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The Stress Acceleration Hypothesis of Nightmares.

Tore Nielsen

Frontiers in Neurology June 1, 2017 DOI: 10.3389/fneur.2017.00201 (opens in new tab)

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AI-extracted from the abstract
Characteristics Theoretical or philosophical paper Peer reviewed
Topics Dreaming
Keywords Trauma Affective disorders Nightmares Adverse childhood experiences Infantile amnesia Stress acceleration
Key points Proposes that idiopathic nightmares may originate in adverse experiences during the infantile amnesia period, which ends around age 3½, via two mechanisms: disruption of infantile amnesia allowing early memories to influence later dream content, and altered emotion regulation increasing fear sensitivity and impairing fear extinction within a fear network involving the amygdala, hippocampus, and medial prefrontal cortex.

Abstract

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.

Comparable studies

Other theoretical and historical papers on dreaming, most cited first.

Study Year Design Participants
Dreaming: a conceptual framework for philosophy of mind and empirical research 2016 Theoretical or philosophical paper
Metaphor and hyperassociativity: the imagination mechanisms behind emotion assimilation in sleep and dreaming 2015 Theoretical or philosophical paper
Varieties of Lucid Dreaming Experience 2000 Theoretical or philosophical paper
Experimental Research on Dreaming: State of the Art and Neuropsychoanalytic Perspectives 2011 Theoretical or philosophical paper
The Neurobiology of Consciousness: Lucid Dreaming Wakes Up 2009 Theoretical or philosophical paper

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