Impaired secondary somatosensory gating in patients with schizophrenia

• Published in: Psychiatry research 2007-06, Vol.151 (3), p.189-199
• Main Authors: Thoma, Robert J, Hanlon, Faith M, Huang, Mingxiong, Miller, Gregory A, Moses, Sandra N, Weisend, Michael P, Jones, Aaron, Paulson, Kim M, Irwin, Jessica, Cañive, Jose M
• Format: Article
• Language: English
• Subjects: Adult; Adult and adolescent clinical studies; Arousal - physiology; Attention - physiology; Biological and medical sciences; Brain Mapping; Chronic Disease; Cortex; Discrimination (Psychology) - physiology; Dominance, Cerebral - physiology; Electroencephalography; Evoked Potentials, Somatosensory - physiology; Female; Frontal Lobe - physiopathology; Humans; Magnetoencephalography; Male; Median Nerve - physiopathology; Medical sciences; Middle Aged; Parietal Lobe - physiopathology; Psychiatry; Psychology. Psychoanalysis. Psychiatry; Psychopathology. Psychiatry; Psychoses; Reaction Time - physiology; Reference Values; Schizophrenia; Schizophrenia - diagnosis; Schizophrenia - physiopathology; Schizophrenic Psychology; Secondary somatosensory; Sensory gating; Signal Processing, Computer-Assisted; Somatosensory Cortex - physiopathology
• ISSN: 0165-1781; 1872-7123
• DOI: 10.1016/j.psychres.2006.10.011

Abstract A large and growing literature has demonstrated a deficit in auditory gating in patients with schizophrenia. Although that deficit has been interpreted as a general gating problem, no deficit has been shown in other sensory modalities. Recent research in our laboratory has examined sensory gating effects in the somatosensory system showing no difference in gating of the primary somatosensory response between patients with schizophrenia and control subjects. This is consistent with recent structural studies showing no cortical structural abnormality in primary somatosensory area in schizophrenia. However, a significant decrease in cortical thickness and gray matter volume loss in secondary somatosensory cortex has recently been reported, suggesting this as a focus for impaired somatosensory gating. Thus, the current study was designed (1) to replicate previous work showing a lack of schizophrenia deficit in primary somatosensory cortex (SI) gating, and (2) to investigate a possible deficit in secondary somatosensory cortex (SII) gating. In a paired-pulse paradigm, dipolar sources were assessed in SI and SII contralateral to unilateral median nerve stimulation. Patients demonstrated no impairment in SI gating, but a robust gating deficit in SII, supporting the presence of cross modal gating deficits in schizophrenia.