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Nightmares are highly dysphoric dreams that are well-remembered upon awakening. Frequent nightmares have been associated with psychopathology and emotional dysregulation, yet their neural mechanisms remain largely unknown. Our neurocognitive model posits that nightmares reflect dysfunction in a limbic-prefrontal circuit comprising medial prefrontal and anterior cingulate cortices, hippocampus, and amygdala. However, there is a paucity of studies that used brain imaging to directly test the neural correlates of nightmares. One such study compared the regional homogeneity (ReHo) of resting-state functional magnetic resonance imaging blood-oxygen level-dependent signals between frequent nightmare recallers and controls. The main results were greater regional homogeneity in the left anterior cingulate cortex and right inferior parietal lobule for the nightmare recallers than for the controls. In the present study, we aimed to document the ReHo correlates of frequent nightmares using several nightmare severity measures. We acquired resting-state functional magnetic resonance imaging data from 18 frequent nightmare recallers aged 18–35 (3 males and 15 females) and 18 age- and sex-matched controls, as well as retrospective and prospective disturbed dreaming frequency estimates and scores on the Nightmare Distress Questionnaire. While there were inconsistent results for our different analyses (group comparisons, correlational analyses for frequency estimates/Nightmare Distress scores), our results suggest that nightmares are associated with altered ReHo in frontal (medial prefrontal and inferior frontal), parietal, temporal and occipital regions, as well as some subcortical regions (thalamus). We also found a positive correlation between retrospective disturbed dreaming frequency estimates and ReHo values in the hippocampus. These findings are mostly in line with a recent SPECT study from our laboratory. Our results point to the possibility that a variety of regions, including but not limited to the limbic-prefrontal circuit of our neurocognitive model, contribute to nightmare formation.

AimRapid eye movement (REM) sleep, non-rapid eye movement (NREM) sleep, and sleep spindles are all implicated in the consolidation of procedural memories. Relative contributions of sleep stages and sleep spindles were previously shown to depend on individual differences in task processing. However, no studies to our knowledge have focused on individual differences in experience with Vipassana meditation as related to sleep. Vipassana meditation is a form of mental training that enhances proprioceptive and somatic awareness and alters attentional style. The goal of this study was to examine a potential role for Vipassana meditation experience in sleep-dependent procedural memory consolidation.MethodsGroups of Vipassana meditation practitioners (N = 22) and matched meditation-naïve controls (N = 20) slept for a daytime nap in the laboratory. Before and after the nap they completed a procedural task on the Wii Fit balance platform.ResultsMeditators performed slightly better on the task before the nap, but the two groups improved similarly after sleep. The groups showed different patterns of sleep-dependent procedural memory consolidation: in meditators, task learning was positively correlated with density of slow occipital spindles, while in controls task improvement was positively associated with time in REM sleep. Sleep efficiency and sleep architecture did not differ between groups. Meditation practitioners, however, had a lower density of occipital slow sleep spindles than controls.ConclusionResults suggest that neuroplastic changes associated with meditation practice may alter overall sleep microarchitecture and reorganize sleep-dependent patterns of memory consolidation. The lower density of occipital spindles in meditators may mean that meditation practice compensates for some of the memory functions of sleep.

Adverse childhood experiences can deleteriously affect future physical and mental health, increasing risk for many illnesses, including psychiatric problems, sleep disorders, and, according to the present hypothesis, idiopathic nightmares. Much like post-traumatic nightmares, which are triggered by trauma and lead to recurrent emotional dreaming about the trauma, idiopathic nightmares are hypothesized to originate in early adverse experiences that lead in later life to the expression of early memories and emotions in dream content. Accordingly, the objectives of this paper are to (1) review existing literature on sleep, dreaming and nightmares in relation to early adverse experiences, drawing upon both empirical studies of dreaming and nightmares and books and chapters by recognized nightmare experts and (2) propose a new approach to explaining nightmares that is based upon the Stress Acceleration Hypothesis of mental illness. The latter stipulates that susceptibility to mental illness is increased by adversity occurring during a developmentally sensitive window for emotional maturation—the infantile amnesia period—that ends around age 3½. Early adversity accelerates the neural and behavioral maturation of emotional systems governing the expression, learning, and extinction of fear memories and may afford short-term adaptive value. But it also engenders long-term dysfunctional consequences including an increased risk for nightmares. Two mechanisms are proposed: (1) disruption of infantile amnesia allows normally forgotten early childhood memories to influence later emotions, cognitions and behavior, including the common expression of threats in nightmares; (2) alterations of normal emotion regulation processes of both waking and sleep lead to increased fear sensitivity and less effective fear extinction. These changes influence an affect network previously hypothesized to regulate fear extinction during REM sleep, disruption of which leads to nightmares. This network consists of a fear circuit that includes amygdala, hippocampus, and medial prefrontal cortex and whose substantial overlap with the stress acceleration findings allows the latter to be incorporated into a wider, more developmentally coherent framework.