[Posttraumatic stress disorder (PTSD) as a consequence of the interaction between an individual genetic susceptibility, a traumatogenic event and a social context].
Why are some individuals more likely than others to develop a posttraumatic stress disorder (PTSD) in the face of similar levels of trauma exposure? Monitoring the traumatic process combining the antecedents, the determinants of the psychic trauma and the acute symptoms can clarify the causes of the final onset of a chronic repetition syndrome. Epidemiologic research has clarified risk factors that increase the likelihood of PTSD after exposure to a potentially traumatic event. PTSD is an interaction between a subject, a traumatogenic factor and a social context. With each epidemiological, psychopathological and more particularly neurogenetic study, we will expand on the impact of these interactions on the therapeutic treatment of psycho-traumatised persons.
Most studies have shown that unrelated to the traumatic event, additional risk factors for developing PTSD include younger age at the time of the trauma, female gender, lower social economic statuts, lack of social support, premorbid personality characteristics and preexisting anxiety or depressive disorders increase the risk of PTSD. The psychic trauma is firmly attached to the repetition and the previous traumas are as many risks of developing a subsequent PTSD in the wake of a new trauma: PTSD in adults may represent a prolonged symptomatic reaction to prior traumatic assault, child abuse and childhood adversities. Related to the traumatic event, the organic pain, the traumatic brain injury, but also the sight of blood can lead to a trauma being considered as more serious or more harmful to life. It is useful to recognize the acute reactions of exhaustion stress as they can guide both the pharmacotherapeutic and the psychotherapeutic treatment thanks to debriefings. Even though the majority of people with acute stress disorder subsequently develop PTSD, the current data indicate that too many people can develop PTSD without initially displaying acute stress disorder. Though peritraumatic dissociation and peritraumatic distress have emerged as the strongest predictors for PTSD and have to be treated as soon as possible with the debriefing or the pharmacology; initial evidence suggests the potential benefits of early intervention, shortly after the trauma, and psychological debriefing has received increasing interest from the scientific community. However the Anglo-Saxon techniques (such as Critical Incident Stress Debriefing also known as the Mitchell model) are in total contrast with the French approach. In the first case the emotional response is controlled to ensure the pursuit of the group action, whilst in the second case the debriefing concerns patients with acute symptoms in order to prevent the development of a PTSD structuring of the latter. The facts, emotions and thoughts are not partitioned but inter-linked, thus enabling a fragmentation of the traumatic experience. In the face of the annihilation experienced, speech production by the subject is restored linking the person to the human community, once abandoned. However, debate continues on the efficacy of single session debriefing in the prevention of PTSD. At the time of the acute stress reactions, benzodiazepines are contraindicated at this stage as they promote dissociation and ulterior revivals. On the other hand, treatment with propranolol could be proposed: a two or three week course of propranolol begun in the aftermath of a traumatic event can reduce subsequent PTSD symptoms.
A genetic polymorphism is evidently at work in the development of a PTSD via the regulation of the expression of genes of interest to the serotoninergic system and the adrenocorticotropic axis. The 5-HTTLPR (promoter region of SLC6A4 witch encodes the serotonin transporter) constitutes a genetic candidate region that may modulate emotional responses to traumatic events. The interaction between variation at the 5HTTLPR and stressful life events could predict depression and PTSD. Considering the dopaminergic pathway, the A1 allele coding the type 2 dopaminergic receptor is associated with a severe comorbidity of PTSD with the presence of somatic disorders, anxiety, social change and depression. For noradrenergic neuromodulation, an interaction between the polymorphism of gene GABRA2 and the occurrence of PTSD is described whereas an interaction between the number of traumatic events and Val(158)Met polymorphism of the gene coding for catecholamine-o-methyltransferase has also been found. The role of polymorphisms in FKBP5 (a co-chaperone of hsp 90 which binds to the glucocorticoid receptor) in predicting PTSD too, with a gene-by-environment point of view. These gene-by-environment studies are needed to focus more on distinct endophenotypes and influences from environmental factors. If several candidate genes are involved, a weighting of susceptibility to such and such a neurological regulation system will imply various endophenotypes. According to the monoamine predominantly incriminated, PTSD can take on a more hyper-vegetative clinical expression linked with noradrenergic overuse. Differently, avoidance behaviour and the depressive aspect invoke more a modification of the serotoninergic modulation whilst posttraumatic psychotic reactions question the role of dopaminergic pathways. Neuroscientific discoveries interesting the biological support of PTSD can thus modify our view of the conception of the disorder in relation to different therapeutic prospects.
Chronic PTSD can manifest itself in different clinical forms. The repetition syndrome can appear a long time after the traumatic event, following a paucisymptomatic latency period, which can last several years or even decades. The absence of complaints from the patient is common, the latter suffering in silence. Often other comorbid disorders and other complaints arise sooner than the clinical picture. Thus a depressive episode characterised as drug-seeking behaviour is frequently encountered. The therapeutic accompaniment traditionally combines a pharmacological and a psychotherapeutic treatment even if recommendations are rare. A posttraumatic stress disorder is never just a coincidence. The different stages of the evolution and the establishment of a PTSD are the expression of an interaction between the outside and the inner self. Despite a known progression of the posttraumatic stress disorder, this deleterious evolution is far from being a foregone conclusion. On the contrary, several levels of prevention are possible at each stage of its structuration to propose treatments to subjects who are vulnerable and/or present symptoms. No neurobiological study has yet found a biological marker, which would apparently and inevitably destine a subject to structure, a posttraumatic stress disorder in reaction to a stress. Conversely, the psychopathological study finds afterwards that a particular subject has necessarily built a traumatic repetition syndrome according to the concordance of significant data relative to his/her history. The event strikes a repression or an anterior biographical deadlock and of which the thematic questions the fundamentals of human culture in its emancipation with nature, like the question of death and its consequences: bereavement, parentality, transgenerational transmission and organicity often linked to the illness. A therapeutic proposal constitutes an environmental factor par excellence which can be either protective or deleterious. If the traumatic repetition syndrome has been known since Antiquity, the birth of PTSD has followed the chronology of the DSM according to the sociopolitical contexts encountered. A PTSD does not occur by chance: the conditions of possibility of the trauma are established by genetic and psychological determinants interactively integrated at the heart of a social context. After the increase in a psychotraumatic interest in international publications since the 1980s, a fight against over-victimisation seems to be setting in. The advances in genetic and neuroimaging techniques are in the process of superseding psychometric studies in terms of reliability and validity; maybe we should see in this social evolution the changes of tomorrow concerning the clinical of PTSD and its treatment. The healing of the psycho-traumatised subject cannot just be established on the passive status of victim, which would be detrimental to reflection and ultimately reconstruction: the rebirth of the subject will require active commitment, which could distract from the deadly repetition. Whilst the confrontation with death resembled nonsense, the subject will question the psychotraumatic determinants of his/her life history to reinstate this tragic event within a search for meaning. Such restructuring is built on the intersubjectivity of the clinical relationship, which occurs within a social context. PTSD is a pathology which interacts with the societal context: on the one hand the trauma is established on the brutal reconsideration of social values which seem immutable and on the other hand, the clinical and nosographical concept of PTSD is changing with the evolution of society.
Auxéméry Y
《ENCEPHALE-REVUE DE PSYCHIATRIE CLINIQUE BIOLOGIQUE ET THERAPEUTIQUE》
[The Gulf War Syndrome twenty years on].
After Operation Desert Storm which took place in Iraq from August 1990 to July 1991 involving a coalition of 35 countries and a 700,000 strong contingent of mainly American men, some associations of war veterans, the media and researchers described a new diagnostic entity: the Gulf War Syndrome (GWS).
GWS seems to be a new disorder which associates a litany of functional symptoms integrating the musculoskeletal, digestive, tegumentary and neurosensory systems. The symptoms presented do not allow a syndrome already known to be considered and the aetiology of the clinical picture remains unexplained, an increasing cause for concern resulting from the extent of the phenomenon and its media coverage. It quickly appears that there is no consensus amongst the scientific community concerning a nosographic description of GWS: where can all these functional complaints arise from? Different aetiopathogenic hypotheses have been studied by the American administration who is attempting to incriminate exposure to multiple risks such as vaccines and their adjuvants, organophosphorous compounds, pyridostigmine (given to the troops for the preventive treatment of the former), impoverished uranium, and the toxic emanations from oil well fires. But despite extremely in-depth scientific investigations, 10 years after the end of the war, no objective marker of physical suffering has been retained to account for the disorders presented. It would appear that the former soldiers are in even better objective health than the civil population whereas their subjective level of health remains low. Within this symptomatic population, some authors have begun to notice that the psychological disorders appear and persist associating: asthenia, fatigability, mood decline, sleep disorders, cognitive disorders and post-traumatic stress disorder (PTSD). Within the nosological framework, does GWS cause functional disorders or somatisation? Finally, 20 years after the end of the fighting, only PTSD has been causally attributed to military deployment.
Certain functional symptoms of GWS occur during the latent phase of a future reexperiencing syndrome, latent phase which is the locus of nonspecific symptoms. The psychotraumatised subject does not express himself spontaneously and waits to be invited to do so: if the social context does not allow this expression, the suffering can remain lodged in a few parts of the body. How can the inexpressible part of the trauma be recounted, particularly if the social context does not allow it? For civil society, calling into question "the somatic word" of veterans is difficult: why were they sent to face these hardships? What could we learn from these soldiers we do not wish to listen to: the horror of the war, the aggressive impulse of men, and the confrontation with death? Another obstacle to this reflection is the reference to stress as a prevalent aetiopathogenic model of the psychological trauma. A model like this, considering that PTSD is a normal reaction to an abnormal situation, finally discredits the subject and society and disempowers them by freezing them in a passive status of victim.
However, as GWS affects approximately a quarter of subjects deployed, it is not very likely that all these symptoms are caused by a psychotraumatic reaction. Many veterans suffering from GWS have themselves rejected the diagnosis of PTSD, arguing that they do not suffer repetition nightmares. What the veterans rightly tell us here is that the notions of stress and trauma cannot strictly be superimposed. A subject may have been intensely stressed without ever establishing traumatic flashbacks and likewise; a psychological trauma can be experienced without stress and without fear but in a moment of terror. This clarification is in line with the first criterion of the DSM-IV-TR which necessarily integrates the objective and subjective dimensions as determinants of PTSD. Yet, scientific studies relating to GWS are struggling to establish opposition or continuity links between the objective external exposure (smoke from petrol wells, impoverished uranium, biological agents, chemicals) and the share of inner emotion albeit reactive and characterised by a subjective stress. There were no lack of stress factors for the troops deployed: repeated alerts of chemical attacks, hostility of the environment with its sandstorms and venomous animals, climatic conditions making long hours of backup and static observation difficult, collecting bodies, lack of knowledge of the precise geography of their movements and uncertainty of the duration of the conflict. The military anti-nuclear-bacteriological-chemical uniform admittedly provided protective confinement, shutting out the hostile world from which the threat would come but, at the same time, this isolation increases the fear of a hypothetical risk whilst the internal perceptions are increased and can open the way to future somatisations. In a context like this, the somatic manifestations of anxiety (palpitations, sweating, paresthesia…) are willingly associated with somatised functional disorders to which can also be assigned over-interpretations of bodily feelings according to a hypochondriacal mechanism. The selective attention to somatic perceptions in the absence of mentalisations, the request for reassurance reiterated and the excessive use of the treatment system will be diagnostic indices of these symptoms caused by the stress. Rather than toxic exposure to such and such a substance, the non-specific syndrome called "Gulf War Syndrome" is the result of exposure to the eponymous operational theatre. But if the psychological and psychosomatic suffering occurring in veterans is immutable throughout history, the expression of these difficulties has specificities according to the past cultural, political and scientific context. In the example of GWS, the diffusion of the fear of a pathology resulting from chemical weapons has promoted this phenomenon. In the end, biochemical and biological weapons have not been used on a large scale but the mediatisation of this possibility has led to a deleterious… To spare the bother of a group psychological reflection, the scientific and political authorities chose to investigate the implication of environmental factors in the genesis of the disorder. At individual as well as social level, rather than accept a psychogenic origin, a common defence mechanism is to assign the suffering to an external cause. With the perspective of preventing the risk of diffusion of other unexplained syndromes, which could occur following future armed conflicts, new epidemiological diagnostic models must be defined. The media also has considerable responsibility for the diffusion of epidemic psychological reactions but at the same time, they can inform the population about certain individual or group psychopathological mechanisms.
The GWS exists: it is not an "imaginary illness" but a serious public health issue which has led to tens of thousands of complaints and swallowed up millions of dollars. To reply to human suffering, a new nosographic entity can spread through society taking the epidemic expression of a somatised disorder via identification, imitation and suggestion mechanisms. This possibility questions not only mental health but also the sociology and politics. It is necessary to inform the leaders and the general population of the possibility of this type of mass reaction, which can take the shape of a highly contagious complex functional syndrome.
Auxéméry Y
《ENCEPHALE-REVUE DE PSYCHIATRIE CLINIQUE BIOLOGIQUE ET THERAPEUTIQUE》
[Clinical forms of post-traumatic depression].
As a result of determinants specific to the psychopathological structure of the psychological trauma, psycho-traumatised patients very rarely solicit the health care system directly with a request for treatment centred on their trauma. The medical profession is consulted for non-specific symptoms and complications, which are mainly somatoform, addictions and depressive disorders. After a few epidemiological reminders followed by a discussion concerning contemporary depressive and post-traumatic nosographic features, we define, through our clinical experience collated with the data in the literature, different clinical and etiopathogenic contexts of post-traumatic depression in order to control their therapeutic treatment.
Burnout post-traumatic depression in response to re-experiencing is the most common: it is a reactive psycho-physiological burnout in response to the emotional distress re-experienced during flashbacks, insomnia, a constant feeling of insecurity and the deleterious consequences of this symptomatology in terms of social adaptation. A common genetic predisposition affecting serotoninergic regulation seems to be a vulnerability marker of both depressive and psychotraumatic symptoms. In this case, SSRI will be effective on sadness. In addition, these antidepressants have been widely prescribed for the first-line treatment of depressive and psychotraumatic symptoms. However, this pharmacological class is often insufficient in relieving autonomic hyperactivity such as re-experiencing which are mediated more by noradrenergic hyperactivity. SNRI such as venlafaxine can be used as a first-line treatment. Post-traumatic depression with psychotic features congruent with mood is dominated by a feeling of incurability; the subject blames himself and feels guilty about the traumatic event and its consequences. Symptoms of denial of identity are sometimes observed: confined by an intense depersonalization, the psycho-traumatised subject evokes that he is "no longer himself" and that his mind "is disconnected". Confronted with the psychological emptiness of the traumatic scene, the psycho-traumatised subject remains devoid of thought as if their mind has left him. In addition to antidepressant therapy, an atypical antipsychotic drug must be prescribed to relieve the melancholic symptoms as well as the concomitant psychotraumatic symptoms. Post-traumatic depression masked by peripheral physical injuries is the result of accidents combining psychological and physical impairment. The physical pain resulting from the accident regularly recalls the drama in the same way as traumatic re-experiencing. Depression masked by this somatic suffering is difficult to diagnose, but the repeated somatic complaints at the forefront of the request for treatment, the breakdown of self-esteem as well as the level of subjective strain due to pain and dysesthesia are all indications. The psychotherapy will focus on the symbolic reconstruction of the organs that have been damaged or destroyed, with the aim of healing the extensive narcissistic impairment. Post-concussive depression is diagnosed following a head trauma, however severe. It is sometimes assigned to neurological lesions and at other times recognised as the expression of a purely psychological reaction. Antidepressant therapy, or possibly trial therapy, is often indicated. The terms traumatic grief and post-traumatic grief are often used synonymously in publications: a conceptual opposition must however been recalled. If the traumatic grief is the result of the loss of an object that holds much psychological importance for the individual, the subject has not however been traumatised by this event and is not suffering and will not suffer from re-experiencing. The therapy will include methods used in the psychotherapeutic treatment of grief; antidepressants are often insufficient. Differently, post-traumatic grief takes shape when the loss of another is concomitant with the confrontation with the reality of the death witnessed in a moment of peri-traumatic dissociation. This grief is often observed following the discovery of the body of a close friend or family member who has committed suicide, or when part of a family has been decimated by an accident whilst the survivors watch their close relations die pending the arrival of the emergency services, or when a military comrade is wounded in combat in front of his partner. The mourning process cannot really begin until the flashbacks cease.
Clinical depression or even melancholia, possibly masked by somatic or post-concussive complaints, is often the initial mode of contact with the health care system for the psycho-traumatised subject. The different clinical and etiopathogenic contexts of post-traumatic depression that we have developed in this work use specific therapies which need to be clarified by further research based on this nosography.
Auxéméry Y
《ENCEPHALE-REVUE DE PSYCHIATRIE CLINIQUE BIOLOGIQUE ET THERAPEUTIQUE》
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