P279 Short-latency afferent inhibition from the dorsolateral prefrontal cortex in patients with schizophrenia: A TMS-EEG study

Abstract

Introduction Transcranial magnetic stimulation (TMS) techniques provide a non-invasive indication of various inhibitory and excitatory processes in the human brain. One such a paradigm involves short-latency afferent inhibition (SAI) that captures a central cholinergic activity traditionally from the motor cortex (M1). Recently, we have established a method to index SAI in the dorsolateral prefrontal cortex (DLPFC), an area implicated in the pathophysiology of schizophrenia (SCZ). Objectives Here, we aimed to investigate SAI in both M1 and the DLPFC in patients with SCZ compared to healthy controls (HC). We hypothesized that modulation of the N100 on TMS-evoked potential (TEP) at the left frontal area would be reduced in patients with SCZ compared to that of HC. Methods Twelve right-handed SCZ (8 male, mean age 41 ± 10 yrs) and 12 HC (6 male, mean age 39 ± 12 yrs) were examined with combined TMS-electroencephalography (EEG). Individual N20 latency was determined from somatosensory-evoked potentials prior to the SAI procedure. SAI from the left motor cortex (M1-SAI) and the DLPFC (DLPFC-SAI) was indexed by conditioning a single suprathreshold TMS pulse with right median nerve stimulation at interstimulus intervals of N20 +2 (M1-SAI) and N20 +4 ms (DLPFC-SAI), respectively. Results In patients with SCZ, there were no significant TEP N100 change with M1-SAI (t 11 = −2.30, p = 0.822) or no significant difference in modulation of TEP N100 between SCZ and HC (t 22 = 1.917, p = 0.068). However, we observed a significant TEP N100 attenuation at the left frontal area with DLPFC-SAI ( t 11 = −7.756, p 22 = 5.299, p Conclusion Taken together, the modulation of TEP N100 by DLPFC-SAI may reflect the specific pathophysiology at the frontal area in SCZ. Therefore, the N100 modulation with DLPFC-SAI paradigm could be a potential biomarker to detect the cholinergic dysfunction from the prefrontal cortex in patients with SCZ. These findings warrant further study which may help to understand high smoking rates among SCZ.