Nightmares , Bad Dreams , and Emotion Dysregulation A Review and New Neurocognitive Model of Dreaming

Nightmares—vivid, emotionally dysphoric dreams—are quite common and are associated with a broad range of psychiatric conditions. However, the origin of such dreams remains largely unexplained, and there have been no attempts to reconcile repetitive traumatic nightmares with nontraumatic nightmares, dysphoric dreams that do not awaken the dreamer, or with more normative dreams. Based on recent research in cognitive neuroscience, sleep physiology, fear conditioning, and emotional-memory regulation, we propose a multilevel neurocognitive model that unites waking and sleeping as a conceptual framework for understanding a wide spectrum of disturbed dreaming. We propose that normal dreaming serves a fear-extinction function and that nightmares reflect failures in emotion regulation. We further suggest that nightmares occur as a result of two processes that we term affect load—a consequence of daily variations in emotional pressures—and affect distress—a disposition to experience events with high levels of negative emotional reactivity. KEYWORDS—nightmares; dreaming; emotion regulation Nightmares—vivid and highly emotionally dysphoric dreams that awaken the individual from sleep—are among the most commonly experienced sleep disorders (for extensive reviews of this literature, see Levin & Nielsen, 2007; Nielsen & Levin, 2007). While fear and terror are the predominant emotions associated with nightmares, other emotions such as rage are not uncommon (Zadra, Pilon, & Donderi, 2006). Like most dreams, nightmares typically occur during rapid-eye-movement (REM) sleep. Nightmares typically imply nocturnal awakening (Levin & Nielsen, 2007), whereas bad dreams are usually defined as negatively toned dreams that do not awaken the dreamer (Levin & Nielsen, 2007; Zadra & Donderi, 2000; Zadra et al., 2006). Despite phenomenological similarities between nightmares and bad dreams, it remains unknown whether they are two qualitatively distinct phenomena or a single phenomenon varying in intensity. We suggest that bad dreams involve similar processes and merely differ in how effective (or ineffective) they are in regulating shifting surges of current affect levels, a process we refer to as regulating affect load (see below for further discussion). Accordingly, we use the term disturbed dreaming (DD) when referring to both nightmares and bad dreams. PREVALENCE AND DEMOGRAPHIC CHARACTERISTICS OF DD Occasional episodes of DD are ubiquitous in the general population. Epidemiological studies indicate that about 85% of adults report experiencing at least one nightmare within the previous year (Levin, 1994), with about 2 to 6% of respondents reporting weekly nightmares. Furthermore, nightmare incidence is reported at significantly higher rates in younger adults starting at age 14, in women after age 14, and in clinical populations (Levin, 1994; Nielsen, Stenstrom, & Levin, 2006). As nightmares are rarely reported spontaneously as clinical problems or inquired about in routine health screenings, true prevalence rates are likely higher. In addition, retrospective reporting significantly underestimates true DD prevalence and incidence rates (Zadra & Donderi, 2000). Perhaps the most robust finding in the DD literature is the strong association between DD frequency and waking psychopathology (e.g., Berquier & Ashton, 1992; Blagrove, Farmer, & Williams, 2004; Hartmann, Russ, Oldfield, Sivan, & Cooper, 1987; Levin & Fireman, 2002; Levin & Nielsen, 2007; Nielsen, Laberge, Tremblay, Vitaro, & Montplaisir, 2000). Because most Address correspondence to Ross Levin, Ferkauf Graduate School of Psychology, Albert Einstein College of Medicine, 145 Rousso Bld., 1165 Morris Park Ave., Bronx, NY 10461; rlevin@yu.edu. CURRENT DIRECTIONS IN PSYCHOLOGICAL SCIENCE 84 Volume 18—Number 2 Copyright r 2009 Association for Psychological Science of these clinical disorders are marked by considerable waking emotional distress, their association with nightmares suggests that nightmare production is related to a personality style characterized by intense reactive emotional distress (Belicki, 1992; Blagrove et al., 2004; Levin & Fireman, 2002; Levin & Nielsen, 2007; Nielsen et al., 2000). Furthermore, it has long been noted that DDs are often precipitated by stressful life events (Berquier & Ashton, 1992; Hartmann et al., 1987). DDs are most commonly associated with trauma exposure and posttraumatic stress disorder (PTSD), and there is a strong link between trauma exposure and subsequent DD (e.g., Mellman, David, Kulick-Bell, Hebding, & Nolan, 1995; Woodward, Arsenault, Murray, & Bliwise, 2000). Further evidence for a link between increased stress and DD comes from a landmark prospective study by Wood, Bootzin, Rosenhan, Nolen-Hoeksema, and Jourden (1992), who found nightmare incidence to be twice as high immediately after the 1989 San Francisco earthquake in two San Francisco Bay-area groups than in an Arizona sample, despite equal baseline frequencies. Importantly, these differences were dose-response specific to proximity to the earthquake epicenter—those who were closer had more nightmares. THE AMPHAC/AND NEUROCOGNITIVE MODEL OF DISTURBED DREAMING Despite the proliferation of recent experimental work on DD, nightmare pathogenesis remains largely unexplained. Current work by us (Levin & Nielsen, 2007; Nielsen & Levin, 2007) incorporating recent advances in cognitive neuroscience, sleep neurophysiology, and fear conditioning—particularly in relation to PTSD and sociocognitive-based diathesis (i.e., vulnerability)– stress models of psychopathology—supports a multilevel model of dream function and nightmare production that unites neural and cognitive processes in both waking and sleeping. The neurophysiological branch of this model is termed the AMPHAC network, after its presumed underlying neurophysiological centers: the amygdala (A), the medial prefrontal cortex (MP), the hippocampus (H), and the anterior cingulate cortex (AC). The cognitive branch is termed the affect network dysfunction (AND) model. Together, the two branches integrate explanatory concepts at both a neural level (i.e., a cohesive and interconnected network of limbic and forebrain regions underlying emotional expression and representation) and a cognitive level (i.e., a dream-production system that transforms fear memories into dream and nightmare imagery). Disruption of processes at these levels can account for a variety of features associated with nightmare imagery (lack of emotional control, bizarre features, or replay of traumatic memories). The AMPHAC/AND model stipulates that DD results from dysfunction in a network of affective processes that, during normal dreaming, are presumed to serve the adaptive function of fear-memory extinction. Indeed, the underlying neurophysiology and biochemistry of REM sleep appears to be primed to activate these very systems. At the cognitive level, dreaming is proposed to facilitate fear-memory extinction by three processes: memory-element activation, memory-element recombination, and emotional expression. The first process refers to the increased availability of a wide range of memory elements during dreaming. For example, it has long been noted that, with the exception of trauma memories, dreams often do not represent coherent episodic memories; the deconstruction of memories into isolated elements or basic units is considered by most dream and sleep researchers to be a cardinal phenomenal feature of dreaming. The second process, memory-element recombination, is largely responsible for the continuous assembly of isolated memory units into a constant and phenomenologically coherent flow of dream imagery. We propose that this organization occurs during dreaming: New image contexts are produced for highly emotionally arousing memorial elements. We propose that these new memorial components are rendered into virtual simulations that maximize their impact on limbic structures, in a manner functionally identical to that which occurs during waking. Limbic structures respond more readily to perceptual stimuli than to imaginal stimuli. The new representations are then recombined to introduce contextual elements that are incompatible with existing fear memories, thus facilitating emotional processing by providing novel contexts for fear that reinforce the development of new extinction memories. The reality mimesis endemic to dream phenomenology (i.e., that dreams feel real and are experienced as waking perception, not simply as hallucination) ensures that fear memories are processed in a medium similar to that in which they were first encoded, thus facilitating emotion regulation. We consider the third process, emotional expression, to be a necessary step in dreaming’s fear-extinction function, as it maximizes the involvement of neural structures—primarily but not limited to those of the limbic system—to further ensure the adequate deployment of attentional resources in order to downregulate negative emotional arousal. We suggest that engagement of these fear-extinction processes may be the default function of REM sleep, with dreaming representing the experienced result of these mechanisms. Representation of specific memorial components in dream content is then determined by ongoing daytime demands on the emotionalmemory system—in other words, we dream about what we are emotionally preoccupied by in waking. We use the term affect load (AL) to refer to the ongoing accumulation of stressful and emotional negative events that impinge on an individual’s capacity to effectively regulate emotion. AL, in our model, is a state (i.e., transitory) factor considered to be a primary determinant of DD incidence. Thus, as AL increases, so does the probability of DD. In contrast, affect distress (AD), defined as a dispositional tendency to experience heightened distress in response to emotional stimuli, is proposed to be a major determinant of whether DDs will become clinical Volume 18—