Si certains refusent la réalité de l’entité de syndrome post-commotionnel (SPC) pour la confondre dans la dépression masquée, les somatisations ou l’état de stress post-traumatique, nous avons voulu réaffirmer son existence sans en nier les intrications avec d’autres troubles psychiatriques. On note une différence évidente de gravité initiale entre les conséquences somatiques graves d’un traumatisme crânien « sévère » comparées à celles, apparemment bénignes d’un traumatisme crânien « léger ». Pourtant les conséquences à long terme des deux types de chocs sont loin d’être négligeables : le SPC est source de morbidité. Le pronostic des traumatismes crâniens « légers » est bénin sur le plan vital, mais nombre de patients vont développer des plaintes durables qui contrastent avec la négativité de l’examen clinique et des explorations complémentaires. L’origine de ces symptômes questionne leurs étiologies organiques et psychiques potentiellement associées ou intriquées. Le SPC réside aux confins de symptômes somatiques (céphalées, vertiges, fatigue), cognitifs (trouble de mémorisation et de concentration) et affectifs (irritabilité, labilité émotionnelle, dépressivité, anxiété, trouble du sommeil). Pris isolément, les symptômes du SPC sont non spécifiques et rejoignent d’autres cadres nosographiques comme l’épisode dépressif caractérisé et l’état de stress post-traumatique. Le traumatisme peut être entendu comme épreuve de l’onde de choc sur le cerveau et comme évènement psychotraumatique. L’approche psychopathologique apporte un éclairage supplémentaire là où les études de neuro-imagerie peinent à établir des corrélations anatomocliniques précises entre lésions neurotraumatiques, état de stress post-traumatique et SPC. S’éloignant d’une vision uniquement scientifique pour s’inscrire dans la subjectivité, le SPC peut s’établir chez des sujets sans aucun antécédent de traumatisme crânien en venant ainsi témoigner d’une souffrance purement psychique. L’ancienne dénomination de « syndrome subjectif des traumatisés crâniens » n’aurait-elle plus lieu d’être parce que des atteintes neurobiologiques sont devenues objectivables ? Pourtant ces dernières n’expliquent pas nécessairement les symptômes somatiques présentés. Au-delà de toute opposition d’une causalité psychique ou somatique, cela montre la complexité de cette interaction. Certes la recherche d’une atteinte neuropathologique est cardinale pour proposer un modèle étiologique et objectiver des lésions qui devront être documentées dans une logique médicolégale. Mais dans le cadre des soins, cette division théorique du cerveau et de l’esprit devient moins opérante : l’accompagnement psychothérapique viendra au contraire étayer l’indivisibilité du sujet, lui, qui a été confronté au « fracas ».

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.

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.

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.

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.

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”.