https://orcid.org/0000-0001-8566-3572
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Abstract
Background
Sleep disturbances (SD) are the most impactful and commonly reported symptoms in post-traumatic stress disorder (PTSD). Yet, they are often resistant to primary PTSD therapies. Research has identified two distinct SDs highly prevalent in PTSD; insomnia and nightmares. Those who report SDs prior to a traumatic event are at greater risk for developing PTSD; highlighting that sleep potentially plays a role in PTSD’s pathology. To further understand the pathobiological mechanisms that lead to the development of PTSD, it is first imperative to understand the interplay which exists between sleep and PTSD on a biological level. The aim of this systematic review is to determine if biological or physiological markers are related to SD in PTSD.
Methods
A systematic literature search was conducted on the electronic databases; Medline, Embase, AMED and PsycINFO, using Medical Subject Headings and associated keywords.
Results
Sixteen studies were included in the final analyses. Physiological makers of autonomic function, and biochemical markers of HPA-axis activity; inflammatory processes; and trophic factor regulation were related to the severity of SDs in PTSD.
Conclusion
These findings add to the growing literature base supporting a central focus on sleep in research aiming to define the pathophysiological processes which result in PTSD, as well as emphasising the importance of specifically targeting sleep as part of a successful PTSD intervention strategy. Resolving SDs will not only reduce PTSD symptom severity and improve quality of life but will also reduce all-cause mortality, hospital admissions and lifetime healthcare costs for those with PTSD. Limitations of the current literature are discussed, and key recommendations future research must adhere to are made within.
Abbreviations
PTSD, post-traumatic stress disorder; SD, sleep disturbances; DSM-5, Diagnostic and statistical manual of mental disorders 5th edition; CBT, cognitive behavioural therapy; CBT-I, cognitive behavioural therapy for insomnia; PCL, PTSD checklist; PVN, paraventricular nucleus; CRH, corticotrophin-releasing hormone; AVP arginine vasopressin; ACTH, adrenocorticotrophic hormone; FKBP5, FK506 binding protein; IL-6, interleukin-6, IL-1β; TNF-α, tumour necrosis factor-α; INF-γ, interferon gamma; SCN, suprachiasmatic nuclei; CRP, C-reactive protein; MeSH, Medical Subject Headings; EEG, electroencephalogram; PSG, polysomnography; HR, heart rate; HRV, heart rate variability; nHF, normalised high frequency; LF, low frequency; BRS, baroreceptor sensitivity; BP, blood pressure; SCL, skin conductance level; ERRT, exposure, relaxation and rescripting therapy; TLR, toll-like receptor; CVD, cardiovascular disease.
Disclosure
MWR is a paid employee of Randox Laboratories but holds no shares in the company. No other authors have any conflicts of interests to declare.