Pharmacopsychiatry 2019; 52(04): 186-192
DOI: 10.1055/a-0695-9138
Original Paper
© Georg Thieme Verlag KG Stuttgart · New York

Augmentation of Pharmacotherapy by Sleep Deprivation with Sleep Phase Advance in Treatment-Resistant Depression

Ewa Kurczewska
1   Department of Adult Psychiatry, Poznan University of Medical Sciences, Poznan, Poland
,
Ewa Ferensztajn-Rochowiak
1   Department of Adult Psychiatry, Poznan University of Medical Sciences, Poznan, Poland
,
Anna Jasińska-Mikołajczyk
1   Department of Adult Psychiatry, Poznan University of Medical Sciences, Poznan, Poland
,
Maria Chłopocka-Woźniak
1   Department of Adult Psychiatry, Poznan University of Medical Sciences, Poznan, Poland
,
Janusz K. Rybakowski
1   Department of Adult Psychiatry, Poznan University of Medical Sciences, Poznan, Poland
› Author Affiliations
Further Information

Publication History

received 28 June 2018
revised 28 June 2018

accepted 08 August 2018

Publication Date:
10 September 2018 (online)

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Abstract

Introduction The aim was to assess the efficacy of total sleep deprivation (TSD) with sleep phase advance (SPA) in treatment-resistant depression (TRD) and associated biochemical factors.

Methods We studied nine males and 12 females, aged 49±14 years, with treatment-resistant unipolar or bipolar depression, receiving antidepressant and mood-stabilizing drugs. The four-day schedule included single TSD and three consecutive nights with SPA. Biochemical markers were measured on the day before and on 1st, 7th and 14th day after the TSD.

Results Ten subjects met criteria for response, defined as a reduction of ≥50% in the Hamilton Depression Rating Scale, on the 14th day. Concentrations of cortisol at baseline were lower in responders, and they decreased during therapy in both groups. In responders, there was an increase of interleukin-10 (IL-10) and IL-1β on the 14th day.

Discussion Our preliminary study demonstrated the efficacy of pharmacotherapy augmentation by TSD and SPA in half of the patients with TRD. The main biochemical factors related to clinical response included status of cortisol and increase in IL-10 and IL-1β levels.