Deficient Inhibitory Cortical Networks in Antipsychotic-Naive Subjects at Risk of Developing First-Episode Psychosis and First-Episode Schizophrenia Patients: A Cross-Sectional Study
Biological Psychiatry, 04/19/2012Hasan A et al.
The results indicate specific alterations in inhibitory cortical networks in subjects at risk and in first–episode patients. It appears that there is already a cortical inhibitory deficit in at–risk individuals. These results suggest a possible gamma–aminobutyric acid (GABA) type A dysfunction early in the disease course, whereas alterations in GABA type B functionality seem to occur later in the disease's progression.
A total of 18 subjects at risk, 18 first-episode schizophrenia patients, and 18 healthy control subjects were included in this study.
Transcranial magnetic stimulation over the left primary motor cortex was used to determine short-latency intracortical inhibition, intracortical facilitation, and the contralateral silent period (CSP).
Short-latency intracortical inhibition can be considered as a parameter of GABA type A (GABAA)-mediated inhibition and it has been proposed that CSP can test GABA type B (GABAB)-mediated inhibitory intracortical networks.
Subjects at risk and first-episode patients showed a reduced short-latency intracortical inhibition compared with healthy control subjects, suggesting reduced GABAA-mediated inhibition.
First-episode patients had a prolonged CSP duration compared with the other two groups, implying a GABAB imbalance only in patients with full-blown psychosis.
Analyses did not reveal group differences for intracortical facilitation.
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