(20)(21)(22)(23)(24)(25). Some older studies present several methodologic problems.…”

Section: Discussionmentioning

confidence: 99%

“…The other results of Touchon et al (2) are not comparable, since they did not document the effects of the first administration of drug and did not verify the effects of CBZ on healthy volunteers. Gann et al (25) did not detect changes in REM sleep parameters (except for a reduction in REM density) in a group of healthy volunteers treated with CBZ for 5 consecutive nights. However, the dosage used in that experiment was 200 mg twice daily.…”

Section: Discussionmentioning

confidence: 99%

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Nocturnal Sleep and Daytime Somnolence in Untreated Patients with Temporal Lobe Epilepsy: Changes After Treatment with Controlled‐Release Carbamazepine

et al. 1997

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Summary:Purpose: To define sleep disturbances in patients with temporal lobe epilepsy (TLE) and explore the association between carbamazepine (CBZ) therapy, sleep, and daytime somnolence.Methods: We recorded nocturnal polysomnography and measured subjective and objective daytime somnolence in a group of newly diagnosed TLE patients, who had no evidence of anatomic brain lesion on neuroimaging and had never been treated before. Recordings were performed at baseline, after the initial administration of 400 mg CBZcontrolled release (CR) and after 1 month of treatment (400 mg twice daily b.i.d.). The findings were compared with those of a group of young healthy volunteers, both at baseline and after the first administration of CBZ. The chronic effect of CBZ-CR treatment was evaluated only in TLE patients.Results: At baseline, nocturnal sleep patterns of TLE patients did not show marked alterations when the influence of seizures, cerebral lesions, and drugs had been ruled out. In both the TLE and the control groups, initiation of CBZ therapy provoked a reduction and a fragmentation of rapid eye movement (REM) sleep and an increase in the number of sleep stage shifts. In the TLE group, these effects were almost completely reversed after 1 month of treatment, and no significant difference was noted between baseline condition and long-term follow-up. With regard to daytime sleepiness, initial administration of the drug caused an increase in objective sleepiness only in the control group. Subjective sleepiness was higher in the control group than in the TLE group but was not modified by the drug.Conclusions: We conclude that CBZ-CR has negative effects on REM sleep during initial administration but chronic treatment does not significantly modify nocturnal sleep or daytime somnolence.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Nocturnal Sleep and Daytime Somnolence in Untreated Patients with Temporal Lobe Epilepsy: Changes After Treatment with Controlled‐Release Carbamazepine

et al. 1997

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“…Regarding the sleep EEG parameters, CBZ has been shown to increase SWS [72][73][74] from 6.8 B 5.3 to 13.2 B 7% in healthy subjects. These data are strikingly close to our data in BPD patients.…”

Section: Discussionmentioning

confidence: 99%

“…It has also been reported to increase adrenocorticotropin (ACTH) response to the hypothalamic corticotrophin-releasing factor (CRF) [70,71]. Regarding sleep EEG in healthy subjects, CBZ has been shown to increase slow wave sleep (SWS) [72][73][74] and not to modify REM latency and REM duration [74]. Yang et al [72] described a reduction in REM sleep.…”

Section: Introductionmentioning

confidence: 99%

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Effects of Carbamazepine on Dexamethasone Suppression and Sleep Electroencephalography in Borderline Personality Disorder

Fuente

Bobes²,

Vizuete³

et al. 2002

Neuropsychobiology

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The pathophysiology of borderline personality disorder (BPD) remains obscure, but there is mounting evidence of brain dysfunction without focal abnormality. The dexamethasone suppression test (DST) and sleep electroencephalography (sleep EEG) have been studied in BPD, but the findings seem to be related to a concomitant axis I diagnosis of major depression (MD) rather than to BPD itself. There is no effective treatment for BPD. Carbamazepine (CBZ) has shown contradictory results and in a previous study, our results were negative. In this study, we investigated the effects of CBZ versus placebo on the DST and sleep EEG in a sample of 20 BPD patients without concomitant MD. CBZ given at doses that are therapeutic for epilepsy and affective disorders may have an effect on the DST and sleep EEG in BPD. CBZ significantly increased the postdexamethasone plasma cortisol values. This did not parallel MD or an increase in the Hamilton depression rating scores. CBZ also increased slow wave sleep (SWS). The mechanisms by which CBZ increased postdexamethasone plasma cortisol levels and SWS in BPD are discussed.

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Effects of Anticonvulsant Medication on EEG Sleep Architecture

Geurkink

Gidal

Hermann

2000

Epilepsy & Behavior

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The influence of carbamazepine on sleep-EEG and the clonidine test in healthy subjects: Results of a preliminary study

Cited by 41 publications

References 16 publications

Nocturnal Sleep and Daytime Somnolence in Untreated Patients with Temporal Lobe Epilepsy: Changes After Treatment with Controlled‐Release Carbamazepine

Nocturnal Sleep and Daytime Somnolence in Untreated Patients with Temporal Lobe Epilepsy: Changes After Treatment with Controlled‐Release Carbamazepine

Effects of Carbamazepine on Dexamethasone Suppression and Sleep Electroencephalography in Borderline Personality Disorder

Effects of Anticonvulsant Medication on EEG Sleep Architecture

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