The present study identified independent relations among earlier-life trauma exposure and REM sleep fragmentation during adulthood. The current findings elucidate the important role that earlier-life trauma exposure may have in the development of REM sleep physiology, and how this altered sleep physiology may have dynamic influences on subsequent PTSD associated symptoms, such as disruptive nocturnal behaviors. Furthermore, the REM sleep fragmentation profile was described with visually scored, as well as quantitative EEG measures. The confluence of the current findings can extend existing psychobiological models (see: [Germain et al., 2008
; Spilsbury, 2009
]) by providing insight into early-life experience and REM sleep physiology. These models may ultimately be used to predict the developmental course of psychiatric adversities subsequent to trauma, and may provide insight into timing for early intervention.
The independent relations among earlier-life trauma with sleep and PTSD associated behaviors during adulthood were calculated; there were striking associations between earlier-life trauma and REM sleep fragmentation during adulthood. Previous work has identified more proximal associations between trauma exposure, and REM sleep disturbance among humans (Habukawa et al., 2007
; Mellman et al., 2002
), also replicated in the current study; however, the current work demonstrates the prolonged influence that earlier-life trauma may have on the development of REM sleep physiology. This finding replicates, and thus translates to humans, similar findings previously described by experimental animal models that identified the prolonged effect that fear-conditioning has on sleep physiology (DaSilva et al., 2011
; Madan et al., 2008
). Furthermore, earlier-life trauma was independently associated with REM sleep fragmentation whereas later-life trauma was limited to a non-significant trend. This particular finding provides insight into the interaction between early-development and adverse early-life experiences, which may have a salient effect on developmental trajectories of sleep physiology. This finding does not discount the relation between REM sleep fragmentation and later-life trauma since the non-significant association was likely due to low statistical power.
The unique relation between earlier-life trauma and fragmented REM sleep in the pathogenesis of PTSD symptomatology necessitated further examination. Additional analyses identified that REM sleep fragmentation carried an indirect association between earlier-life trauma and disruptive nocturnal behaviors that are characteristic to PTSD. Disruptive nocturnal behaviors, measured by the PSQI-A, have predictive validity in discriminating individuals with and without PTSD (Germain et al., 2005
) and were in fact associated with daytime PTSD severity symptoms among the current sample. REM sleep fragmentation associated with earlier-life trauma may have pervasive influences on subjective sleep quality in adulthood. These pervasive influences could potentially propagate the discrepancies found between subjective and objective sleep measures among individuals who suffer from PTSD (e.g. references [Klein et al., 2003
; Dagan et al., 1997
; Kobayashi et al., 2007
]). Thus, earlier-life trauma associated REM sleep fragmentation may increase vulnerability to psychopathologies in adulthood, especially among military veterans.
Study results guided a further dissection of REM sleep fragmentation that provided a detailed analysis and description of its profile. Visually scored EEG data were examined to better understand the REM fragmentation profile. REM sleep fragmentation was most strongly associated with non-REM during a REM sleep period, wake during a REM sleep period, and micro arousals during REM sleep, respectively. Recent work has demonstrated that these micro-level sleep stage transitions can predict subjective sleep quality over-and-beyond commonly used sleep architecture measures, and can be used to more intricately understand sleep continuity (Laffan et al., 2010
). QEEG calculations during REMs indicated that REMs fragmentation was associated with decreased qEEG delta and increased qEEG beta bands. These results are congruent with previous work that identified self-reported psychological stress as associated with decreased qEEG delta and increased qEEG beta bands during non-REM sleep among insomniacs (Hall et al., 2007
). Although previous work has examined qEEG among military veterans to identify a neurobiological basis for PTSD (e.g. references [Begic et al., 2001
; Jokic-Begic & Begic, 2003
; Woodward et al., 2000
]), the current results provide the initial qEEG report on the physiology of REM sleep in relation to earlier-life trauma associated REM sleep fragmentation.
During early-life, changes in sleep and brain development are drastic and are sensitive to peripheral factors such as stress (Perry et al., 1995
); thus, early-life trauma may have a long-term effect on sleep physiology. Separate research areas indicate that trauma can permanently alter the hypothalamic-pituitary-adrenal axis physiology among children (Neigh et al., 2009
) and normal developmental changes in sleep physiology are most pronounced during early-life (Iglowstein et al., 2003
; McLaughlin & Williams, 2009
; Ohayon et al., 2004
). For instance, the natural developmental decrease in REMs during early-life coincides with a high volume of neurological changes, including a decrease in noradrenergic inhibition (see review [Garcia-Rill, Charlesworth, Heister, Ye, & Hayar, 2008
]). A body of work conducted by Mellman and colleagues has indicated that noradrenergic hyperactivity, possibly due to lack of noradrenergic inhibition, during REM sleep may lead to REM sleep disturbance, which appears to be central to the development of PTSD (Ross et al., 1989
; also, see review [Mellman & Hipolito, 2006
]). Decreased noradrenergic tone is thought to be the primary mechanism underlying the efficacy of prazosin, a α-1 adrenergic antagonist, to treat nightmares and sleep disturbances that are associated with PTSD (Raskind et al., 2003
; Raskind et al., 2007
). When synthesized with the current results, traumatic events that occur during earlier-life, in sequence with normal developmental changes in sleep physiology, may permanently alter noradrenergic regulation and REM sleep physiology, thus resulting in life-long REMs disturbances as described by Garcia-Rill and colleagues (2008)
. This interpretation is congruent with previous longitudinal work that identified a strong association between adverse early-life experiences and poor self-reported sleep quality in adulthood (Koskenvuo et al., 2010
). However, further research is necessary to identify the effects of timing, frequency, intensity, and contexts of trauma exposure during early-life on specific developmental features of sleep physiology, especially REM sleep.
Evidence continues to build to support the function of sleep, and particularly REM sleep, in the process of memory consolidation (see review [Stickgold & Walker, 2005
]). REM sleep and memory have direct implications for emotional memory processing that are fundamental to various stress-related psychopathologies including PTSD. A ‘sleep to forget
and sleep to remember
hypothesis’ has been postulated and highlights the role that REM sleep disturbance has in emotional memory processing, that when present, can initiate and maintain mood disturbances (Walker & van der Helm, 2009
). The current findings support this hypothesis, and together direct future research to identify mechanisms that reveal the relations between early-life trauma, REM sleep physiology, and emotional memory processing.
Recent research has sought to identify various genetic and transgenerational mechanisms that influence adverse reactions to early-life traumatic experiences. A large epidemiological study identified that childhood maltreatment predicted later-life depression only among individuals who possessed a short ‘s’ allele in the 5-HTT gene-linked polymorphic region; additionally, these individuals were more likely to demonstrate adverse psychiatric reactions to stressful life events compared to individuals who did not have the long allele (Caspi et al., 2003
). Furthermore, increased methylation has been shown to result from early-life adversity (Beach et al., 2010
) and appears to moderate the relation between the 5-HTT polymorphism and adverse psychiatric reactions to stress; thus, identifying an epigenetic gene-by-environment interaction (van IJzendoorn et al., 2010
). Additionally, early-life stress can also have a transgenerational effect on subsequent generations that did not directly experience the stressor. For example, male mice who received a salient stressor during postnatal days 1-14, as well as their offspring who did not receive the stressor, demonstrated methylation changes and depressive-like behaviors compared to control mice (Franklin et al., 2010
). Thus, the search for early-life stress related mechanisms that lead to adverse developmental and psychiatric trajectories are at the forefront of science. Future research can be deeply enriched by further examining the novel contributions that REM sleep physiology has among these adverse trajectories. Furthermore, REM sleep physiology may be a viable and non-invasive biomarker to detect the pathogenesis of PTSD development, or susceptibility, following trauma exposure (e.g. Mellman & Hipolito, 2006
All of the current findings were in their expected directions, were identified despite relevant control variables, and aggregated together to bolster the study interpretations. Nevertheless, methodological limitations need to be considered when interpreting results from the current study. The current sample was assembled out of convenience from multiple studies, which limited the research design to a cross-sectional analysis without a control group. Following the sleep disorders screening and adaption night, 23.81% of participants were administered one PSG study night whereas the remainder were administered two PSG study nights. Participants who were administered one study night had longer REM sleep latency than those who were administered two study nights; however, the two groups did not differ on any other REMs variable. Subtle differences in REM sleep values can be expected. Previous research among military veterans with PTSD indicated that participants demonstrated higher REMs density during the first PSG night compared to their second PSG night (Ross et al., 1999
). Furthermore, previous work among healthy community based participants has indicated that the first-night effect during ambulatory PSG can extend beyond one night (Le Bon et al., 2001)—a methodological limitation that can impact a majority of PSG sleep research studies. Nevertheless, the primary study variable, REM sleep fragmentation, did not differ as a function of the number of PSG study nights. As expected, the sample demonstrated high daytime PTSD severity, poor sleep quality, and high disruptive nocturnal behavior prevalence. The CAPS scores may appear low for the particular sample; however, a conservative analytic approach was taken to remove the sleep item scores from the CAPS.
In order to utilize the most accurate amount of data from the THQ, trauma history was limited to the report of discrete events experienced during earlier-life and later-life. Age during each traumatic event was not examined because some participants chose not to provide that level of detail in response to some questions, but rather provided an age range. However, the correlation between later-life trauma with the CAPS (gold-standard) demonstrated the effectiveness of the THQ. Furthermore, the prevalence rate of 65.08% who experienced at least one earlier-life traumatic event is consistent with data from the Center for Disease Control, indicating that two thirds of the general population report childhood adverse events (Centers for Disease Control and Prevention, 2010
). Later-life trauma was associated with daytime PTSD severity and disruptive nocturnal behaviors, which was anticipated because these particular traumatic events are the expected antecedents to PTSD severity and symptoms. The association between earlier-life and later-life trauma was also anticipated because early-life trauma exposure is associated with a higher propensity for re-exposure to trauma (Widom et al., 2008
). Contrary to expectations, there was not a significant association between earlier-life trauma and daytime PTSD severity. The relation between earlier-life trauma and daytime PTSD severity may have been influenced by the retrospective study design, lack of the trauma measurement sensitivity, or the high experience of later-life trauma that may have overshadowed the recollection of earlier-life traumas. When appropriate, future research should utilize prospective designs, a multidimensional assessment battery to probe trauma exposure, and diverse samples to better identify the etiology and effects of earlier-life trauma (e.g. Bernstein et al., 1994
; Briere, 1996
Although a convenience sample was utilized, military veterans are an enriched population to examine post-trauma REM sleep disturbances due to their high-risk for trauma exposure and high rates of PTSD (Hoge et al., 2004
; RAND, 2008
). Knowledge accrued from military samples can be specifically utilized to help identify basic physiological mechanisms that result from trauma-exposure and that contribute to adverse psychiatric conditions. Additionally, such physiological results can be applied to detect signals of trauma-related adversities that may be expressed more subtly among other high-risk civilian populations, such as public service employees (e.g. police officers, firefighters, emergency medical technicians), victims of violence (e.g. rape, physical assaults, terroristic attacks), and individuals who suffer from the aftermath of natural disasters (e.g. hurricanes, tornados, wildfires, floods, tsunamis).