Abstract
Recent MRI studies have shown that schizophrenia is characterized by reductions in brain gray matter, which progress in the acute state of the disease. Cortical circuitry abnormalities in gamma oscillations, such as deficits in the auditory steady state response (ASSR) to gamma frequency (>30-Hz) stimulation, have also been reported in schizophrenia patients. In the current study, we investigated neural responses during click stimulation by BOLD signals.We acquired BOLD responses elicited by click trains of 20, 30, 40 and 80-Hz frequencies from 15 patients with acute episode schizophrenia (AESZ), 14 symptom-severity-matched patients with non-acute episode schizophrenia (NASZ), and 24 healthy controls (HC), assessed via a standard general linear-model-based analysis. The AESZ group showed significantly increased ASSR-BOLD signals to 80-Hz stimuli in the left auditory cortex compared with the HC and NASZ groups. In addition, enhanced 80-Hz ASSR-BOLD signals were associated with more severe auditory hallucination experiences in AESZ participants. The present results indicate that neural over activation occurs during 80-Hz auditory stimulation of the left auditory cortex in individuals with acute state schizophrenia. Given the possible association between abnormal gamma activity and increased glutamate levels, our data may reflect glutamate toxicity in the auditory cortex in the acute state of schizophrenia, which might lead to progressive changes in the left transverse temporal gyrus.
Highlights
In a recent Global Burden of Disease Study, ‘acute’ schizophrenia received the highest disability weight out of 220 health state valuations (0–76, where 0 equals no disability and 1 equals complete disability) (Salomon et al, 2012)
We examined beta (ASSR to 20-Hz click trains), low gamma (ASSR to 30 and 40-Hz click trains), and high gamma (ASSR to 80-Hz click trains) auditory steady state response (ASSR)-blood oxygenation level dependent (BOLD) signals in healthy controls (HC), patients with acute episode schizophrenia (AESZ), and patients with non-acute phase schizophrenia (NASZ)
Given the potential for increased spontaneous gamma activities during auditory stimulation in the acute state, we hypothesized that BOLD signals elicited by the higher frequency periodic click stimuli would be elevated in the AESZ but not the non-acute episode schizophrenia (NASZ) group
Summary
In a recent Global Burden of Disease Study, ‘acute’ schizophrenia received the highest disability weight out of 220 health state valuations (0–76, where 0 equals no disability and 1 equals complete disability) (Salomon et al, 2012). The precise neurobiological mechanisms underlying progressive deterioration in the left transverse temporal gyrus and left planum temporale in schizophrenia are unknown, a growing body of work has implicated abnormal excitatory amino acid neurotransmission, possibly mediated by a deficit in recurrent inhibition (Coyle and Konopaske, 2016) Controversial, this mechanism could elicit ongoing, use-dependent cellular damage mediated via excitotoxic effects. ASSR deficits in individuals with chronic schizophrenia have been correlated with reduced evoked gamma responses (Tsuchimoto et al, 2011) and increased spontaneous gamma activities (Hirano et al, 2015) during auditory stimulation, indicating that neural circuitry abnormalities in schizophrenia patients may be associated with an imbalance between excitatory glutamate and inhibitory GABA neurotransmission. Given the potential for increased spontaneous gamma activities during auditory stimulation in the acute state, we hypothesized that BOLD signals elicited by the higher frequency periodic click stimuli would be elevated in the AESZ but not the NASZ group
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