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Sleep spindle and slow wave activity in Bipolar Disorder: preliminary observations from a high–density EEG study

Published online by Cambridge University Press:  19 July 2023

C. Sanguineti ,
F. L. Donati ,
M. Sala ,
C. Carrara ,
C. Casetta ,
C. Zangani ,
A. Mayeli ,
A. Castelnovo ,
M. P. Canevini  and
A. D’Agostino
C. Sanguineti*
Affiliation:
Department of Health Sciences
F. L. Donati
Affiliation:
Department of Health Sciences
M. Sala
Affiliation:
Department of Pathophysiology and Transplantation, Università degli Studi di Milano
C. Carrara
Affiliation:
Department of Health Sciences
C. Casetta
Affiliation:
San Carlo Hospital, ASST SS. Paolo e Carlo, Milano, Italy
C. Zangani
Affiliation:
Warneford Hospital, Department of Psychiatry, University of Oxford, Oxford, United Kingdom
A. Mayeli
Affiliation:
Department of Psychiatry, University of Pittsburgh, Pittsburgh, United States
A. Castelnovo
Affiliation:
Sleep Center, Neurocenter of Southern Switzerland, Civic Hospital of Lugano, Lugano, Switzerland
M. P. Canevini
Affiliation:
Department of Health Sciences San Paolo Hospital, Epilepsy Center - Sleep Medicine Center, Childhood and Adolescence Neuropsychiatry Unit, ASST SS. Paolo e Carlo
A. D’Agostino
Affiliation:
Department of Health Sciences Department of Mental Health and Addiction, ASST Santi Paolo e Carlo, Milano, Italy
*
*Corresponding author.

Abstract

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Introduction

Recent research on Schizophrenia (SCZ) suggests that reduced sleep spindle and slow wave density could be particularly informative of underlying thalamocortical and cortical synchronization mechanisms and dysfunctions. Although sleep disturbances are also highly prevalent across all stages of Bipolar Disorder (BD), the objective evaluation of sleep macrostructure and microstructural oscillatory activity remains understudied in this population.

Objectives

We aimed to investigate sleep EEG activity in BD, with a focus on sleep architecture, sleep spindles and slow waves.

Methods

We recorded high-density EEG (64–channel BrainAmp, Brain Products GmbH, Germany) during sleep in 18 euthymic patients with BD and 18 age/gender-matched healthy control (HC) subjects. After sleep scoring and EEG artifact rejection, several parameters of sleep spindles (12-16 Hz), including density and amplitude, and slow waves (0.1-4 Hz) were identified for the first cycle of sleep using automated algorithms and compared between groups using non-parametric statistics.

Results

BD subjects showed significantly higher Wake After Sleep Onset and lower Sleep Efficiency (Table 1). Total (12 - 16 Hz), slow (12 - 14 Hz) and fast (14 - 16 Hz) sleep spindle parameters of density (Image 1) and amplitude did not differ significantly between groups. On the other hand, slow wave density was reduced in a large frontal cluster of electrodes in the BD group (Image 2).Table 1

BD (n = 18)HC (n = 18)Difference(p value)
WASO (min ± sd)140,61 ± 74,2384,34 ± 59,840,017
Sleep efficiency (% ± sd)72,47 ± 14,3382,43 ± 11,580,028

Image:

Image 2:

Conclusions

The absence of sleep spindle deficits in the BD group suggests that the systems involved in generating and maintaining these thalamocortical oscillations are presevered during periods of clinical stability in Bipolar Disorder. Conversely, reduced sleep slow wave density points to an altered cortical synchronization, which might represent a common neurophysiological feature shared with Schizophrenia. Further research is needed to confirm these preliminary observations in all–night recordings and with a direct comparison of larger cohorts of patients with both diagnoses.

Disclosure of Interest

None Declared

Type
Abstract
Information
European Psychiatry , Volume 66 , Special Issue S1: Abstracts of the 31st European Congress of Psychiatry , March 2023 , pp. S506 - S507
Creative Commons
Creative Common License - CCCreative Common License - BY
This is an Open Access article, distributed under the terms of the Creative Commons Attribution licence (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted re-use, distribution, and reproduction in any medium, provided the original work is properly cited.
Copyright
© The Author(s), 2023. Published by Cambridge University Press on behalf of the European Psychiatric Association
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