TY - JOUR
T1 - Effects of trazodone versus cognitive behavioral therapy in the insomnia with short sleep duration phenotype
T2 - A preliminary study
AU - Vgontzas, Alexandros N.
AU - Puzino, Kristina
AU - Fernandez-Mendoza, Julio
AU - Krishnamurthy, Venkatesh Basappa
AU - Basta, Maria
AU - Bixler, Edward O.
N1 - Funding Information:
All authors have seen and approved the manuscript. Work for this study was performed at the Sleep Research and Treatment Center, Penn State Health Milton S. Hershey Medical Center, Pennsylvania State University, College of Medicine, Hershey, PA. This study was funded by internal funding from the Department of Psychiatry at Penn State Health Milton S. Hershey Medical Center. The authors report no conflicts of interest.
Publisher Copyright:
© 2020 American Academy of Sleep Medicine. All rights reserved.
PY - 2020/12/15
Y1 - 2020/12/15
N2 - Study Objectives: The insomnia with objective short sleep duration phenotype is associated with increased risk for adverse health outcomes, physiological hyperarousal, and a blunted response to cognitive behavioral therapy for insomnia (CBT-I).Whether insomnia with objective short sleep duration responds better to pharmacological treatment compared to CBT-I has not been examined. Methods: Participants included 15 patients with chronic insomnia (86.7% female), aged 45.3 ± 8.1 years. Eight patients were randomized to CBT-I and 7 to trazodone. Patients were examined with 2 weeks of actigraphy, salivary cortisol, and the insomnia severity index at 3 time points (pretreatment, 3-month posttreatment, and 6-month follow-up). Mixed between-within-subjects analysis of variance and univariate analysis of covariance were conducted to assess the impact of trazodone and CBT-I on patients' total sleep time, salivary cortisol, and insomnia severity index scores across the 3 time points. Results: Trazodone, but not CBT-I, significantly lengthened total sleep time (when measured with actigraphy) both at posttreatment (51.01 minutes vs -11.73 minutes; P =.051; Cohen's d = 1.383) and at follow-up (50.35 minutes vs -7.56 minutes; P =.012; Cohen's d = 1.725), respectively. In addition, trazodone, but not CBT-I, showed a clinically meaningful decrease in salivary cortisol from pretreatment to posttreatment (-36.07% vs -11.70%; Cohen's d = 0.793) and from pretreatment to follow-up (-21.37%vs -5.79%; Cohen's d = 0.284), respectively. Finally, therewere no differences on insomnia severity index scores between the trazodone and the CBT-I groups. Conclusions: The current preliminary, open-label, randomized trial suggests that trazodone, but not CBT-I, significantly improves objective sleep duration and reduces hypothalamic-pituitary-adrenal axis activation, suggesting a differential treatment response in the insomnia with objective short sleep duration phenotype.
AB - Study Objectives: The insomnia with objective short sleep duration phenotype is associated with increased risk for adverse health outcomes, physiological hyperarousal, and a blunted response to cognitive behavioral therapy for insomnia (CBT-I).Whether insomnia with objective short sleep duration responds better to pharmacological treatment compared to CBT-I has not been examined. Methods: Participants included 15 patients with chronic insomnia (86.7% female), aged 45.3 ± 8.1 years. Eight patients were randomized to CBT-I and 7 to trazodone. Patients were examined with 2 weeks of actigraphy, salivary cortisol, and the insomnia severity index at 3 time points (pretreatment, 3-month posttreatment, and 6-month follow-up). Mixed between-within-subjects analysis of variance and univariate analysis of covariance were conducted to assess the impact of trazodone and CBT-I on patients' total sleep time, salivary cortisol, and insomnia severity index scores across the 3 time points. Results: Trazodone, but not CBT-I, significantly lengthened total sleep time (when measured with actigraphy) both at posttreatment (51.01 minutes vs -11.73 minutes; P =.051; Cohen's d = 1.383) and at follow-up (50.35 minutes vs -7.56 minutes; P =.012; Cohen's d = 1.725), respectively. In addition, trazodone, but not CBT-I, showed a clinically meaningful decrease in salivary cortisol from pretreatment to posttreatment (-36.07% vs -11.70%; Cohen's d = 0.793) and from pretreatment to follow-up (-21.37%vs -5.79%; Cohen's d = 0.284), respectively. Finally, therewere no differences on insomnia severity index scores between the trazodone and the CBT-I groups. Conclusions: The current preliminary, open-label, randomized trial suggests that trazodone, but not CBT-I, significantly improves objective sleep duration and reduces hypothalamic-pituitary-adrenal axis activation, suggesting a differential treatment response in the insomnia with objective short sleep duration phenotype.
UR - http://www.scopus.com/inward/record.url?scp=85097933845&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85097933845&partnerID=8YFLogxK
U2 - 10.5664/jcsm.8740
DO - 10.5664/jcsm.8740
M3 - Article
C2 - 32780015
AN - SCOPUS:85097933845
VL - 16
SP - 2009
EP - 2019
JO - Journal of Clinical Sleep Medicine
JF - Journal of Clinical Sleep Medicine
SN - 1550-9389
IS - 12
ER -