Katharina Haß1, Nikolaj Bak2, Gregor R Szycik3, Birte Y Glenthøj4, Bob Oranje5. 1. Clinic for Psychiatry, Social Psychiatry and Psychotherapy, Hannover Medical School, Hanover, Germany; Center for Neuropsychiatric Schizophrenia Research (CNSR) and Center for Clinical Intervention and Neuropsychiatric Schizophrenia Research (CINS), Mental Health Center Glostrup, Mental Health Services, Capital Region of Denmark, University of Copenhagen, Denmark. Electronic address: hass.katharina@mh-hannover.de. 2. Center for Neuropsychiatric Schizophrenia Research (CNSR) and Center for Clinical Intervention and Neuropsychiatric Schizophrenia Research (CINS), Mental Health Center Glostrup, Mental Health Services, Capital Region of Denmark, University of Copenhagen, Denmark. 3. Clinic for Psychiatry, Social Psychiatry and Psychotherapy, Hannover Medical School, Hanover, Germany. 4. Center for Neuropsychiatric Schizophrenia Research (CNSR) and Center for Clinical Intervention and Neuropsychiatric Schizophrenia Research (CINS), Mental Health Center Glostrup, Mental Health Services, Capital Region of Denmark, University of Copenhagen, Denmark; University of Copenhagen, Faculty of Health and Medical Sciences, Dept. of Clinical Medicine, Denmark. 5. Center for Neuropsychiatric Schizophrenia Research (CNSR) and Center for Clinical Intervention and Neuropsychiatric Schizophrenia Research (CINS), Mental Health Center Glostrup, Mental Health Services, Capital Region of Denmark, University of Copenhagen, Denmark; University of Copenhagen, Faculty of Health and Medical Sciences, Dept. of Clinical Medicine, Denmark; Department of Psychiatry, Brain Center Rudolf Magnus, University Medical Center, Utrecht, The Netherlands.
Abstract
OBJECTIVES: To investigate whether the typically reported deficient sensorimotor gating in patients with schizophrenia using unimodal paradigms can also be detected by a cross-modal paradigm which made use of an electrocutaneous-acoustic coupling of stimuli. METHODS: Twenty-one male schizophrenia patients took part in a prepulse inhibition (PPI) paradigm with an electrocutaneous prepulse and an acoustic startle-eliciting pulse. Their results were compared with those from nineteen healthy males. RESULTS: As expected, the patients showed significantly lower PPI than controls. No associations were found between measures of illness severity and PPI. DISCUSSION: To the best of our knowledge, this is the first study showing reduced PPI in patients with schizophrenia by using an electrocutaneous-acoustic prepulse-pulse combination. Hence, this study gives further evidence of a modality-independent sensorimotor gating deficit in schizophrenia. Furthermore, as PPI was also lower than usual in controls using unimodal paradigms, results are interpreted in favour of longer processing times of the electrocutaneous prepulse, which probably led to a shorter perceived stimulus onset asynchrony (SOA) in the brain.
OBJECTIVES: To investigate whether the typically reported deficient sensorimotor gating in patients with schizophrenia using unimodal paradigms can also be detected by a cross-modal paradigm which made use of an electrocutaneous-acoustic coupling of stimuli. METHODS: Twenty-one male schizophreniapatients took part in a prepulse inhibition (PPI) paradigm with an electrocutaneous prepulse and an acoustic startle-eliciting pulse. Their results were compared with those from nineteen healthy males. RESULTS: As expected, the patients showed significantly lower PPI than controls. No associations were found between measures of illness severity and PPI. DISCUSSION: To the best of our knowledge, this is the first study showing reduced PPI in patients with schizophrenia by using an electrocutaneous-acoustic prepulse-pulse combination. Hence, this study gives further evidence of a modality-independent sensorimotor gating deficit in schizophrenia. Furthermore, as PPI was also lower than usual in controls using unimodal paradigms, results are interpreted in favour of longer processing times of the electrocutaneous prepulse, which probably led to a shorter perceived stimulus onset asynchrony (SOA) in the brain.