Hostname: page-component-586b7cd67f-rdxmf Total loading time: 0 Render date: 2024-11-29T12:45:38.933Z Has data issue: false hasContentIssue false

CS03-03 - Sleep and sleep disorders in somatoform pain disorder

Published online by Cambridge University Press:  16 April 2020

G. Saletu-Zyhlarz
Affiliation:
Department of Psychiatry and Psychotherapy, Medical University of Vienna, Vienna, Austria
W. Prause
Affiliation:
Sozialpsychiatrisches Zentrum Wien, Vienna, Austria
M. Aigner
Affiliation:
Department of Psychiatry and Psychotherapy, Medical University of Vienna, Vienna, Austria
P. Anderer
Affiliation:
Department of Psychiatry and Psychotherapy, Medical University of Vienna, Vienna, Austria
E. Grätzhofer
Affiliation:
Department of Psychiatry and Psychotherapy, Medical University of Vienna, Vienna, Austria
S. Klug
Affiliation:
Department of Psychiatry and Psychotherapy, Medical University of Vienna, Vienna, Austria
B. Saletu
Affiliation:
Institute of Sleep Medicine, Rudolfinerhaus, Vienna, Austria

Abstract

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.
Introduction

Somatoform pain disorder (SPD) is frequently associated with sleep disorders, specifically restless legs syndrome and insomnia, which in turn lowers the pain threshold and worsens pain.

Objectives

The aim of the present study was to investigate differences in wake-EEG by low-resolution electromagnetic tomography (LORETA) and objective and subjective sleep and awakening quality in SPD patients as compared with controls and study acute and chronic effects of trazodone CR on these variables and pain measures.

Methods

Fifteen patients with SPD (F45.4) and co-morbid insomnia (F51.0) were compared with 15 controls and participated in a single-blind, placebo-controlled, cross-over study on the acute effect of 100 mg trazodone CR, followed by a six-week open titration period. Statistics involved clinical, EEG-LORETA, PSG and psychometry.

Results

LORETA showed reduced power, mainly in the beta band in almost all pain matrix areas (SI, SII, ACC, SMA, PFC, PPC, insula, amygdala, hippocampus). PSG demonstrated a lack of deep sleep and increased arousals and stage shifts, with opposite changes induced by trazodone after acute and chronic therapy. Improvement of sleep was associated with improvement of pain, evaluated by visual-analog scales.

Conclusion

Our LORETA findings demonstrate a dysfunctional pain modulation in SPD. Trazodone induced changes in subjective and objective sleep and awakening quality that were opposite to the differences between SPD patients and controls (key-lock principle) and associated with pain improvement.

Type
Research Article
Copyright
Copyright © European Psychiatric Association 2011
Submit a response

Comments

No Comments have been published for this article.