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Posttraumatic Stress Disorder With Amnesia Following Asphyxiation
Abstract
We describe five cases of traumatic asphyxiation injury, each meeting diagnostic criteria for posttraumatic stress disorder (PTSD) and characterized by a range of postinjury cognitive impairment. Four patients exhibited dense retrograde amnesia, including absence of conscious memory for the traumatic event. Appreciation of these asphyxiation cases, which involve temporally extended trauma exposure, may help resolve arguments regarding the possibility of co-occurrence of PTSD and neurological amnesia based exclusively on observations of much briefer duration events (specifically, motor vehicle crashes). These five cases also provide evidence that cognitive symptoms of PTSD can develop in the absence of conscious memory for the event.
... 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). ...
... 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). ...
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 posttraumatic 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 before maturation of the neural systems supporting declarative memory to assess the necessity of early memory to the later life development of PTSD-related symptoms.
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 or elevated plus maze or sacrificed for basal diurnal corticosterone and quantification of neuronal glucocorticoid and neuropeptide Y receptors.
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 glucocorticoid receptors, decreased time spent in the open arm of an elevated plus maze, and an odor aversion associated with early-life footshocks.
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.
... A third mechanism can exert influence in the absence of any explicit, declarative memory at all (Layton & Wardi-Zonna, 1995). This is consistent with neurocognitive and psychoanalytic perspectives that do not stipulate a necessary role for explicit memories within traumatic etiology with or without TBI (Brewin, Dalgleish, & Joseph, 1996; Layton & Krikorian, 2002; Layton, Krikorian, Dori, Martin, & Wardi, 2006; Yovell, 2000). In a series of 105 cases of mild TBI, the presence or absence of amnesia for the traumatic event did not differentiate PTSD incidence within the sample (Bryant & Harvey, 1999). ...
... When considering the objectively documented nature of incidents leading to TBI, malevolent actions, intentions , or responsibility of self or other often feature. The survivor may have been injured as a result of the actions of another driver (intentional or otherwise), a purposeful assault, or the neglect or human error of an industrial colleague or superior (Bell, 1998; Layton et al., 2006). Perhaps, in addition, the survivor may have inadvertently caused the death of a significant other in the same incident (e.g., in a car crash) or may experience guilt through the very fact of his or her survival when others have died. ...
Posttraumatic stress disorder (PTSD) has been identified in survivors of traumatic brain injury (TBI), sustained from road traffic ac-cidents, assaults, or industrial accidents. This article reviews the small literature on this population, which is predominantly charac-terized by integrations of cognitive neuropsychology and cognitive behavior therapy. While these perspectives have been applied to identify etiological processes and treatment options, one insufficiently specified domain in this literature is the role of interpersonal relationships. This includes interpersonal etiological mechanisms and social outcomes, but also therapeutic process for PTSD after TBI. In response, object-relations psychoanalytic concepts of symbolizing (Segal, 1957) and containing–contained (Bion, 1962) mechanisms are applied. These concepts are used to consider the aforementioned factors while permitting close conceptual links to neurological and cognitive vulnerabilities for this clinical group. This article finishes with a therapeutic application of these concepts, from the perspective of a neurorehabilitation team.
... Hypoxia is a factor in ptsD allowing memory loss of a traumatic event in ptsD patients [72]. Post-avalanche survivors develop ptsD in approximately 11% of cases and it is presumable, but not demonstrated, that suffering hypoxia is a factor in this development [73]. ...
COVID-19 affects brain function, as deduced by the “brain fog” that is often encountered in COVID-19 patients and some cognitive impairment that is observed in many a patient in the post-COVID-19 period. Approximately one-third of patients, even when they have recovered from the acute somatic disease, continue to show posttraumatic stress disorder (PTSD) symptoms. We hypothesized that the persistent changes induced by COVID-19 on brain structure would overlap with those associated with PTSD. We performed a thorough PubMed search on 25 April 2023 using the following strategy: ((posttraumatic OR PTSD) AND COVID-19 AND (neuroimaging OR voxel OR VBM OR freesurfer OR structural OR ROI OR whole-brain OR hippocamp* OR amygd* OR “deep gray matter” OR “cortical thickness” OR caudate OR striatum OR accumbens OR putamen OR “regions of interest” OR subcortical)) OR (COVID-19 AND brain AND (voxel[ti] OR VBM[ti] OR magnetic[ti] OR resonance[ti] OR imaging[ti] OR neuroimaging[ti] OR neuroimage[ti] OR positron[ti] OR photon*[ti] OR PET[ti] OR SPET[ti] OR SPECT[ti] OR spectroscop*[ti] OR MRS[ti])), which produced 486 records and two additional records from other sources, of which 36 were found to be eligible. Alterations were identified and described and plotted against the ordinary PTSD imaging findings. Common elements were hypometabolism in the insula and caudate nucleus, reduced hippocampal volumes, and subarachnoid hemorrhages, while white matter hyperintensities were widespread in both PTSD and post-COVID-19 brain infection. The comparison partly supported our initial hypothesis. These data may contribute to further investigation of the effects of long COVID on brain structure and function.
... that characterise the disorder (APA, 2013, p. 5th ed.) are not contingent on memory and can occur in its absence (King, 2001;Russell & Curran, 2002;Turnbull, Campbell, & Swann, 2001). Examples include psychological trauma occurring in the context of traumatic brain injury (TBI; Bryant et al., 2009;McNeil, 1996), asphyxiation (Layton, Krikorian, Dori, Martin, & Wardi, 2006), drug-facilitated sexual assault (Fitzgerald & Riley, 2000;Gauntlett-Gilbert, Keegan, & Petrak, 2004) and intensive care treatment (Jones, Griffiths, Humphris, & Skirrow, 2001). ...
Background:
It is possible for people to have post-traumatic stress disorder (PTSD) without memory of the trauma event, such as in drug-facilitated sexual assault. However, there is little evidence available on treatment provision for this population.
Objective:
This study aimed to address this gap by exploring the experiences of people who have had psychological intervention for PTSD without memories (PwM).
Method:
Interpretative phenomenological analysis was used to explore the lived experience of nine women with PwM, who had sought psychological assessment/therapy. Participants were recruited via social media and completed semi-structured interviews online/via telephone.
Results:
Identified themes concerned two broad areas: (i) the challenges of having therapy whilst lacking memories and (ii) what was helpful in therapy. Challenges included: delayed help-seeking; having emotional/sensory reactions in the absence of recognisable triggers; experiencing therapy as more applicable to remembered trauma (vs. unremembered); and difficulty discussing and processing unremembered trauma. However, participants also described helpful aspects of therapy including: feeling safe and supported; working with emotional and sensory forms of experience; having scientific explanations for trauma and memory; and having 'permission' from therapists not to remember.
Conclusions:
Recommendations for clinicians included: being aware that clients with PwM may have more difficulty accessing treatment and perceive it as less applicable to them; focussing on clients' emotions and sensations (not cognitive memories) in therapy; and supporting clients to develop a more self-compassionate understanding of their experiences and lack of memory, thus supporting them to accept that not remembering is 'permitted'.
Highlights:
• Having therapy for unremembered trauma involves unique challenges, but aspects of therapy can still be helpful.• Suggested 'dos and don'ts' for therapists include recognising the additional barriers to treatment, focussing on emotions (not memories), and normalising memory loss.
... When footshock stress is administered to rats too young to acquire Pavlovian contextual fear, the rats still exhibit fear sensitization when tested as adults [21]. Similarly, human patients with amnesia of an acutely traumatic event can still exhibit symptoms of PTSD [22]. We are aware of only one study showing that fear sensitization requires Pavlovian conditioned fear. ...
Stressful experiences ca cause long-lasting sensitization of fear and anxiety that extends beyond the circumstances of the initial trauma. The neural mechanisms of these stress effects have been studied extensively in rats using the stress-enhanced fear learning (SEFL) paradigm, in which exposure to footshock stress potentiates subsequent fear conditioning. Here we establish a mouse version of the SEFL. Male and female 129s6 mice received four 1-mA foot shocks or equivalent context exposure without shock. Shock exposure induced Pavlovian fear conditioning to the shock context and produced three more general effects: (1) suppression of open field exploration, (2) potentiated unconditioned fear of a novel tone stimulus, and (3) enhanced fear conditioning in a novel context. To determine whether these effects of footshock stress reflect generalized Pavlovian fear conditioning versus nonassociative fear sensitization, some mice received extinction training in the footshock stress context, which reduced contextual fear to the levels of unstressed control mice. Extinction restored normal open field exploration, suggesting that this effect of stress reflects generalized Pavlovian fear. In contrast, extinction failed to attenuate stress-enhanced fear, indicating that stress-enhanced fear is nonassociative and mechanistically distinct from Pavlovian fear conditioning. The effects of footshock stress were similar in male and female mice, although female mice displayed larger acute responses to fear-inducing stimuli than did males. The results demonstrate that footshock stress influences emotional behavior through distinct associative and nonassociative mechanisms, which likely involve unique neural underpinnings.
... 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). ...
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.
... For instance, as illustrated inFigure 1, a very intense stressor could result in a more short-lived excitatory phase of hippocampal function and a faster onset of its inhibitory phase. In fact, it is possible that traumatic stressors could force the hippocampus into a refractory phase immediately following the onset of stress, which may explain the phenomenon of traumatic amnesia (Bryant et al., 2009; Layton, Krikorian, Dori, Martin, and Wardi, 2006). In addition, individual differences, such as different physiological responses to stress, different perceptions of the stressor, or different perceived controllability over the stress, could also influence the model. ...
Stress exerts complex effects on cognition. While stress can enhance learning and result in powerful memories that last a lifetime, it can also impair learning and cause us to be forgetful in our everyday lives. Over the past several years, it has become apparent that the types of effects that stress exerts on learning and memory depend critically on several factors related to the organism being studied, the learning experience, and the timing of the stressor. For instance, post-learning stress often facilitates long-term memory, while pre-learning and pre-retrieval stress effects are more variable and can involve enhancements or impairments of memory. In addition, stressors that are administered immediately before learning seem to result in amygdala-induced enhancements of hippocampal neuroplasticity, which promote learning, whereas stressors that are temporally separated from the learning experience result in amygdala-induced suppression of hippocampal neuroplasticity, which impairs learning. In the present review, we provide a comprehensive discussion of factors that mediate stress-induced alterations of hippocampus-dependent learning and memory and contend that the neurochemicals released following stress (e.g., cortisol, norepinephrine, glutamate, etc.) exert temporally distinct effects on brain areas devoted to processing emotional and cognitive information, such as the amygdala, hippocampus, and prefrontal cortex. We also propose that such stress-memory interactions differ significantly between males and females, which may be attributable, at least in part, to differences in amygdala activity and temporal dynamics of the stress response. Collectively, understanding the neurobiological basis of stress-memory interactions and how sex mediates such effects will facilitate the scientific community's understanding of traumatic memory formation and the onset of stress-related psychological disorders, such as post-traumatic stress disorder.
Stress-enhanced fear learning (SEFL) refers to the long-lasting nonassociative sensitization produced by intense stress (e.g., repeated and unpredictable footshock) that results in increased fear learning to a mild conditioning regimen (e.g., one shock). SEFL experiments suggest that one component of posttraumatic behavior is inappropriately strong fear conditioning occurring to relatively mild stressors. Past reports of SEFL have used the same intensity (1 mA) of footshock to cause both the sensitization and conditioning of new fear. SEFL would be a particularly problematic component of posttrauma behavior if intense stress results in substantial fear conditioning under conditions that would not normally support conditioning. Therefore, we determined if SEFL occurred when the conditioning shock was substantially milder than the SEFL-inducing shock. The results indicate that exposure to a sensitizing regimen of shock can convert a mild footshock that normally does not support measurable levels of fear conditioning into one that causes substantial learned fear. Moreover, as the intensity of single footshock increases, so does the capacity of the prior stressor to contribute to the sensitization of fear responses. Consistent with prior studies, males acquired and retained a greater level of fear conditioning than female rats, however the level of sensitization did not differ between sexes. (PsycINFO Database Record (c) 2015 APA, all rights reserved).
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.
This report documents a case of posttraumatic stress disorder (PTSD) following psychological trauma with cerebral insult and amnesia for the traumatic event. The case history demonstrates the role of implicit memory in PTSD and indicates that the mechanisms of psychopathology are one-trial sensitization and conditioned emotional responses.
This study indexed the profile of posttraumatic stress disorder (PTSD) after severe traumatic injury to the brain.
Patients who sustained a severe traumatic brain injury (N=96) were assessed for PTSD 6 months after the injury with the PTSD Interview, a structured clinical interview based on DSM-III-R criteria.
PTSD was diagnosed in 26 (27.1%) of the patients. While only 19.2% (N=5) of the patients with PTSD reported intrusive memories of the trauma, 96.2% (N=25) reported emotional reactivity. Intrusive memories, nightmares, and emotional reactivity had very strong positive predictive values for the presence of PTSD.
These findings indicate that PTSD can develop after severe traumatic brain injury. The predominance of emotional reactivity and the relative absence of traumatic memories in patients with PTSD who suffered impaired consciousness during trauma suggest that traumatic experiences can mediate PTSD at an implicit level.
The authors present a new theory of the neurobiological mechanisms mediating the memory processes involved in posttraumatic stress disorder (PTSD). The current fear-conditioning model accounts for learning that underlies certain central features of PTSD, but it fails to account for peritraumatic memory disturbances, episodic memory phenomena that also are characteristic of the disorder. A more comprehensive model of PTSD, consistent with the clinical phenomenology of the disorder, is proposed on the basis of observations from human memory experiments. It is argued that the amygdala is the locus of consolidation of the core of the traumatic experience and that amygdalar inhibition of hippocampal function at high levels of emotional arousal mediates diminution of conscious memory for peritraumatic events. The model is amenable to specific experimental manipulations that should yield information pertinent to further development of theory and, ultimately, to more rational clinical intervention.
Memory mechanisms in posttraumatic stress disorder: implicit memory in posttraumatic stress disorder with amnesia for the traumatic event
- Layton B.