M Stephane1, S Barton, N N Boutros. 1. Department of Psychiatry, Johns Hopkins Medical Institutions, JHOC Research Room # 3245, 601 North Caroline Street, Baltimore, MD 21287, USA.
Abstract
OBJECTIVE: to evaluate the neural substrate of auditory verbal hallucinations (AVH), the correlation between AVH and subvocal speech (hereafter SVS), and the relationship between speech and AVH. METHOD: we reviewed the papers found by an electronic literature search on hallucinations and speech. The review was extended to the papers cited in these publications and to classical works. RESULTS: there is no conclusive evidence of structural abnormality of the speech perception area in hallucinating schizophrenic patients. However there is evidence of electrophysiological abnormalities of the auditory and speech perception cortices. Functional imaging data are inconsistent, yet point to the left superior temporal gyrus as one of the neural substrates for AVH. There is also evidence that SVS could accompany the experience of AVH. CONCLUSION: there is evidence that dysfunction of brain areas responsible for speech generation is a fundamental mechanism for generating AVH in schizophrenia. It results in a secondary activation of Wernicke's area (speech perception) and Broca's area (speech expression). The first leading to the experience of hallucinations, and the second, eventually, gives rise to a variable degree of vocal muscle activity detectable by EMG, and/or faint vocalizations detectable by sensitive microphones placed at proximity of the larynx. Direct stimulation or disease of Wernicke's area produces AVH without SVS.
OBJECTIVE: to evaluate the neural substrate of auditory verbal hallucinations (AVH), the correlation between AVH and subvocal speech (hereafter SVS), and the relationship between speech and AVH. METHOD: we reviewed the papers found by an electronic literature search on hallucinations and speech. The review was extended to the papers cited in these publications and to classical works. RESULTS: there is no conclusive evidence of structural abnormality of the speech perception area in hallucinating schizophrenicpatients. However there is evidence of electrophysiological abnormalities of the auditory and speech perception cortices. Functional imaging data are inconsistent, yet point to the left superior temporal gyrus as one of the neural substrates for AVH. There is also evidence that SVS could accompany the experience of AVH. CONCLUSION: there is evidence that dysfunction of brain areas responsible for speech generation is a fundamental mechanism for generating AVH in schizophrenia. It results in a secondary activation of Wernicke's area (speech perception) and Broca's area (speech expression). The first leading to the experience of hallucinations, and the second, eventually, gives rise to a variable degree of vocal muscle activity detectable by EMG, and/or faint vocalizations detectable by sensitive microphones placed at proximity of the larynx. Direct stimulation or disease of Wernicke's area produces AVH without SVS.
Authors: Nadine Donata Wolf; Fabio Sambataro; Nenad Vasic; Karel Frasch; Markus Schmid; Carlos Schönfeldt-Lecuona; Philipp Arthur Thomann; Robert Christian Wolf Journal: J Psychiatry Neurosci Date: 2011-11 Impact factor: 6.186
Authors: Guillermo Horga; Eduard Parellada; Francisco Lomeña; Emilio Fernández-Egea; Anna Mané; Mireia Font; Carles Falcón; Anna B Konova; Javier Pavia; Domènec Ros; Miguel Bernardo Journal: J Psychiatry Neurosci Date: 2011-09 Impact factor: 6.186