Abstract

The physiological basis for musical hallucinations (MH) is not understood. One obstacle to understanding has been the lack of a method to manipulate the intensity of hallucination during the course of experiment. Residual inhibition, transient suppression of a phantom percept after the offset of a masking stimulus, has been used in the study of tinnitus. We report here a human subject whose MH were residually inhibited by short periods of music. Magnetoencephalography (MEG) allowed us to examine variation in the underlying oscillatory brain activity in different states. Source-space analysis capable of single-subject inference defined left-lateralised power increases, associated with stronger hallucinations, in the gamma band in left anterior superior temporal gyrus, and in the beta band in motor cortex and posteromedial cortex. The data indicate that these areas form a crucial network in the generation of MH, and are consistent with a model in which MH are generated by persistent reciprocal communication in a predictive coding hierarchy.

Highlights

  • Hallucinations are false percepts in the waking state that are not consequences of stimuli in the external environment, and can involve any sensory modality

  • The experiment was conducted on a subject with Musical hallucinations (MH) in the context of hearing loss who had typical phenomenology for this group

  • These results provide proof of principle for the use of residual inhibition (RI) to study MH, though it is not clear at present the proportion of the MH population in whom RI can be achieved

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Summary

Introduction

Hallucinations are false percepts in the waking state that are not consequences of stimuli in the external environment, and can involve any sensory modality. While hallucinations of music can occasionally result from focal brain lesions and psychiatric disorders (Keshavan, David, Steingard, & Lishman, 1992; Warren & Schott, 2006; Saba & Keshavan, 1997) the most common cause is hearing loss in the absence of other pathology (Berrios, 1990). This latter group raises the question of how hearing loss alone can lead to the development of complex MH, which is the focus of this study. A wide range of cortical and sub-cortical areas, which are inconsistent across studies, have been implicated in MH

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