[Study of agency in the discourse of women suffering from post-traumatic stress disorder in the aftermath of domestic violence]. / Étude de l'agentivité dans le discours de femmes souffrant de trouble de stress post-traumatique dans les suites de violences conjugales.

INTRODUCTION: In the absence of appropriate care, psychotraumatic consequences (revival, hyperarousal, avoidance strategies, dissociation and other clinical forms of post traumatic symptoms) can take control of a large part of the subject's existence (psychological, physical, social) and affect the ability of the victim to regain ground on the intrusions that harass, and to take up new life projects. More objective than the current semiological and psychometric approaches, and in the absence of biomarkers that may be used in clinical practice, psycholinguistics opens up an epistemological renewal of the conception of trauma and its clinical consequences, in particular through the definition of the Psycho Linguistic Traumatic Syndrome (SPLIT). If such conceptions have been developed based on the analysis of traumatic accounts of subjects injured in war and attacks, other forms of psychotraumatic confrontations also deserve to be considered. In this paper, our objective was to better characterize the pronominal forms of agency in the traumatic and non-traumatic narratives produced by women victims of domestic and/or sexual violence. METHODS: Nineteen women aged 20 to 60 victims of domestic violence and diagnosed with post-traumatic stress disorder (Mini International Neuropsychiatric Interview) as well as a matched control group participated in the study. The subjects completed the French versions of Post Traumatic Checklist (PCL-5), Dissociative Experience Scale (DES) and Hospital and Anxiety Depression Scale (HAD). Traumatic and non-traumatic narratives were linguistically coded and scored on the SPLIT-10 scale. RESULTS: Traumatic narratives contained significantly more first person singular pronouns than the non-traumatic narratives of controls or the non-traumatic narratives of psychically injured people. Traumatic narratives contained significantly more of the direct object pronoun "me" as well as indirect object pronouns. In traumatic narratives, the frequency of use of the subject pronoun "I" tended to correlate negatively with the HAD-A, HAD-D and SPLIT-10, while the frequency of use of the direct object pronoun "me" tended to correlate positively with DES, HAD-A, HAD-D as well as SPLIT-10. Finally, traumatic narratives contained significantly more verbs in the passive voice than non-traumatic narratives. DISCUSSION: There was a gradient in the use of the first person singular pronoun that was inversely correlated to the degree of traumatic valence of the narratives: the control group used "I" less often than the psychically injured people who appeared to use this pronoun all the more as their narratives had a traumatic valence. In other words, even in the so-called "non-traumatic" narratives produced by subjects suffering from post-traumatic stress disorder, the trauma seemed to be inscribed in the discourse, testimony to dissociation, as the seen in the correlation of this pronominal expression dimension of "I" with the SPLIT-10 scale. The use of the direct object complement was correlated with greater psycho-traumatic morbidity (dissociative, depressive and anxious) than the use of the "I", the latter remaining however a pathological mark instead of the use of the pronouns "we" or "one". Saying "I" translated less symptomatology than saying "me", but it was when the subject said "we" or "one" that he appeared to have returned to a normal discourse, no longer suffering from the torments of reliving or pathological dissociation. The identification of linguistic markers deserves to be pursued in order to better objectively describe post-traumatic psychiatric disorders, to better identify them in clinical practice in the field and to monitor the efficiency of the recommended psychotherapies. More generally, we may put forward the hypothesis that the direct modification of the patient's language, thanks to the intervention of the practitioner, from a speech composed of linguistic markers testifying to the trauma towards a normalized speech could help to treat post-traumatic symptoms.

Post-concussion syndrome: Still forgotten? From the disappearance of the DSM-5 to a multidisciplinary consultation.

OBJECTIVES: Following the presence of both post-traumatic stress disorder (PTSD) and post-concussion syndrome (PCS) in the nosography since the publication of DSM-IV, large-scale studies investigated the links between these two entities: exposure to a mild traumatic brain injury was correlated with the presence of PTSD and vice versa, and the strongest factor associated with PCS was the presence of PTSD. But PCS entity was recently suppressed from the 5th edition of the American diagnostic and statistical classification of neuropsychiatric disorders (DSM-5, 2013). In the 11th edition of the CIM, PCS is also likely to be omitted. This elimination raises more questions if we take into consideration the emancipation of PTSD, which now includes the full category of "disorders related to trauma and stressors" to which PCS could have legitimately been added. METHODS: We discuss current scientific literature and clinical practices with a socio-anthropological point of view. RESULTS: Post-concussion and post-traumatic clinical entities often show similar anamnestic temporalities, with an initial acute phase where memory (amnesia following TBI; dissociative post-traumatic amnesia) and consciousness (initial loss of consciousness secondary to TBI; peri-traumatic psychic dissociation) impairments predominate, followed by a pauci-symptomatic latency phase. Finally, a symptomatic phase occurs in which similar symptoms for both entities are observed (sleep disorders, anxiety and depression, irritability, fatigue, attention disorder, tendency to avoidance). If similar therapies (pharmacological and psychological) are effective in treating the clinical consequences of head and mental trauma, this suggests that they have common etiopathogenic origins. CONCLUSIONS: Yet, post-concussion syndrome remains a clinical-biological reality. If a diffusion tensor imaging MRI in the acute phase is likely to provide predictive elements for subsequent cognitive dysfunctions, it would appear useful to consider combining biomarkers, and linguistics markers, with the creation of a clinical-radio-bio- neuropsychological score in order to differentiate benign outcomes from neuro- and/or psycho-traumatic disorders.

[Somatic treatments in psychiatry: A descriptive study of laboratory tests and systematic involvement in terms of overall care]. / Les soins somatiques en psychiatrie : étude descriptive d'un bilan biologique systématique et implication en termes de prise en charge globale.

BACKGROUND: Somatic suffering concerns mental health in many ways, but numerous psychiatrists are still reluctant to take an interest in somatic care due to a supposed lack of expertise and an alteration of the psychotherapeutic link, whilst in parallel numerous fellow physicians are quite apprehensive about treating patients with mental disorders. OBJECTIVES: We have undertaken a targeted clinical audit regarding the somatic treatment of in-patients in a psychiatric unit to propose the implementation of measures of improvement. MATERIAL AND METHODS: Our study focused on the identification and treatment of abnormal liver function tests, a subject that has been overlooked in the literature, yet from clinical experience the results are often abnormal in psychiatric unit in-patients. We analysed retrospectively over a period of two years the medical records of psychiatric unit in-patients with abnormal results for at least one of the following hepatic markers: aspartate-aminotransferase (AST), alanine transaminase (ALT), gamma-glutamyltransferase (GGT), alkaline phosphatase (ALP) and bilirubin. RESULTS: In total, 188 liver test results were abnormal, with an average of 1.7 per patient. The abnormal test results were in decreasing order: elevation in GGT (80 % of patients), elevation in transaminases (65.5 % for each), elevation in ALP (19.1 %) and elevation in bilirubin (7.27 %). Abnormal transaminase levels were lower than 10N, with a peak between 1N and 3N for ALT and a peak between 1N and 5N for AST. The elevation in GGT was between 1N and 34N, although 71.6 % of these values were below 5N. ALP was below 3N. The medical history was traced in 93.6 % of the records. A somatic clinical examination was only reported in 39 records (35.5 %) and was carried out by a hepato-gastroenterologist (HGE) in 30.8 % of cases, the establishment's emergency physician in 25.7 % of cases and the psychiatrists in 12.9 % of cases. Patients with abnormal liver function test results frequently underwent other biological and morphological examinations. A discharge letter was found in almost all cases. Abnormal liver function test results were indicated in less than 45 % of these discharge letters, whilst over half reported the establishment of a future treatment coordinated by the GP, in close collaboration with the gastroenterologist in at least half the cases. DISCUSSION: Our study was carried out in an open psychiatric unit in the heart of a general hospital that mainly receives patients suffering from thymus and anxiety disorders, addictive disorders, somatoform disorders, personality disorders and psycho-organic disorders. Patients suffering from schizophrenia or schizoaffective disorders comprised less than 10 % of admissions. Our retrospective study of over 750 hospital admissions over a period of two years found only 62.93 % of patients underwent liver function tests, which proved to be pathological in nearly 30 % of cases. Following a well-defined anamnesis, just over a third of patients underwent a physical examination whilst in hospital, more often a while after admission and not in the psychiatric unit. The consultation of fellow hospital physicians was limited even if the gastroenterologist was called upon in 30 % of cases. It was sometimes the treatment pathway or the fortuitous presence of co-morbidities that enabled the anaesthetist or emergency physician to carry out this clinical examination. However, when this physical examination was scheduled, clinical hepatobiliary signs were discovered in 30 % of patients. CONCLUSION: An accurate, formalised reference database detailing the principles of the somatic treatment of psychiatric unit in-patients should be established. Our results indicate the necessity of a referring physician in each psychiatric department.

[Perstimulus asystole during electroconvulsive therapy: Clinical case and critical literature review]. / Asystolie perstimulus résultant d'une hypertonie parasympathique au cours des électroconvulsivothérapies : cas clinique, brève revue de la littérature et discussion.

INTRODUCTION: Electroconvulsive therapy (ECT) is most frequently indicated for episodes of melancholic depression, but is also useful in the treatment of maniac syndrome and some schizophrenia subtypes. ECT is part of the treatment of movement disorders, neuroleptic malignant syndrome and even in the treatment of severe conversions. Although the therapeutic results are excellent when used appropriately, the mortality rate is estimated between 2 and 4 for 100,000 shocks. Despite this mortality rate, the benefit-risk ratio remains very positive and serious complications are extremely rare. ECT results in a biphasic cardiological effect: firstly a perstimulus parasympathetic hypertonia contemporary to the seizure's tonic phase, then a phase of contemporary sympathetic hypertonia during the epileptic clonic movement. We will focus on the perstimulus asystole as it is by far the most frequent. Very few cases and even less studies have been referenced in the literature; here, we present a clinical case followed by a discussion. CLINICAL CASE: The patient is in his fifties and has been treated for many years for a unipolar mood disorder with recurrent melancholic depressive episodes. With each new depressive episode, the clinical evolution is rapidly positive after a few sessions of ECT. Maintenance ECT was not retained due to the supra-annual periodicity of the melancholic depressive episodes and rapid recovery after electric treatment. Then, this patient developed another depressive decline in mood comparable to the previous one, despite adapted blood lithium levels associated with a new generation antidepressant treatment. According to his history, a hospitalisation was programmed to carry out a new course of ECT. Considering the short duration of the first seizures, the intensity of the stimulus was progressively increased. At 180 joules, the patient presented an immediate per-stimulus asystole of 20seconds which ceased spontaneously. The specialized cardiologic consultation following the rhythmic episode was reassuring: the patient's cardiac condition remained stable. However, after discussion with the patient and his family, we decided to stop the ECT. Was this a reasonable decision? DISCUSSION: According to the literature, the patient's medical history, sex, psychiatric diagnosis, the shock parameters (level of energy applied, duration of the stimulus, number of shocks) and clinical results, are not predictive factors in the occurrence of an asystole. Concerning the ECT protocol, the vagus nerve seems less stimulated during bifrontal stimulations in opposition to unilateral stimulations. Perasystolic patients are younger and have less prior history of cardiovascular disease or ECG abnormalities. Although the patients receiving ECT are often taking several medications (antipsychotics, benzodiazepines, antidepressants, anticholinergic correctors, calcium channel blockers, loop diuretics, converting enzyme inhibitors), these drugs are not considered as facilitating asystoles. No increase in the frequency of asystole had been observed when taking an average dose psychotropic treatment allowing the continuation of an antidepressant treatment at the recommended dose. Differently, lithium is regularly stopped during the shock phase as it could - even a few days after being stopped - potentiate the effects of succinylcholine and increase the vagal tone. Succinylcholine seems to promote asystole, whilst caffeine, methohexital and trimethaphan do not. The hypersympathetic phase can be controlled by a betablocker (propranolol, esmolol, labetalol) that does not increase the prior risk of asystole. Anticholinergic premedication using atropine does not appear to be systematic and could even potentially induce tachy-dysarrhythmia. However, in the case of perstimulus asystole, most authors recommend continuing the shocks with doses of atropine around 0.4 to 1mg. PHYSIOPATHOLOGY: Vagal stimulation is preferentially central and directly linked to the electric excitation of the lateral dorsal motor nucleus of the vagus nerve. Younger patients with no cardiac history are more at risk. This could be explained by the fact that juvenile tissue conducts electricity more rapidly than senescent (the difference being probably due to the fibrosis and adipose tissue which reduce its conductive capacity). Finally, it is appropriate to question the direct therapeutic aspect of vagal stimulation which constitutes an experimental treatment of resistant depression. CONCLUSIONS: The occurrence of perstimulus asystole is not considered as a serious complication of ECT and therefore as a contra-indication to any future sessions. On the contrary, most authors are campaigning for the continuation of shocks with the possibility of adding prophylactic intravenous atropine. Cardiac arrest reminds us that ECT requires a special attention to its cardiovascular effect, which emphasizes the role of interdisciplinarity between anaesthesiologists and psychiatrists.

[Clinical forms of post-traumatic depression]. / Formes cliniques des dépressions post-traumatiques.

INTRODUCTION: 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. CLINICAL FINDINGS: 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. CONCLUSIONS: 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.

[Correlation between specific and nonspecific posttraumatic stress disorder symptoms with healthcare consumption among 340 French soldiers]. / État de stress post-traumatique et consommation de soins sur l'année écoulée: étude menée auprès de 340 militaires français de cinq unités combattantes de l'armée de terre.

BACKGROUND: The psychotraumatic disorders are often difficult to diagnose because the specific symptoms of posttraumatic stress disorder (revival, hyperarousal, avoidance) are rarely a direct demand for health care: for reasons determined by the psychopathological structure of trauma, its symptomatology and course, the psychotraumatised subjects seek a care system for nonspecific psychological or somatoform symptoms: depressive episode, cognitive disorders, other anxiety disorders, histrionic and obsessive symptoms, changes in personality, pain disorders and somatization. Somatic pain may also result from a war injury and psychosomatic complications, addictive or consequences of risk behaviours during the evolution of posttraumatic stress disorder. OBJECTIVES: To establish a correlation between the PCLS and the evaluation of the healthcare consumption in a military population. METHODS: We conducted a multicenter epidemiological study analyzing the PCLS and a questionnaire assessing health care consumption. The PCLS has been studied in various forms: quantitative (17 to 85), in qualitative classes (<33, 33 to 43 and ≥44), and in five sub-dimensions (flashbacks, avoidance, dissociation, depression and hyperactivity). The sub-dimension revival was then studied item by item. The criteria used care consumption over the last twelve months is the numbers of days of sick leave, days of unavailability (of certain jobs or military activities) and consultations. RESULTS: Our population of 340 subjects cannot be considered representative of the French military population even if only a few characteristics differ. Sixteen of 340 subjects show a positive PCLS is 4.70% of our sample. PCLS average of 23 (±9.4) with a median of 19 objectifying much of PCLS have almost zero score. Validating our main hypothesis, we found a statistically significant relationship between elements of the PCLS and variables care consumption: this link exists mainly between the score, classes and sub-dimensions of the PCLS in one hand and number of days of sick leave and unavailability on the other hand. DISCUSSION: Towards a strategy for tracking psychotraumatic disorders, could be developed a score of health care consumption which would include the number of days of sick leave and unavailability, the number and quality of medical consultations, the number and quality of drug and laboratory requirements, the number of hospitalisations. To the identification of posttraumatic stress disorder, the PCLS score as well as the consumer healthcare score are valuable tools but do not replace the subjectivity of the clinical relationship: return to this shared subjectivity with the practitioner remains a diagnostic dimension, but also therapeutic, fundamental.

[The Gulf War Syndrome twenty years on]. / Le syndrome de la guerre du Golfe vingt ans après.

INTRODUCTION: 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). LITERATURE FINDINGS: 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. CLINICAL FINDINGS: 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. DISCUSSION: 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. CONCLUSION: 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.

[Mild traumatic brain injury and postconcussive syndrome: a re-emergent questioning]. / Traumatisme crânien léger et syndrome post-commotionnel : un questionnement ré-émergent.

INTRODUCTION: Blast injuries are psychologically and physically devastating. Notably, primary blast injury occurs as a direct effect of changes in atmospheric pressure caused by a blast wave. The combat-related traumatic brain injuries (TBI) resulting from exposure to explosions is highly prevalent among military personnel who have served in current wars. Traumatic brain injury is a common cause of neurological damage and disability among civilians and servicemen. Most patients with TBI suffer a mild traumatic brain injury with transient loss of consciousness. A controversial issue in the field of head injury is the outcome of concussion. LITERATURE FINDINGS: Most individuals with such injuries are not admitted to emergency units and receive a variable degree of medical attention. Nevertheless, cranial traumas vary in their mechanisms (blast, fall, road accident, bullet-induced craniocerebral injury) and in their gravity (from minor to severe). The majority of subjects suffering concussion have been exposed to explosion or blast injuries, which have caused minor cranial trauma. Although some authors refuse to accept the reality of post-concussion syndrome (PCS) and confuse it with masked depression, somatic illnesses or post-traumatic stress, we have raised the question again of its existence, without denying the intricate links with other psychiatric or neurological disorders. Although the mortality rate is negligible, the traumatic sequel after mild traumatic brain injury is clear. A difference in initial somatic severity is noted between the serious somatic consequences of a severe cranial trauma compared with the apparently benign consequences of a minor cranial trauma. However, the long-term consequences of the two types of impacts are far from negligible: PCS is a source of morbidity. The prognosis for minor cranial traumas is benign at vital level but a number of patients will develop long-term complaints, which contrast with the negativity of the clinical examination and complementary explorations. The origin of these symptoms questions their organic and psychological aetiologies, which are potentially associated or intricately linked. After a cerebral concussion patients report a cluster of symptoms referred to as postconcussive. CLINICAL FINDINGS: Post-concussion syndrome lies within the confines of somatic symptoms (headaches, dizziness, and fatigue), cognitive symptoms (memory and concentration problems) and affective symptoms (irritability, emotional lability, depression, anxiety, trouble sleeping). The nosographical entity of post-concussion syndrome is still in the process of elaboration following the input of new research intended to determine a cluster of specific symptoms. The persistent post-concussion syndrome is believed to be due to the psychological effects of the injury, biological factors, or a combination of both. Considered in isolation, the symptoms of post-concussion syndrome are non-specific and come together with other diagnostic frameworks such as characterised depressive episodes and post-traumatic stress. Post-concussion syndrome is not specific to concussion but can be present in subjects without any previous cranial trauma. DISCUSSION: Blast trauma can thus be understood as experiencing a shockwave on the brain and as a psycho-traumatic event. The major methodological problem of the studies is the quantification of the functional symptoms present in different nosographical frameworks, which are often co-morbid. Post-traumatic stress disorder is one of several psychiatric disorders that may increase suffering and disability among people with mild traumatic brain injury; in addition mood disorders also seem to be frequent psychiatric complications among these patients. Psychotic disorders after TBI have been associated with several brain regions. The establishment of a causative relationship between TBI and psychiatric disorders is interesting in terms of our understanding of these possible sequelae of TBI. The grey substance of the grey nuclei of the base can also be altered by a scissoring mechanism of the perforating arteries. A cortical contusion through impression of the cortex on the contours of the cranium is frequent. The most common type of injury is traumatic axonal injury. Cerebral lesions that are secondary to TBI associate cell deaths through the mechanisms of apoptosis and necrosis concerning the nerve and glial cells. The scientific objective is to discover an anatomoclinical correlation between the symptoms of post-concussion syndrome and objectifiable brain damage. The predictive value of serum concentrations of the specific serum markers S-100B and neurone specific enolase has been established. CONCLUSION: Cerebral imaging will allow the mechanisms concerned in cranial trauma to be better understood and thus may allow these mechanisms to be linked with co-morbid post-traumatic psychiatric disorders such as depression. The pyschopathological approach provides supplementary enlightenment where neuroimaging studies struggle to establish precise anatomoclinical correlations between neurotraumatic lesions, state of post-traumatic stress, and PCS. Moving away from a purely scientific view to focus on subjectivity, PCS can establish itself in subjects with no history of head trauma thus showing purely psychic suffering. Is the former name of "subjective post-head injury syndrome" no longer pertinent since the neurobiological affections can be objectified? Yet, the latter does not necessarily explain the somatic symptoms. Beyond any opposition of a psychic or somatic causality, it shows the complexity of this interaction. Admittedly, looking for a neuropathological affection is particularly cardinal to propose an aetiological model and objectify the lesions, which should be documented using a forensic approach. However, within the context of treatment, this theoretical division of the brain and the mind becomes less operative: the psychotherapeutic support will on the contrary back the indivisibility of the subject, he/she, who faced the "clatter".

[Posttraumatic stress disorder (PTSD) as a consequence of the interaction between an individual genetic susceptibility, a traumatogenic event and a social context]. / L'état de stress post-traumatique comme conséquence de l'interaction entre une susceptibilité génétique individuelle, un évènement traumatogène et un contexte social.

INTRODUCTION: 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. LITERATURE FINDINGS: 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. DISCUSSION: 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. CONCLUSION: 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.

[Posttraumatic stress disorder endophenotypes: several clinical dimensions for specific treatments]. / Les endophénotypes de l'etat de stress post-traumatique: plusieurs dimensions cliniques pour des prises en charge spécifiques.

Posttraumatic stress disorder is a syndrome with a very complex clinical that it is useful to describe according to a multidimensional approach. Following a critical review of the international literature, we have been able to highlight the genetic supports of posttraumatic stress disorder in the perspective of returning to the source of the clinical of this syndrome in order to steer its treatment better. We consider in succession the neuromodulation pathways involving dopamine, serotonine and noradrenaline to describe the hyperdomaminergic, hyposerotoninergic and hypernoradrenergic endophenotypes of posttraumatic stress disorder. Neurogenetic studies have affirmed two essential proposals. On the one hand, the pharmacological treatment of psychotraumatic disorders can be very closely adjusted to the different endophenotypes. On the other hand, the psychotherapeutic approach retains all its importance in the sense that it is the subjective implication that generated the trauma, subjectivity interacting with a genetic heritage and environmental factors integrating a social context. The changing definition of posttraumatic stress disorder over time comes from scientific exploration in part determined by a sociocultural context and, reciprocally, the psychic trauma is caused by the collapse of reassuring social values which were considered as immutable. The clinical is not developed according to fixed references: the evolution of neurogenetic techniques changes our perception of psychic traumas and the therapeutic possibilities.

[Psychosis and trauma. Theorical links between post-traumatic and psychotic symptoms]. / Psychose et traumatisme psychique. Pour une articulation théorique des symptômes psycho-traumatiques et psychotiques chroniques.

INTRODUCTION: The co-occurrence between post-traumatic symptoms and psychotic symptoms is well described in the immediate suites of a trauma but can also be chronic. This symptomatic co-occurrence, rarely studied in the literature, is often approached under the sole angle of a primary post-traumatic stress disorder (PTSD) or of a primary psychosis, without federative will to unify the psychotic and post-traumatic symptoms within the same nosological framework. Individuals with schizophrenia or schizoaffective disorder report higher rates of trauma and assault than the general population. LITERATURE FINDINGS: High rates of PTSD have been noted in severe mental illness cohorts. Psychotic phenomena may be a relatively common manifestation in patients with chronic PTSD. AIM: The purpose of this paper is to expose the various theorical psychopathological aspects between the symptoms of psychosis and PTSD. In populations of veterans, positive and negative symptoms of psychosis in PTSD are described as delusional thoughts and hallucinations often combat-specific. CLINICAL FINDINGS: When a PTSD becomes established at a subject to the personality of neurotic structure, the intensity of the PTSD's symptoms lead to a psychotic expression which constitutes a factor of seriousness. Besides, PTSD often induces a risk of substance use disorder supplying psychotic symptoms. Cannabis increases the hallucinations, cocaine strengthens an underlying paranoid tone, and alcohol implies withdrawal hallucinosis. Moreover, such consumption could be a risk factor for the future development of chronic psychosis. From another point of view, by basing themselves on the plasma dopamine beta-hydroxylase activity, some authors made the analogy between psychotic major depression and PTSD with psychotic features (also characterized as a distinct psychotic subtype of PTSD). However, other studies found no correlation between PTSD with psychotic features and family predisposition for schizophrenia or schizoaffective disorder. DISCUSSION: The determination of the structure of personality seems fundamental in the understanding of the symptoms. A personality of psychotic structure increases the risk of traumatization and PTSD. At the same time, the fragility of this structure causes an increased sensitivity to the trauma, which takes on a particular echo. Moreover, a trauma can test a latent psychotic structure to reveal its existence. The experience of psychosis may be traumatic in itself for patients with, notably, seclusion and sedation during hospitalization. Lastly, the symptoms of this post-traumatic psychosis will be differentiated from neurological confusion caused by a traumatic brain injury. Clinicians often fail to screen routinely for trauma and PTSD symptoms in patients with severe mental illness because few systematic guidelines exist for the identification and treatment of this comorbidity. CONCLUSION: The links between psychotic and psycho-traumatic symptoms are complex and multidirectional; this co-occurrence is a factor of seriousness. The clinician, while paying attention to these symptoms, has to distinguish the structure of the personality of the subject to articulate the psychotherapy and the pharmacological treatment. Further investigational studies may determine whether antipsychotics will enhance treatment response in PTSD patients with psychotic features.

[Psychogenic non epileptic seizures: a review]. / Crises psychogènes non épileptiques. Revue de la littérature.

OBJECTIVE: This paper summarizes the recent literature on the phenomena of psychogenic non epileptic seizures (PNES). DEFINITION AND EPIDEMIOLOGY: PNES are, as altered movement, sensation or experience, similar to epilepsy, but caused by a psychological process. Although in the ICD-10, PNES belong to the group of dissociative disorders, they are classified as somatoform disorders in the DSM-IV. That represents a challenging diagnosis: the mean latency between manifestations and diagnosis remains as long as 7 years. It has been estimated that between 10 and 30% of patients referred to epilepsy centers have paroxysmal events that despite looking like epileptic episodes are in fact non-epileptic. Many pseudo epileptic seizures have received the wrong diagnosis of epilepsy being treated with anticonvulsants. The prevalence of epilepsy in PNES patients is higher than in the general population and epilepsy may be a risk factor for PNES. It has been considered that 65 to 80% of PNES patients are young females but a new old men subgroup has been recently described. POSITIVE DIAGNOSIS AND PSYCHIATRIC COMORBIDITIES: Even if clinical characteristics of seizures were defined as important in the diagnosis algorithm, this point of view could be inadequate because of its lack of sensitivity. Because neuron-specific enolase, prolactin and creatine kinase are not reliable and able to validate the diagnosis, video electroencephalography monitoring (with or without provocative techniques) is currently the gold standard for the differential diagnosis of ES, and PNES patients with pseudoseizures have high rates of psychiatric disorders such as depression, anxiety, somatoform symptoms, dissociative disorders and post-traumatic stress disorder. We found evidence for correlations between childhood trauma, history of childhood abuse, PTSD, and PNES diagnoses. PNES could also be hypothesized of a dissociative phenomena generated by childhood trauma. PATHOPHYSIOLOGY: Some authors report that PNES can be associated with a physical brain disorder playing a role in their development: head injury may contribute to the pathogenesis of PNES. New-onset psychogenic seizures after resective epilepsy surgery or other intracranial neurosurgery have been described. Recent studies found psychogenic seizure disorders associated with brain pathology in the right hemisphere, non specific interictal electroencephalography abnormalities, magnetic resonance imaging changes and neuropsychological deficits. However, complex partial seizures of frontal origin might present similar characteristics with PNES and could be confused with the latter. PROGNOSIS AND TREATMENT: There is actually no clear agreement as the best treatment plan for PNES patients. The PNES diagnosis has to be clearly communicated to the patient. Nevertheless, even after a correct diagnosis is made a high proportion of PNES patients continue to have seizures, serious disability and bad self-reported quality of life. Furthermore, seizure remission cannot be considered a comprehensive measure of medical or psychosocial outcome. Nearly half of the patients who become seizure free remain unproductive and many of these patients continue to have symptoms of psychopathology including other somatoform, depressive, and anxiety disorders. Even if psychiatric comorbidities have to be treated by a psychiatrist? who could also suggest a psychotherapy, in all cases the importance of a neurologist continuing to follow post-diagnosis PNES patients is essential. CONCLUSIONS: PNES is a diagnostic and therapeutic challenge that is costly to patients and to society at large. Further studies are needed to understand this dissociative psychiatric disorder and to propose therapeutic guidelines.

The "near-death experience" during comas: psychotraumatic suffering or the taming of reality?

An near death experience (NDE) is the experience of an atypical state of consciousness that is induced by the neuropsychological consequences of a passage near death. Far from being a psychologically traumatic event, these experiences never cause flashbacks and can even eliminate the fear of death. Listening to patients who have shared their near death sensations has encouraged the reevaluation of the medical standards associated with NDEs. Over several decades, the patient has been positioned at the center of management decisions, with his or her will taken into account. Certain patients can be revived following neurological events, but their resuscitation is performed with the possibility of serious neurological sequelae, which might prevent a return to normal life. The patient may also remain unconscious, either transiently or in a more long term coma or persistent vegetative state. Nonetheless, several works have demonstrated the presence of neuronal activity, however little, in patients suffering from prolonged comas. The medical team then does not act as if the patient were not there but, on the contrary, considers the patient to be the subject, although unable to speak directly, to whom one speaks and of whom one speaks between caregivers.

[Post-traumatic stress disorder: Clinical aspects and pharmacological approach]. / Une conception moderne du traumatisme psychique à l'usage des médecins somaticiens : des différentes formes cliniques du trauma à leurs perspectives pharmacologiques.

All medical specialities are interested in the clinical aspects of psychological trauma. Due to psychopathological determinants which structure the trauma, although pathognomonic of posttraumatic stress disorder, flashbacks are rarely highlighted by the psychotraumatised patient in their contact with the health care system. Contact with the medical profession is expressed by somatic symptoms or psychiatric comorbidities. Addictive and suicidal problems, as well as somatisations and physical pain, are more traditional methods of contact with the health care system. In relation to the evolution of investigative techniques, modern wars have highlighted other dissociative and psychotic dimensions of the psycho- and craniatraumatic repercussions. These different clinical forms of posttraumatic stress disorder can receive a specific pharmacological treatment according to the predominant impairment of the incriminated monoaminergic neuromodulatory system.