Grey matter density changes of structures involved in Posttraumatic Stress Disorder (PTSD) after recovery following Eye Movement Desensitization and Reprocessing (EMDR) therapy

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Neuroticism Modifies Psychophysiological Responses to Fearful Films

Background: Neuroticism is a personality component frequently found in anxious and depressive psychiatric disorders. The influence of neuroticism on negative emotions could be due to its action on stimuli related to fear and sadness, but this remains debated. Our goal was thus to better understand the impact of neuroticism through verbal and physiological assessment in response to stimuli inducing fear and sadness as compared to another negative emotion (disgust).¦Methods: Fifteen low neurotic and 18 high neurotic subjects were assessed on an emotional attending task by using film excerpts inducing fear, disgust, and sadness. We recorded skin conductance response (SCR) and corrugator muscle activity (frowning) as indices of emotional expression.¦Results: SCR was larger in high neurotic subjects than in low neurotics for fear relative to sadness and disgust. Moreover, corrugator activity and SCR were larger in high than in low neurotic subjects when fear was induced.¦Conclusion: After decades of evidence that individuals higher in neuroticism experience more intense emotional reactions to even minor stressors, our results indicate that they show greater SCR and expressive reactivity specifically to stimuli evoking fear rather than to those inducing sadness or disgust. Fear processing seems mainly under the influence of neuroticism. This modulation of autonomic activity by neurotics in response to threat/fear may explain their increased vulnerability to anxious psychopathologies such as PTSD (post traumatic stress disorder)

MOSAIC: A New Pain-Free Psychotherapy for Psychological Trauma

International audienceEye movements and alternating stimuli for brain integration (MOSAIC) is a promising but untested new therapy. Its four-step protocol is based on the effects of bilateral alternating stimulation (BAS) (as in eye movement desensitization and reprocessing therapy) on the brain. This solution-oriented therapy promotes experiencing solutions through bodily sensations. Through BAS and bodily sensations, MOSAIC therapy aims to enrich the traumatic memory neuronal network with new information so that the client's psychological trauma is no longer distressing. Thus, MOSAIC can be used to treat psychological trauma without the pain associated with reliving the traumatic situation. This method may be particularly adaptive for patients who have experienced complex trauma and who have dissociative experiences

Mécanismes périphériques et centraux impliqués dans le stress post-traumatique & son traitement

Bien que la plupart des personnes soient exposées à un traumatisme au cours de leur vie, toutes ne développent pas de stress-post traumatique (PTSD). La prévalence de vie du PTSD est en effet estimée à 10%. Il peut survenir à la suite d un événement traumatique tel un accident, agression, deuil, viol ou incendie, mais aussi un désastre naturel (inondation, tremblement de terre ) ou humain (guerre, terrorisme ). En raison de l augmentation contemporaine des sources traumatiques, les rapports récents de l'Organisation Mondiale de la Santé décrivent le PTSD comme un problème de santé mondiale croissant, en raison de sa fréquence, sévérité, comorbidité et de son coût élevé. Un corpus de recherche enquête sur divers aspects du PTSD concernés par les pensées intrusives, l'hypervigilance, les déficits émotionnels, les troubles cognitifs et les problèmes de mémoire.Comme d'autres problèmes de santé mentale, le PTSD est à ce jour assez méconnu. Comme d'autres troubles anxieux, il est surtout marqué par une peur excessive. Il n'est donc pas surprenant que l'hypothèse la plus répandue dans le PTSD soit celle d'un déficit du traitement de la peur. S il est vrai que la conceptualisation du PTSD comme un trouble de la peur parait phénoménologiquement étroite, elle a été néanmoins pragmatique en permettant l approfondissement de la recherche translationnelle de l'animal à l humain, en passant par la paillasse. Les études sur le sujet ont suggéré que les déficiences centrales et périphériques du PTSD tourneraient autour d altérations du réseau neuronal de la peur. Ceci impliquerait un dérèglement des mécanismes qui sous-tendent le conditionnement à la peur, ainsi que le traitement des émotions et de l'attention, qui sont en effet bouleversés dans le PTSD.Although most people encounter at least one traumatic event over their lifetime, not all of them will develop post-traumatic stress disorder (PTSD). Lifetime prevalence of full-blown PTSD, known as an anxiety disorder, is in fact around 10%. In addition to accidents, aggression, grief, rape, fires, traumatic events can be caused by natural (flooding, earthquake ) or man-made stressors (war, terrorism ). With the contemporary rise in traumatic sources the World Health Organization recent reports describe PTSD as an increasing global health issue, due to its high frequency, severity, comorbidity and cost. A body of research has thus started investigating various aspects of PTSD concerned with intrusive thoughts, hypervigilance, emotional deficits, cognitive disturbances and memory issues. Similarly to other mental health problems, much remains unknown about PTSD, and similarly to other anxiety disorders it is marked by excessive fear. It comes as no surprise that the most prevalent hypothesis in PTSD is that of a fear-processing deficit. Conceptualizing PTSD as a fear disorder can be phenomenologically quite narrow. It has been nonetheless pragmatic in allowing thorough translational research from animal to bench-side and clinical studies. Most studies have suggested that central and peripheral impairments in PTSD revolve around altered neural fear processing network. These alterations involve mechanisms implicated in fear conditioning, as well as emotional and attentional processing, all of which are altered in PTSD.AIX-MARSEILLE2-Bib.electronique (130559901) / SudocSudocFranceF

EMDR Therapy Mechanisms Explained by the Theory of Neural Cognition

International audienceEye Movement Desensitization and Reprocessing (EMDR) is a therapy of choice for post-traumatic stress disorder (PTSD). The mechanism of EMDR therapy is still unknown but it is hypothesized to favor memory reconsolidation. A new learning occurs relieved from the emotional load. Based on the Theory of neural Cognition (TnC), we propose an explanation of this phenomenon that implicates hebbian synaptic plasticity, i.e., long-term potentiation (LTP) and long-term depression (LTD). The new learning is mediated by the bilateral alternating stimulations (BAS) that are essential to the EMDR therapy. These repeated BAS modify the neural traces of a traumatic memory through the incorporation of newly activated cortical columns. These activated columns form a sparse coding representation of the situation called the global state of activation (GSA). Some of these added cortical activities will eventually crystallize in a column’s activation that is able to join the current GSA, making a new GSA, i.e., a stable network of activity. This process (trauma recall and BAS) is repeated several times, and each time, the activity of new columns is being added to the current GSA, until a GSAn totally cleared of its emotional content is obtained. Each GSA is a stable network of activity which gets reinforced thanks to LTP. Each time, a lessened traumatic memory is experienced. These modifications end up with a shift from the amygdalae’s involvement in the traumatic memory towards a more cognitive representation of the traumatic event, exempt from the previously associated strong negative feeling

Cracking the EMDR code: Recruitment of sensory, memory and emotional networks during bilateral alternating auditory stimulation

International audienceIntroduction: The inability to extinguish a conditioned fear is thought to be at the core of post-traumatic stress disorder. Eye movement desensitization and reprocessing therapy has been efficacious for post-traumatic stress disorder, but the brain mechanisms underlying the effect are still unknown. The core effect of eye movement desensitization and reprocessing therapy seems to rely on the simultaneous association of bilateral alternating stimulation and the recall of the traumatic memory. To shed light on how eye movement desensitization and reprocessing therapy functions, we aimed to highlight the structures activated by bilateral alternating stimulation during fear extinction and its recall. Methods: We included 38 healthy participants in this study. Participants were examined twice in functional magnetic resonance imaging, over 2 consecutive days. On the first day, they performed two fear conditioning and extinction procedures, one with and one without the bilateral alternating stimulation during the fear extinction learning phase in a counterbalanced order across the participants. On the second day, participants completed the fear extinction recall procedure, in the same order as the previous day. Statistical significance of maps was set at p < 0.05 after correction for family-wise error at the cluster level. Results: The analysis revealed significant activation with versus without bilateral alternating stimulation at the early extinction in the bilateral auditory areas, the right precuneus, and the left medial frontal gyrus. The same pattern was found in the early recall on the second day. The connectivity analysis found a significant increase in connectivity during bilateral alternating stimulation versus without bilateral alternating stimulation in the early extinction and recall between the two superior temporal gyri, the precuneus, the middle frontal gyrus and a set of structures involved in multisensory integration, executive control, emotional processing, salience and memory. Conclusion: We show for the first time that in the eye movement desensitization and reprocessing therapy the bilateral alternating stimulation is not a simple sensory signal and can activate large emotional neural networks

Bilateral Alternating Auditory Stimulations Facilitate Fear Extinction and Retrieval

International audienceDisruption of fear conditioning, its extinction and its retrieval are at the core of posttraumatic stress disorder (PTSD). Such deficits, especially fear extinction delay, disappear after alternating bilateral stimulations (BLS) during eye movement desensitization and reprocessing (EMDR) therapy. An animal model of fear recovery, based on auditory cued fear conditioning and extinction learning, recently showed that BLS facilitate fear extinction and fear extinction retrieval. Our goal was to determine if these previous results found in animals can be reproduced in humans. Twenty-two healthy participants took part in a classical fear conditioning, extinction, and extinction recall paradigm. Behavioral responses (fear expectations) as well as psychophysiological measures (skin conductance responses, SCRs) were recorded. The results showed a significant fear expectation decrease during fear extinction with BLS. Additionally, SCR for fear extinction retrieval were significantly lower with BLS. Our results demonstrate the importance of BLS to reduce negative emotions, and provide a successful model to further explore the neural mechanisms underlying the sole BLS effect in the EMDR

A case-control study of skin conductance biofeedback on seizure frequency and emotion regulation in drug-resistant temporal lobe epilepsy

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Increased perception of loudness in autism

Abstract Clinical reports on autism describe abnormal responses to auditory stimuli such as intolerance to sounds. The present study assessed subjective perception of loudness in subjects with autism compared to healthy controls, using two psychoacoustic tests. First, the auditory dynamic range was evaluated at six different tone frequencies. Secondly, loudness growth as a function of the intensity level of a 1 kHz tone was estimated. Verbal responses from a group of 11 children and adolescents with autism were compared to responses of 11 age-and gender-matched healthy controls. Smaller auditory dynamic ranges were found in the autistic group than in the control group, as well as increased perception of loudness, indicating hyperacusis in subjects with autism