[The aetiopathogenesis of auditory hallucinations in psychosis].
BACKGROUND
Auditory hallucinations is one of the core symptoms of psychosis. Two main different approaches have been made in recent years in order to understand this perceptual abnormality. The psycho-social approaches is trying to explain auditory hallucinations as a common human phenomenon that only environmental factors cause them to be pathological. It propose psychotherapeutic techniques based on the cognitive model, paying special attention to the emotional component. The neurobiological approach, specially with neuroimaging techniques, is giving us new information about abnormal activation in specific neural networks, particularly in language areas. It propose biological treatments with antipsychotics and transcranial magnetic stimulation. Neither of these approaches are listening to each other. Neither of them look at the molecular genetic vulnerability to auditory hallucinations in psychosis.


METHODS
From a review of the literature and our own findings, we present a genetic-environmental model of auditory hallucinations in psychoses. We hypothesize two types of genetic vulnerability: vulnerability to hearing voices -that could be related with genes that are expressed in language areas and are related with language abnormalities (FOXP2)-, and vulnerability to abnormal emotional response to voices -that could be related with genes that are involved in the regulation of dopamine in the limbic system (5-HTT, CCK-AR)-. Finally, environmental and cultural factors explain the content and social adjustment to auditory hallucinations.


CONCLUSIONS
Our model allow the integration of many data from epidemiology and neuroimaging, to psychopharmacology in the understanding of the aetiology of auditory hallucinations.
Sanjuan
J
J
Unidad de Psiquiatría, Facultad de Medicina. Universidad de Valencia, 46010 Valencia, Espana. julio.sanjuan@uv.es
D001921:Brain / Q000033:anatomy & histology / Q000502:physiology; D051858:Forkhead Transcription Factors / Q000235:genetics / Q000378:metabolism; D006212:Hallucinations / Q000209:etiology* / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology; D006801:Humans; D011618:Psychotic Disorders / Q000150:complications* / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology*; D043886:Receptor, Cholecystokinin A / Q000235:genetics / Q000378:metabolism; D011985:Receptors, Serotonin / Q000235:genetics / Q000378:metabolism; D050486:Serotonin Plasma Membrane Transport Proteins / Q000235:genetics / Q000378:metabolism
C465448:FOXP2 protein, human; D051858:Forkhead Transcription Factors; D043886:Receptor, Cholecystokinin A; D011985:Receptors, Serotonin; D050486:Serotonin Plasma Membrane Transport Proteins