There has been a recent surge of interest in auditory hallucinations (AH) in schizophrenia compared to those experienced by non-clinical (i.e. healthy) individuals. This interest stems in no small part from a keen awareness of the fact that progress in developing more effective treatments for AH in psychosis has been seriously hampered by our limited understanding of the cognitive and biological mechanisms involved. The prevailing notion that AH in clinical and non-clinical populations share the same features and underlying mechanisms - the continuum hypothesis - has been seriously challenged by a growing list of differences, as well as similarities, between these groups. At the phenomenological level this is exemplified in the highly negative content of AH in patients and the markedly earlier age of onset of AH in non-patients. Similarly, several recent studies point to significant differences in cognition, language lateralization and, possibly, dopamine function between these groups. These findings have important implications for the design of future studies, and raise considerable doubt about the adequacy of modelling the functional mechanisms of clinical AH on the basis of non-clinical populations. In short, the time seems ripe to re-evaluate the continuum hypothesis and provide a forum to present alternative perspectives on the functional pathways leading to AH in clinical and non-clinical groups. Such a forum is also timely in view of the renewed interest in AH in other (non-schizophrenic) clinical groups, again examining similarities and differences between such groups. Preliminary studies, for instance, have shown that AH in certain clinical populations (e.g. bipolar disorder, borderline personality disorder, dissociative disorder) share similar phenomenological features with AH in schizophrenia. However, the implications of such findings are not fully understood, and studies have not adequately examined potential differences between AH in these groups.
The goal of this Frontiers Research Topic, therefore, is take the opportunity to bring together research exploring differences and similarities in mechanisms of AH in clinical and non-clinical groups and to stimulate the development of new explanatory models which explicitly link the phenomenological characteristics of AH with underlying mechanisms. We welcome original research studies covering different levels of analysis, including cognition, neurophysiology, neuroimaging and neurotransmitter function, each of which might provide new targets for treatment development. We particularly encourage submission of studies that directly compare clinical and non-clinical AH groups. We also aim to encourage reviews and opinion pieces which aim to synthesize available data; develop integrated, testable models of AH; and propose new directions for the treatment of AH explicitly grounded in the emerging evidence base. Finally we also welcome critical commentary from investigators with expertise in “normal” voice perception, since this dialogue seems likely to provide important boundaries for emerging models of abnormal voice perception.
By bringing these papers together we hope to provide an overview of current thinking about AH and open discussion beyond the traditional continuum view to include multiple pathways to developing AH.
There has been a recent surge of interest in auditory hallucinations (AH) in schizophrenia compared to those experienced by non-clinical (i.e. healthy) individuals. This interest stems in no small part from a keen awareness of the fact that progress in developing more effective treatments for AH in psychosis has been seriously hampered by our limited understanding of the cognitive and biological mechanisms involved. The prevailing notion that AH in clinical and non-clinical populations share the same features and underlying mechanisms - the continuum hypothesis - has been seriously challenged by a growing list of differences, as well as similarities, between these groups. At the phenomenological level this is exemplified in the highly negative content of AH in patients and the markedly earlier age of onset of AH in non-patients. Similarly, several recent studies point to significant differences in cognition, language lateralization and, possibly, dopamine function between these groups. These findings have important implications for the design of future studies, and raise considerable doubt about the adequacy of modelling the functional mechanisms of clinical AH on the basis of non-clinical populations. In short, the time seems ripe to re-evaluate the continuum hypothesis and provide a forum to present alternative perspectives on the functional pathways leading to AH in clinical and non-clinical groups. Such a forum is also timely in view of the renewed interest in AH in other (non-schizophrenic) clinical groups, again examining similarities and differences between such groups. Preliminary studies, for instance, have shown that AH in certain clinical populations (e.g. bipolar disorder, borderline personality disorder, dissociative disorder) share similar phenomenological features with AH in schizophrenia. However, the implications of such findings are not fully understood, and studies have not adequately examined potential differences between AH in these groups.
The goal of this Frontiers Research Topic, therefore, is take the opportunity to bring together research exploring differences and similarities in mechanisms of AH in clinical and non-clinical groups and to stimulate the development of new explanatory models which explicitly link the phenomenological characteristics of AH with underlying mechanisms. We welcome original research studies covering different levels of analysis, including cognition, neurophysiology, neuroimaging and neurotransmitter function, each of which might provide new targets for treatment development. We particularly encourage submission of studies that directly compare clinical and non-clinical AH groups. We also aim to encourage reviews and opinion pieces which aim to synthesize available data; develop integrated, testable models of AH; and propose new directions for the treatment of AH explicitly grounded in the emerging evidence base. Finally we also welcome critical commentary from investigators with expertise in “normal” voice perception, since this dialogue seems likely to provide important boundaries for emerging models of abnormal voice perception.
By bringing these papers together we hope to provide an overview of current thinking about AH and open discussion beyond the traditional continuum view to include multiple pathways to developing AH.
