Almost a decade ago, Anne Germain summarized the research of the previous decade. It supported a “paradigm shift, reconceptualizing sleep disturbances as biologically relevant and modifiable predisposing, precipitating, and perpetuating factors of PTSD (Germain et al., 2017, p. 84).” However, since that review almost nothing has been done to integrate sleep repair into
trauma treatments. The reason? Sleep has been seen as just another symptom. Any why should any one symptom be given more attention than any other symptom?
In the intervening decade, our understanding of the neurobiology that underpins trauma has revolutionized our understanding of what accounts for both trauma and sleep symptoms. Specifically, it is the unique contribution of brainstem centres, and their powerful neuromodulation of other midbrain and cortical brain centres, that accounts for both the diversity of trauma symptoms as well as the variety of sleep disturbances. The implication of these insights is that trauma treatment must target these deep brain structures directly, to resolve both trauma symptoms as well as disrupted sleep.
· The brainstem plays a pivotal role in survival responses and emotional regulation, particularly during life-threatening situations.
· The first internal centre that detects our location in space and orients to an external danger is at the lower brainstem, in the Superior Colliculus (SC). Antonio Damasio described this as the location of our “proto self.”
· The SC activates our orientation to danger, setting off the body's LC-NE alarm system. These LC-NE reactions coordinate and prioritize survival over other functions, such as restful sleep and memory processing.
· Targeting the brainstem structures that Neuromodulate the brain offers promising avenues to address the dysregulation caused by trauma, helping patients reclaim their sense of self, diminish trauma symptoms and improve sleep.
· Alarm System Activation: Trauma triggers intense responses via the brainstem, specifically through pathways involving the Superior Colliculus-Amygdala-LC axis. These responses amplify emotional and physical reactivity overwhelming the person’s sense of safety.
· Disruption of Autobiographical Memory: Hyperactivation of brainstem survival centers causes fragmented sensory memories, preventing the formation of coherent narrative memories and keeping the individual in a state of hypervigilance.
· Sleep Impairment: The LC-Orexin-Thyroid brainstem circuits also disrupt sleep by maintaining 24-hour wakefulness to avoid perceived threats, leading to insomnia.
· The Short, Fragmented Sleep Insomnia Phenotype: Fragmented, short sleep cycles with little REM sleep characterize chronic insomnia in trauma survivors. This pattern results from heightened cognitive arousal driven by brainstem dysregulation.
· Neuromodulation Strategies: To reverse these effects, treatments need to focus on resetting the brainstem's activity to break the cycle of hyperactivation.
· Techniques addressing brainstem dysregulation through neuromodulation can:
o Silence overactive circuits perpetuating insomnia and hypervigilance.
o Restore normal autobiographical memory function, allowing patients to process and integrate traumatic experiences.
o Enable a return to restorative sleep patterns, essential for emotional and cognitive recovery.
· Only brainstem-focused therapies that reset neuromodulation can offer trauma survivors a pathway to recovery, rebuilding their sense of self and empowering them to move forward.