Posttraumatic Stress Disorder With Amnesia Following Asphyxiation

Layton, Barry S.; Krikorian, Robert; Dori, Galit A.; Martin, G.; Wardi, Katherine

doi:10.1196/annals.1364.048

Cited by 9 publications

(11 citation statements)

References 3 publications

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“…In both of these cases a specific memory for the trauma context is not necessary for sensitization of subsequent fear learning. This augmented fear conditioning is consistent with reports from PTSD patients exhibiting a greater propensity to develop new phobias and a greater reactivity to emotionally salient stimuli even under conditions in which patients may fail to remember the precipitating trauma (4). …”

Section: Discussionsupporting

confidence: 88%

“…In the adult human and rodent, memories established within an emotionally charged environment are generally robust and not readily forgotten (1,2) and thus may provide important insights into the link between trauma related memory and PTSD. This link has been primarily explored in patients with mild traumatic brain injury and/or traumatic asphyxiation injury with post-traumatic amnesia (3,4,5) as well as in subjects with early life trauma occurring during the period of infantile amnesia (6). Despite this, the link between trauma-related memory and PTSD remains a point of controversy (3,4).…”

Section: Introductionmentioning

confidence: 99%

“…This link has been primarily explored in patients with mild traumatic brain injury and/or traumatic asphyxiation injury with post-traumatic amnesia (3,4,5) as well as in subjects with early life trauma occurring during the period of infantile amnesia (6). Despite this, the link between trauma-related memory and PTSD remains a point of controversy (3,4). …”

Section: Introductionmentioning

confidence: 99%

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Amnesia for Early Life Stress Does Not Preclude the Adult Development of Posttraumatic Stress Disorder Symptoms in Rats

Poulos¹,

Reger

Mehta³

et al. 2014

Biological Psychiatry

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Background Traumatic experience can result in life-long changes in the ability to cope with future stressors and emotionally salient events. These experiences, particularly during early development are a significant risk factor for later life anxiety disorders such as post-traumatic stress disorder (PTSD). However, because traumatic experience typically results in strong episodic memories, it is not known whether such long-term memories are necessary for particular features of PTSD such as enhanced fear and anxiety. Here we used a fear conditioning procedure in juvenile rats prior to maturation of the neural systems supporting declarative memory to assess the necessity of early memory to the later life development of PTSD related symptoms. Methods Nineteen-day old rats were exposed to unpredictable and inescapable footshocks and fear memory for the shock context was assessed during adulthood. Thereafter, adult animals were either exposed to single-trial fear conditioning, elevated plus-maze or sacrificed for basal diurnal corticosterone and quantification of neuronal glucocorticoid (G-R) and Neuropeptide Y receptors. Results Early trauma exposed rats displayed stereotypic footshock reactivity, yet by adulthood, hippocampus-dependent contextual fear related memory was absent. However, adult rats showed sensitized fear learning, aberrant basal circadian fluctuations of corticosterone, increased amygdalar G-R, decreased time spent in the open arm of an elevated plus maze and an odor aversion associated with early-life footshocks. Conclusions These results suggest that traumatic experience during developmental periods of hippocampal immaturity can promote lifelong changes in symptoms and neuropathology associated with human PTSD even if there is no explicit memory of the early trauma.

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Section: Discussionsupporting

confidence: 88%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Amnesia for Early Life Stress Does Not Preclude the Adult Development of Posttraumatic Stress Disorder Symptoms in Rats

Poulos¹,

Reger

Mehta³

et al. 2014

Biological Psychiatry

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“…Again, the neurocircuitry of fear learning was altered even though the learning originating in the infantile amnesia period was forgotten. Poulos et al (147) consider this augmented fear conditioning to be analogous to those types of PTSD patients who do not remember their precipitating traumatic event (e.g., asphyxiation with amnesia) yet exhibit a greater propensity for developing phobias and expressing reactivity to other emotional stimuli (148, 149). …”

Section: The Stress Acceleration Hypothesis Of Nightmaresmentioning

confidence: 99%

The Stress Acceleration Hypothesis of Nightmares

Nielsen

2017

Front. Neurol.

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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.

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“…Layton, Krikorian, Dori, Martin, and Wardi (2006) demonstrated that people with amnesia following a trauma may still exhibit avoidance and hyperarousal to traumarelated stimuli in the absence of conscious recollection of the event. First, an overactive amygdala in response to trauma reminders and trauma-unrelated aversive stimuli has been observed in many studies .…”

Section: Structural and Functional Changes In Ptsdmentioning

confidence: 99%

Implications of neuroscientific evidence for the cognitive models of post-traumatic stress disorder

Cruwys

O’Kearney

2008

Clinical Psychologist

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Brewin's dual representation theory, Ehlers and Clark's cognitive appraisal model, and Dalgleish's schematic, propositional, analogue and associative representational systems model are considered in the light of recent evidence on the neural substrates of post-traumatic stress disorder (PTSD). The models' proposals about the cognitive mechanism of memory dysfunction in PTSD are described and evaluated against current knowledge about the neural pathways and functions disrupted in PTSD. A dual pathway model of memory is consistent with neuroscience of memory. The appraisal model also provides an account of the top-down modulation of memory and arousal problems consistent with current neuroscientific evidence of PTSD. Dalgleish's model is less consistent with the evidence because it relies upon assumptions that cannot yet be tested neuroscientifically. All three models under-specify the causal and maintaining influence of hyperarousal relative to the role it plays in current neuroscientific models of PTSD. Implications of the evidence for improving treatment and prevention are discussed.

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Posttraumatic Stress Disorder With Amnesia Following Asphyxiation

Cited by 9 publications

References 3 publications

Amnesia for Early Life Stress Does Not Preclude the Adult Development of Posttraumatic Stress Disorder Symptoms in Rats

Amnesia for Early Life Stress Does Not Preclude the Adult Development of Posttraumatic Stress Disorder Symptoms in Rats

The Stress Acceleration Hypothesis of Nightmares

Implications of neuroscientific evidence for the cognitive models of post-traumatic stress disorder

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