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van Liempt S. Sleep disturbances and PTSD: a perpetual circle?. Eur J Psychotraumatol. 2012;3doi: 10.3402/ejpt.v3i0.19142.
van Liempt, S. (2012). Sleep disturbances and PTSD: a perpetual circle?. European journal of psychotraumatology, 3. https://doi.org/10.3402/ejpt.v3i0.19142
van Liempt, Saskia. "Sleep disturbances and PTSD: a perpetual circle?." European journal of psychotraumatology vol. 3 (2012). doi: https://doi.org/10.3402/ejpt.v3i0.19142
van Liempt S. Sleep disturbances and PTSD: a perpetual circle?. Eur J Psychotraumatol. 2012;3. doi: 10.3402/ejpt.v3i0.19142. Epub 2012 Oct 03. PMID: 23050070; PMCID: PMC3464455.
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Eur J Psychotraumatol. 2012;3. doi: 10.3402/ejpt.v3i0.19142. Epub 2012 Oct 03.

Sleep disturbances and PTSD: a perpetual circle?.

European journal of psychotraumatology

Saskia van Liempt

Affiliations

  1. Military Mental Health, University Medical Centre, Utrecht, The Netherlands.

PMID: 23050070 PMCID: PMC3464455 DOI: 10.3402/ejpt.v3i0.19142

Abstract

BACKGROUND: Sleep facilitates the consolidation of fear extinction memory. Nightmares and insomnia are hallmark symptoms of posttraumatic stress disorder (PTSD), possibly interfering with fear extinction and compromising recovery. A perpetual circle may develop when sleep disturbances increase the risk for PTSD and vice versa. To date, therapeutic options for alleviating sleep disturbances in PTSD are limited.

METHODS: WE CONDUCTED THREE STUDIES TO EXAMINE THE RELATIONSHIP BETWEEN SLEEP AND POSTTRAUMATIC SYMPTOMS: (1) a prospective longitudinal cohort study examining the impact of pre-deployment insomnia symptoms and nightmares on the development of PTSD; (2) a cross-sectional study examining subjective sleep measures, polysomnography, endocrinological parameters, and memory in veterans with PTSD, veterans without PTSD, and healthy controls (HCs); (3) a randomized controlled trial (RCT) (n=14) comparing the effect of prazosin and placebo on sleep disturbances in veterans with PTSD. In addition to these studies, we systematically reviewed the literature on treatment options for sleep disturbances in PTSD.

RESULTS: Pre-deployment nightmares predicted PTSD symptoms at 6 months post-deployment; however, insomnia symptoms did not. Furthermore, in patients with PTSD, a correlation between the apnea index and PTSD severity was observed, while obstructive sleep apnea syndrome was not more prevalent. We observed a significant increase in awakenings during sleep in patients with PTSD, which were positively correlated with adrenocorticotropic hormone (ACTH) levels, negatively correlated with growth hormone (GH) secretion, and the subjective perception of sleep depth. Also, heart rate was significantly increased in PTSD patients. Interestingly, plasma levels of GH during the night were decreased in PTSD. Furthermore, GH secretion and awakenings were independent predictors for delayed recall, which was lower in PTSD. In our RCT, prazosin was not associated with improvement of any subjective and objective sleep parameters. Only a few RCTs have been published. They show promising results for atypical antipsychotics and prazosin, the latter especially on nightmare reduction.

CONCLUSIONS: Disturbed sleep due to nightmares increases the risk for PTSD. PTSD in turn leads to increased sleep fragmentation, decreased GH secretion, and frequent nightmares, which may again compromise fear extinction, synaptic plasticity, and recovery. This suggests that disturbed sleep is a precipitating and perpetuating factor in PTSD symptomatology, creating a perpetual circle. This dissertation suggests that activity of the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system (SNS) is involved in disturbed sleep in patients with PTSD.

Keywords: PTSD; cortisol; growth hormone; memory; nightmares; noradrenalin; polysomnography; sleep

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