Jean-Arthur Micoulaud-Franchi1, William P Hetrick2, Mitsuko Aramaki3, Amanda Bolbecker2, Laurent Boyer4, Sølvi Ystad3, Richard Kronland-Martinet3, Raphaëlle Richieri4, Catherine Faget4, Mélanie Faugere5, Alexandre El-Kaim5, Michel Cermolacce5, Christophe Lancon4, Jean Vion-Dury5. 1. Pôle de Psychiatrie "Solaris", Centre Hospitalier Universitaire de Sainte-Marguerite, 270 Bd de Sainte-Marguerite, 13009 Marseille, France; Unité de Neurophysiologie et Psychophysiologie, Pôle de Psychiatrie Universitaire, CHU Sainte-Marguerite, 270 Bd Sainte-Marguerite, 13009 Marseille, France; Laboratoire de Neurosciences Cognitives (LNC), UMR CNRS 7291, 31 Aix-Marseille Université, Site St Charles, 3 place Victor Hugo, 13331 Marseille Cedex 3, France. Electronic address: jarthur.micoulaud@gmail.com. 2. Department of Psychological and Brain Sciences, Indiana University, 1101 East Tenth Street, Bloomington, IN 47405, United States; Department of Psychiatry, Indiana University School of Medicine, Indianapolis, IN, United States; Larue D. Carter Memorial Hospital, Indianapolis, IN, United States. 3. Laboratoire de Mécanique et d'Acoustique, LMA, CNRS, UPR 7051, Aix-Marseille Univ., Centrale Marseille, F-13402 Marseille Cedex 20, France. 4. Pôle de Psychiatrie "Solaris", Centre Hospitalier Universitaire de Sainte-Marguerite, 270 Bd de Sainte-Marguerite, 13009 Marseille, France; Laboratoire de santé publique évaluation des systèmes de soins et santé perçue, Université de la Méditerranée, EA 3279, Faculté de Médecine, 27 bd Jean Moulin, 13385 Marseille cedex 05, France. 5. Pôle de Psychiatrie "Solaris", Centre Hospitalier Universitaire de Sainte-Marguerite, 270 Bd de Sainte-Marguerite, 13009 Marseille, France; Unité de Neurophysiologie et Psychophysiologie, Pôle de Psychiatrie Universitaire, CHU Sainte-Marguerite, 270 Bd Sainte-Marguerite, 13009 Marseille, France; Laboratoire de Neurosciences Cognitives (LNC), UMR CNRS 7291, 31 Aix-Marseille Université, Site St Charles, 3 place Victor Hugo, 13331 Marseille Cedex 3, France.
Abstract
BACKGROUND: P50 amplitude changes in dual click conditioning-testing procedure might be a neurophysiological marker of deficient sensory gating in schizophrenia. However, the relationship between abnormalities in the neurophysiological and phenomenological dimensions of sensory gating in schizophrenia remains unclear. The aim of the present study was to determine if patients with low P50-suppression (below 50%) report more perceptual anomalies. METHODS: Three groups were compared: twenty-nine schizophrenia patients with high P50-suppression (above 50% amplitude suppression), twenty-three schizophrenia patients with low P50-suppression (below 50%) and twenty-six healthy subjects. The Sensory Gating Inventory (SGI), a four-factor self-report questionnaire, was used to measure perceptual anomalies related to sensory gating. A comparison of demographic and clinical data was also carried out. RESULTS: Patients with low P50-suppression presented: i) significantly higher scores on the SGI (for the overall SGI score and for each of the 4 factors) and ii) significantly larger P50 amplitude at the second click, than both patients with high P50-suppression and healthy subjects. There were no group differences in the most of demographic and clinical data. DISCUSSION: The finding offers support for conceptual models wherein abnormal neurophysiologic responses to repetitive stimuli give rise to clinically relevant perceptions of being inundated and overwhelmed by external sensory stimuli. Further studies are needed to explore the contributions of clinical symptoms, medication and neuropsychological functions to the relationship between P50-suppression and the SGI, and the role of sensory "gating in" versus "gating out".
BACKGROUND: P50 amplitude changes in dual click conditioning-testing procedure might be a neurophysiological marker of deficient sensory gating in schizophrenia. However, the relationship between abnormalities in the neurophysiological and phenomenological dimensions of sensory gating in schizophrenia remains unclear. The aim of the present study was to determine if patients with low P50-suppression (below 50%) report more perceptual anomalies. METHODS: Three groups were compared: twenty-nine schizophreniapatients with high P50-suppression (above 50% amplitude suppression), twenty-three schizophreniapatients with low P50-suppression (below 50%) and twenty-six healthy subjects. The Sensory Gating Inventory (SGI), a four-factor self-report questionnaire, was used to measure perceptual anomalies related to sensory gating. A comparison of demographic and clinical data was also carried out. RESULTS:Patients with low P50-suppression presented: i) significantly higher scores on the SGI (for the overall SGI score and for each of the 4 factors) and ii) significantly larger P50 amplitude at the second click, than both patients with high P50-suppression and healthy subjects. There were no group differences in the most of demographic and clinical data. DISCUSSION: The finding offers support for conceptual models wherein abnormal neurophysiologic responses to repetitive stimuli give rise to clinically relevant perceptions of being inundated and overwhelmed by external sensory stimuli. Further studies are needed to explore the contributions of clinical symptoms, medication and neuropsychological functions to the relationship between P50-suppression and the SGI, and the role of sensory "gating in" versus "gating out".
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