Hotspots in the immediate aftermath of trauma - Mental imagery of worst moments highlighting time, space and motion.

Intrusive memories of trauma (memories that enter consciousness involuntarily) highjack cognitive processing, cause emotional distress, and represent a core symptom of posttraumatic stress disorder. Intrusive memories often contain the worst moment/s ('hotspots') of the trauma memory. Little is known about hotspots shortly after they are formed, i.e., in the first hours after trauma. We investigated the features of hotspots in trauma-exposed individuals (n = 21) within 72 h post-trauma, using linguistic analysis and qualitative coding. On average, participants reported three hotspots per traumatic event (M = 7.8 words/hotspot). Hotspots primarily contained words related to time, space, motion, and sensory processing. Most hotspots contained sensory features (97%) and motion (59%). Few cognitions and no emotion words were identified. Results indicate that hotspots collected shortly post-trauma are expressed as motion-rich sensory-perceptual experiences (mental imagery) with little detail about emotion/cognition. Findings are discussed in terms of the function of hotspots (e.g., preparedness for action) and clinical implications.

Extensive functional connectivity between brain areas implicated in mental imagery production and phobic fear during both emotional and neutral mental imagery.

Mental imagery is used by most people in their day-to-day cognition, for example, in planning, daydreaming, or remembering. Importantly, mental imagery has a powerful influence on emotion and is critically involved in many mental disorders. Thus, understanding the link between mental imagery and emotion is of clinical interest. For example, exposure therapy can be successfully conducted using mental imagery of fear-provoking stimuli, i.e., imaginal exposure. In this vein, accumulating evidence shows that mental imagery of a fearful stimulus produces a similar physiological and neural response as actual perception of the stimulus. Alas, knowledge of the neural processes underlying the link between mental imagery and emotion is limited. Functional magnetic resonance imaging data from a previous study on imaginal exposure (N = 30) was used to examine the functional connectivity during the production of phobic and neutral mental imagery. Regions of interest were selected from meta-analyses on brain regions consistently recruited during mental imagery production and phobic fear, respectively. Results showed that these regions were positively correlated during both phobic and neutral mental imagery production. Very few differences in functional connectivity between phobic and neutral imagery were found. Specifically, weaker functional connectivity between the supplemental motor area and a region including parts of the left insula and inferior frontal gyrus was observed during phobic (vs neutral) imagery. In conclusion, our findings suggest that brain regions previously implicated in mental imagery production and phobic fear are highly interconnected during the production of both phobic and neutral imagery.

Physiological and subjective arousal to prospective mental imagery: A mechanism for behavioral change?

Emotional prospective mental imagery, in which we simulate possible future events within our minds, have a pronounced impact on behavior. For example, repeated engagement in positive prospective imagery can lead to behavioral activation, while negative prospective imagery can lead to catastrophizing and avoidance. Physiological arousal boosts memory consolidation, creating emotional memories. Thus, if emotional prospective imagery produces an arousal response, the memory consolidation of these simulations of the future may be boosted, offering a possible underlying mechanism for the impact of emotional prospective imagery on behavior. In order to examine the feasibility of arousal as a possible mechanism behind the impact of emotional prospective imagery on behavior, sixty participants produced autobiographical prospective imagery of 30 scenes (10 positive, 10 neutral, and 10 negative), during which arousal responses (skin conductance) were measured, and ratings for subjective arousal, valence, and imagery vividness were collected. Moreover, because vividness of prospective imagery has been related to anxiety and depression, the study examined this relation also for event-related autobiographical prospective imagery. The results showed that emotional prospective imagery were associated with higher subjective arousal ratings as compared to neutral imagery. Physiological arousal responses showed a similar pattern, but further data is needed for a firm conclusion. Nevertheless, arousal-boosted consolidation remains a possible contributing mechanism for the impact of emotional prospective imagery on behavior. Moreover, results suggest both anxiety and depression may entail a reduced ability to invent prospective life situations. However, only anxiety was associated with less vivid imaginations, unless the imaginations were of negative content. Hence, anxious individuals may experience negative prospective imagery more vividly than imagery with neutral and positive content.

Imaginal extinction without imagery: Dissociating the effects of visual imagery and propositional thought by contrasting participants with aphantasia, simulated aphantasia, and controls.

Imaginal exposure is a standard procedure of cognitive behavioral therapy for the treatment of anxiety and panic disorders. It is often used when in vivo exposure is not possible, too stressful for patients, or would be too expensive. Peter Lang's Bio-Informational Theory implies that imaginal exposure is effective because of the perceptual proximity of mental imagery to real events, whereas empirical findings suggest that propositional thought of fear stimuli (i.e., thinking about the stimuli without seeing them in the mind's eye) could be sufficient in therapeutical contexts. Exposure to propositional thought, instead of vivid mental imagery, would be more tolerable for patients since vivid imagery is associated with high emotional distress. To investigate whether mental imagery or propositional thought is crucial for the success of imaginal exposure, participants with the rare state of aphantasia (= absence of sensory mental imagery but with intact propositional thought) and two control groups were subjected to a fear conditioning paradigm followed by imaginal exposure and a reinstatement procedure. During imaginal exposure, control group 1 (N = 30) stared at a bright screen to disrupt visual imagery by incoming luminance (= simulated aphantasia), whereas control group 2 (N = 30) and participants with actual aphantasia (N = 30) kept their eyes closed. The results show […].

Imaginal extinction and the vividness of mental imagery: Exploring the reduction of fear within the mind's eye.

Patients are encouraged to produce vivid mental imagery during imaginal exposure, as it is assumed to promote fear reduction. Nevertheless, the link between fear reduction and imagery vividness is unclear. We investigated the impact of vividness on fear responses using an experimental analogue of imaginal exposure - imaginal extinction - in which conditioned fear, measured with skin conductance, is reduced through exposure to mental imagery of the conditioned stimulus. We examined (1) if task-specific vividness (high vs low) of the conditioned stimulus during imaginal extinction moderated the reduction of fear responses, and (2) if task-specific vividness influenced remaining fear responses 24 h later. Findings suggest that high vividness may be advantageous for fear reduction during imaginal extinction, but it may not influence fear responses in the longer term. A possible clinical implication is that high imagery vividness during imaginal exposure may not be vital for overall treatment outcome. As high vividness is associated with increased levels of distress, a future direction would be to explore whether similar fear reduction can be obtained with less vivid imaginal exposure and thereby make treatment tolerable for more patients.

Exploring the neural basis of fear produced by mental imagery: imaginal exposure in individuals fearful of spiders.

Imaginal exposure, i.e. reducing fear using exposure to mental imagery, is a widely used psychological treatment technique for dysfunctional fears. Yet, little is known about its underlying neural mechanisms. The present study examines the neural basis of imaginal exposure using a novel experimental procedure consisting of repeated exposure to flashpoint mental imagery of phobic (spiders) and neutral (gloves) stimuli. Whether the 10 min long imaginal exposure procedure could reduce fear responses was examined one week later. Thirty participants fearful of spiders underwent the experimental procedure. Neural activity was assessed using functional magnetic resonance imaging (session 1). Subjective fear and skin conductance responses were measured throughout the study (sessions 1 and 2). Imaginal exposure evoked intense fear and heightened skin conductance responses, and indicated robust activation in several brain regions, including amygdala, midcingulate cortex and insula. Findings demonstrate that neural activity in fear-processing brain areas can be elicited solely by generating a mental image of a phobic stimulus, that is, in the absence of the percept. Relevant for treatment development, results reveal that a single 10 min session of brief exposures to flashpoint mental imagery can lead to lasting reductions in phobic fear at both the subjective and physiological levels. This article is part of the theme issue 'Offline perception: voluntary and spontaneous perceptual experiences without matching external stimulation'.

Decrease in amygdala activity during repeated exposure to spider images predicts avoidance behavior in spider fearful individuals.

Spider phobia is characterized by exaggerated fear of situations where spiders could be present, resulting in avoidance of such situations and compromised quality of life. An important component in psychological treatment of spider phobia is exposure to phobic situations that reduces avoidance behaviors. At the neural level, amygdala responses to phobic material are elevated, but normalizes following exposure treatment. To what extent amygdala activity decreases during a session of repeated phobic stimulation, and whether activity decrease is related to subsequent avoidance is not well studied. We hypothesized reduced amygdala activity during the course of repeated exposure to spider pictures, and that the degree of reduction would predict subsequent avoidance of spider pictures. To test our hypothesis, functional magnetic resonance imaging was performed in 45 individuals with spider fear during repeated exposure to spider pictures. Results showed that repeated exposure to spider stimuli attenuated amygdala reactivity and individual differences in activity reductions predicted subsequent avoidance behavior to spider pictures in an incentive-conflict task, with larger attenuations predicting less avoidance. At 6-month follow up, initial reductions in amygdala activation still predicted avoidance. This result demonstrates that reduction in amygdala responses is related to clinically meaningful outcomes in human anxiety, and suggests that within-session reductions in amygdala responses could be an important mechanism explaining the clinical effects of exposure therapy.

Detailed analysis of skin conductance responses during a gambling task: Decision, anticipation, and outcomes.

Physiological arousal is considered a key factor of gambling behavior. Hence, to understand gambling behavior it is important to study the arousal responses during gambling. Moreover, crucial mechanisms of action could be uncovered by detailing the situations that produce an arousal response. A gamble, or bet, can be partitioned into three distinct phases: (a) decision phase, during which the information concerning the gamble is presented, outcomes are appraised, and a decision is made on how to gamble; (b) anticipation phase, during which the result of the gamble is awaited; (c) outcome phase, during which the outcome of the gamble is presented. Previous research on arousal responses to gambling have mostly measured tonic changes in arousal, and when phasic responses have been measured, analyses have generally concentrated on one of the gamble phases. The aim of the present study was to map the arousal responses during gambling in more detail by measuring skin conductance responses (SCRs) during all three gamble phases of a simple card game. The anticipation phase was found to produce the largest arousal response, suggesting anticipation to be a major contributor to arousal during gambling behavior. Risk behavior during the gambling task was mirrored in self-reported risk taking in everyday life, and risk-takers displayed smaller SCRs compared to nonrisk-takers during decision making, suggesting this as a possible biomarker for risk-taking individuals.

Biological preparedness and resistance to extinction of skin conductance responses conditioned to fear relevant animal pictures: A systematic review.

Preparedness theory is one of the most influential ideas in explaining the origin of specific phobias. The theory proposes that fear conditioning is selective to animals that have posed a threat to survival throughout human evolution, and that acquired fear memories to such threats are resistant to extinction. We reviewed fear conditioning studies testing whether autonomic responses conditioned to pictures of snakes and spiders show greater resistance to extinction than neutral cues. We identified 32 fear conditioning experiments published in 23 studies including 1887 participants. Increased resistance to extinction of conditioned responses to snake and spider pictures was found in 10 (31%) of the experiments, whereas 22 (69%) experiments did not support the hypothesis. Thus, the body of evidence suggests that preparedness theory does not explain the origin of specific phobias.

Disruption of human fear reconsolidation using imaginal and in vivo extinction.

Memories are not set forever, but can be altered following reactivation, which renders memories malleable, before they are again stabilized through reconsolidation. Fear memories can be attenuated by using extinction during the malleable period. The present study adopts a novel form of extinction, using verbal instructions, in order to examine whether fear memory reconsolidation can be affected by an imaginal exposure. The extinction using verbal instructions, called imaginal extinction, consists of a recorded voice encouraging participants to imagine the scene in which fear was acquired, and to envision the stimuli before their inner eye. The voice signals stimuli appearance, and identical to standard (in vivo) extinction, participants discover that the conditioned stimulus no longer is followed by unconditioned stimulus (UCS). In this way, imaginal extinction translates clinically used imaginal exposure into the standard experimental fear conditioning paradigm. Fear was acquired by pairing pictorial stimuli with an electric shock UCS. Then, both standard and imaginal extinction were given following fear memory reactivation, either after 10min, within the reconsolidation interval, or after 6h, outside of the reconsolidation interval. In vivo and imaginal extinction produced comparable reductions in conditioned responses during extinction and importantly, both disrupted reconsolidation of conditioned fear and abolished stimulus discrimination between reinforced and non-reinforced cues. Thus, disrupted reconsolidation of fear conditioning can be achieved without in vivo stimulus presentation, through purely cognitive means, suggesting possible therapeutic applications.

Disentangling the effects of serotonin on risk perception: S-carriers of 5-HTTLPR are primarily concerned with the magnitude of the outcomes, not the uncertainty.

Serotonin signaling is vital for reward processing, and hence, also for decision-making. The serotonin transporter gene linked polymorphic region (5-HTTLPR) has been connected to decision making, suggesting that short-allele carriers (s) are more risk averse than long-allele homozygotes (ll). However, previous research has not identified if this occurs because s-carriers (i) are more sensitive to the uncertainty of the outcomes or (ii) are more sensitive to the magnitude of the outcomes. This issue was disentangled using a willingness-to-pay task, where the participants evaluated prospects involving certain gains, uncertain gains, and ambiguous gains. The results clearly favored the hypothesis that s-carriers react more to the magnitude of the outcomes. Self-reported measures of everyday risk-taking behavior also favored this hypothesis. We discuss how these results are in line with recent research on the serotonergic impact on reward processing. (PsycINFO Database Record

Think twice, it's all right: Long lasting effects of disrupted reconsolidation on brain and behavior in human long-term fear.

Memories can be modified when recalled. Experimental fear conditioning studies support that amygdala-localized fear memories are attenuated when reconsolidation is disrupted through extinction training immediately following memory activation. Recently, using functional brain imaging in individuals with lifelong spider fears, we demonstrated that fear memory activation followed by repeated exposure to feared cues after 10min, thereby disrupting reconsolidation, attenuated activity in the amygdala during later re-exposure, and also facilitated approach behavior to feared cues. In contrast, repeated exposure 6h after fear memory activation, allowing for reconsolidation, did not attenuate amygdala activity and resulted in less approach behavior as compared to the group that received disrupted reconsolidation. We here evaluated if these effects are stable after 6 months and found that amygdala activity was further reduced in both groups, with a tendency towards greater reductions in the 10min than the 6h group. Hence, disrupted reconsolidation results in long lasting attenuation of amygdala activity. The behavioral effect, with more approach towards previously feared cues, in the 10min than the 6h group also persisted. Thus, the brain effect of disrupted reconsolidation is stable over 6 months and the behavioral effect also remained. We therefore conclude that disrupted reconsolidation result in a long-lasting diminished fear memory representation in the amygdala which may have clinical importance.

Disrupting Reconsolidation Attenuates Long-Term Fear Memory in the Human Amygdala and Facilitates Approach Behavior.

Memories become labile and malleable to modification when recalled [1]. Fear-conditioning experiments in both rodents and humans indicate that amygdala-localized short-term fear memories can be attenuated by disruption of their reconsolidation with extinction training soon after memory activation [2-7]. However, this may not be true for natural long-term fears. Studies in rodents indicate that although it is possible to disrupt the reconsolidation of older memories [8-11], they appear to be more resistant [1, 3, 9, 12, 13]. In humans, 1-week-old conditioned fear memories have been attenuated by behaviorally induced disruption of reconsolidation [14], but it remains to be seen whether this is possible for naturally occurring long-term fears and whether the underlying neural mechanisms are similar to those found in experimental fear-conditioning paradigms. Using functional brain imaging in individuals with a lifelong fear of spiders, we show that fear memory activation followed by repeated exposure to feared cues after 10 min, which disrupts reconsolidation, attenuates activity in the basolateral amygdala at re-exposure 24 hr later. In contrast, repeated exposure 6 hr after fear memory activation, which allows for reconsolidation, did not attenuate amygdala activity. Disrupted, but not undisrupted, reconsolidation facilitated approach behavior to feared cues, and approach behavior was inversely related to amygdala activity during re-exposure. We conclude that memory activation immediately preceding exposure attenuates the neural and behavioral expression of decades-old fear memories and that, similar to experimentally induced fear memories, the basolateral amygdala is crucially involved in this process.

Disruption of Memory Reconsolidation Erases a Fear Memory Trace in the Human Amygdala: An 18-Month Follow-Up.

Fear memories can be attenuated by reactivation followed by disrupted reconsolidation. Using functional magnetic resonance imaging we recently showed that reactivation and reconsolidation of a conditioned fear memory trace in the basolateral amygdala predicts subsequent fear expression over two days, while reactivation followed by disrupted reconsolidation abolishes the memory trace and suppresses fear. In this follow-up study we demonstrate that the behavioral effect persists over 18 months reflected in superior reacquisition after undisrupted, as compared to disrupted reconsolidation, and that neural activity in the basolateral amygdala representing the initial fear memory predicts return of fear. We conclude that disrupting reconsolidation have long lasting behavioral effects and may permanently erase the fear component of an amygdala-dependent memory.

Human reconsolidation: a reactivation and update.

The reconsolidation hypothesis states that memories, when reactivated, enter a transient, labile state followed by a re-stabilization termed reconsolidation. By affecting the reconsolidation process, memory persistence can be influenced, leading to memory enhancement or decrement. This is a time-dependent process and the result of modulating reconsolidation is present only after the reconsolidation process is completed. Historically, reconsolidation research has been performed on non-human animals, since the methods originally used for reconsolidation disruption are not safe. However, there now exist several techniques safe for humans, and consequently, in recent years, papers on human reconsolidation have emerged. Here, the existing literature on human reconsolidation is reviewed and discussed, including studies on fear memories, appetitive memories, procedural memories, and declarative memories. Methods of memory reactivation are compared between studies, and the consistency and lack of consistency in results over reactivation methods and memory types are discussed. These results provide future challenges, both experimental and clinical, in defining the boundary conditions and mechanisms governing the reconsolidation phenomenon. This article is part of a Special Issue entitled 'Memory Enhancement'.

Enlargement of visual processing regions in social anxiety disorder is related to symptom severity.

Social anxiety disorder (SAD) is associated with altered brain function and structure, but most structural studies include small samples and findings are mixed. This study compared regional gray matter volume between 48 SAD patients and 29 healthy controls (HC) as well as the relationship between volume and symptom severity. Structural magnetic resonance images from SAD patients and HC were evaluated using standard voxel-based morphometry (VBM) processing in the SPM8 software package. Social anxiety symptom severity was rated in SAD patients by a clinician using the Liebowitz Social Anxiety Scale (LSAS). SAD patients had greater regional gray matter volume in the lingual gyrus and lateral occipital cortex than the controls, and within the SAD group a positive correlation was found between symptom severity and regional gray matter volume in the lingual gyrus and the retrosplenial cortex. These findings replicate and extend earlier reports of enlarged visual processing areas in SAD. Increased gray matter volume in regions involved in visual processing and self-consciousness could underlie, or be the result of, abnormal emotional information processing and self-focused attention previously demonstrated in patients with SAD.

Disruption of reconsolidation erases a fear memory trace in the human amygdala.

Memories become labile when recalled. In humans and rodents alike, reactivated fear memories can be attenuated by disrupting reconsolidation with extinction training. Using functional brain imaging, we found that, after a conditioned fear memory was formed, reactivation and reconsolidation left a memory trace in the basolateral amygdala that predicted subsequent fear expression and was tightly coupled to activity in the fear circuit of the brain. In contrast, reactivation followed by disrupted reconsolidation suppressed fear, abolished the memory trace, and attenuated fear-circuit connectivity. Thus, as previously demonstrated in rodents, fear memory suppression resulting from behavioral disruption of reconsolidation is amygdala-dependent also in humans, which supports an evolutionarily conserved memory-update mechanism.