Les troubles psychotiques post-traumatiques : un modèle physiopathologique de la schizophrénie

Abstract

Traumatic Brain Injury (TBI) and later serious psychopathology have long been associated in the literature. Psychotic disorder following traumatic head injury is reported to occur in 0.7 to 9% of patients who sustain a head injury. This paper summarizes the recent literature about psychotic symptoms following TBI and try to articulate these psychotic disorders to a pathophysiological model of primary schizophrenia. Psychotic disorder due to a general medical condition (TBI) indicates that the hallucinations or delusions are the direct physical consequences of the medical condition. A contrario, schizophrenia-like psychosis is a secondary schizophreniform syndrom that must be differentiated from posttraumatic schizophrenia where the head trauma is an external factor furthering the onset of a primary psychosis. A dimensional approach could although take place for understanding pathophysiology. Head injury has been reported to increase the likelihood of the development of psychosis disorder due to TBI, schizophrenia-like psychosis and posttraumatic schizophrenia. While TBI is a major public health issue, schizophrenia following TBI is relatively rare and poorly studied. The onset of schizophrenia occurs most commonly from late adolescence to mid-adulthood, in an age group where head injury is more frequent. Even if early illness features of schizophrenia might increase exposure to TBI, posttraumatic schizophrenia could be the result of a gene-environment interaction. The pathophysiology research in psychotic disorders following TBI does not distinguish schizophrenia from other psychotic syndromes but have to consider a dimensional approach of these psychotic phenomena. Family history of schizophrenia and frontal or parietal lobe deficits was more common in patients with posttraumatic psychotic symptoms. Susceptibility to schizophrenia is believed to be due to multiple genetic and interacting factors and mild childhood head injury may play a role in the development and onset of schizophrenia in families with a strong genetic predisposition. The authors suggest hypotheses aimed at furthering the understanding of the physiologic mechanisms relating traumatic brain injuries to psychotic symptoms. Psychotic disorder following TBI, schizophrenia-like psychosis and posttraumatic schizophrenia are a potential interest to clinicians and neuroscientists, as it may provide clues to understanding primary psychotic disorders such as schizophrenia. Schizophrenia is a psychotic disorder commonly attributed to the interaction of genetic vulnerability and environmental events which implies that environmental factors modulate the effects of the genotype. Schizophrenia related to TBI could also be the result of a gene-environment interaction. Schizophrenia genes may increase exposure to head trauma (through agitation or cognitive impairment), with head trauma further increasing the risk for schizophrenia. Further studies are needed to articulate the links between secondary psychotic symptoms and primary schizophrenia in a structure/function paradigm. The new imaging techniques of magnetic resonance imaging, position emission tomography and single-photon emission computed tomography could aid in this sense.