Abnormal auditory sensory gating-out in first-episode and never-medicated paranoid schizophrenia patients: an fMRI study

Abstract

Numerous electrophysiological studies have showed auditory sensory gating-out abnormalities in chronic schizophrenia with antipsychotic medication. Previous research has used functional magnetic resonance imaging (fMRI) with excellent spatial resolution to identify the neural substrates of sensory gating-out deficits revealing increased hemodynamic response in the hippocampus, thalamus and prefrontal cortex. However, such results obtained from medicated patients may be confounded by antipsychotic medication. The present study scanned 15 first-episode schizophrenia patients not yet receiving any medical treatment and 15 healthy controls matched in gender, age and education when they performed a sensory gating-out task adapted for fMRI. The symptoms of the patients were assessed with the positive and negative syndrome scale. Different from previous findings, the schizophrenia patients showed decreased activation in hippocampus and thalamus during sensory gating-out, compared with the normal controls. The results support the theory attributing abnormal sensory gating-out in schizophrenia patients to the dysfunction of hippocampus and thalamus.

Impulsivity is Associated with Early Sensory Inhibition in Neurophysiological Processing of Affective Sounds

“…Deactivations of the dorsolateral prefrontal cortex, hippocampus, insula, and thalamus were observed for P50 during SG ( 25 , 26 ). Unusual activations of hippocampus and thalamus were also observed in patients with schizophrenia ( 31 ). Based on these source findings, habituation to aversive noise likely reduced activity in these areas, inducing SG of P50, as observed in people with higher-scoring RR in the present study.…”

“…Clinical studies have reported that SG functions abnormally in patients with current and developing psychiatric illness ( 16 , 27 ). Patients with schizophrenia, for example, showed higher S2–S1 ratios, that is, lower SG, of the P50 component than non-schizophrenic controls ( 17 , 22 , 28 – 30 ), and attenuated activations in the bilateral thalamus and hippocampus ( 31 ). The SG deficit is likely related to malfunctions of early sensory and attentional processing, which may be related to modulation in the α7 nicotinic receptor system ( 32 ).…”