دانلود رایگان مقاله انگلیسی اختلال خواب مرتبط با تروما: پارازومنی ناشی از تروما - الزویر 2018

summary

Nightmares and disruptive nocturnal behaviors that develop after traumatic experiences have long been recognized as having different clinical characteristics that overlap with other established parasomnia diagnoses. The inciting experience is typically in the setting of extreme traumatic stress coupled with periods of sleep disruption and/or deprivation. The limited number of laboratory documented cases and symptomatic overlap with rapid eye movement sleep behavior disorder (RBD) and posttraumatic stress disorder (PTSD) have contributed to difficulties in identifying what is a unique parasomnia. Trauma associated sleep disorder (TSD) incorporates the inciting traumatic experience and clinical features of trauma related nightmares and disruptive nocturnal behaviors as a novel parasomnia. The aims of this theoretical review are to 1) summarize the known cases and clinical findings supporting TSD, 2) differentiate TSD from clinical disorders with which it has overlapping features, 3) propose criteria for the diagnosis of TSD, and 4) present a hypothetical neurobiological model for the pathophysiology of TSD. Hyperarousal, as opposed to neurodegenerative changes in RBD, is a component of TSD that likely contributes to overriding atonia during REM sleep and the comorbid diagnosis of insomnia. Lastly, a way forward to further establish TSD as an accepted sleep disorder is proposed.

Neurobiological hypothesis of TSD

We propose the interplay of extreme trauma and concurrent sleep deprivation or disturbance can incite measurable changes in the volume, activity, and function of CNS structures that are integral to dream processing and REM sleep, manifesting in the symptomatology of TSD. REM sleep, normally protective for depotentiating traumatic experiences, is disrupted in TSD patients. Multiple factors contribute to the alterations in REM including sleep deprivation and hyperarousal from trauma; these factors lead to hyperactivity of the amygdala during REM. Frontal lobe activity, already reduced in REM, is further impaired in TSD by sleep deprivation and comorbid insomnia, increasing the potential for violent or aggressive behavior. In particular, there is a blunted increase in the activity of the mPFC, which regulates the amygdala. The combination of these changes results in fear and many accompanying downstream effects including increased neuroendocrine activity (via direct stimulation of the HPA axis by the amygdala) that perpetuates hyperarousal in sleep as well as physical expressions of fear (DNB, vocalizations, facial expressions of fear, startle reflex, etc.). The state of hyperarousal present in TSD is further compounded by direct amygdalar stimulation of brainstem REM-off nuclei including the LC, resulting in increased adrenergic activity and the “fight or flight” sympathetic response which has been observed in TSD patients. Additionally, excessive NE release by the LC inhibits REM-on nuclei such as the laterodorsal tegmental and pedunculopontine tegmental nuclei, which may cause RWA and further fragmentation of REM sleep. Trauma also results in dysfunction of other CNS structures including the precuneus and limbic structures such as the hippocampus, ACC, and insula, further contributing to REM sleep disruption and nightmare generation. The clinical manifestations of TSD likely result from the combination of these neurobiological changes, along with others that are not yet discovered or fully elucidated.