Search

BackgroundA number studies have been conducted on abnormalities in the cortical circuitry of gamma oscillations, including deficit in auditory steady-state response (ASSR) to gamma-frequency (≧ 30-Hz) stimulation, in patients with bipolar disorder (BD). In the current study, we investigated neural responses during click stimulation by blood oxygen level-dependent (BOLD) signals. We focused on Broadman 41 and 42, the main sources of ASSR.Materials and methodsWe acquired BOLD responses elicited by click trains of 80-, 40-, 30- and 20-Hz frequencies from 25 patients with BD to 27 healthy controls (HC) with normal hearing between 22 and 59 years of age assessed via a standard general linear-model-based analysis. We extracted contrast values by identifying the primary auditory cortex and Brodmann areas 41 and 42 as regions of interest (ROI)s.ResultsBD group showed significantly decreased ASSR-BOLD signals in response to 40-Hz stimuli compared to the HC group in the right Brodmann areas 41 and 42. We found significant negative correlations between the BOLD change in the right Brodmann areas 41 and 42 and Structured Interview Guide for the Hamilton Depression Rating Scale (SIGH-D) scores, also the BOLD change in the right Brodmann areas 41 and 42 and the Positive and Negative Syndrome Scale (PANSS)-Negative scores.ConclusionThe observed decrease in BOLD signal patterns in the right primary auditory cortex during 40-Hz ASSR may be a potential biomarker option for bipolar disorder.

Patients with alcohol use disorder (AUD) have difficulties controlling alcohol cravings and thus exhibit increased use and earlier relapse. Although patients tend to respond more strongly to alcohol-related images compared with non-alcohol-related images, few researchers examined the factors that modulate cravings. Here, we examined whole-brain blood oxygen level-dependent (BOLD) responses to behavioural cues in individuals with AUD and healthy controls (HCs). The participants included 24 patients with severe AUD and 15 HCs. We presented four beverage images (juice, drinking juice, sake, and drinking sake) and compared participant BOLD responses between the two groups. Multiple comparisons revealed that the AUD group had lower BOLD responses compared with the HC group to images of drinking juice in the left precuneus (p = 0.036) and the left posterior cingulate cortex (PCC) (p = 0.044) and higher BOLD responses to images of drinking sake in the left PCC (p = 0.044). Furthermore, compared to the HCs, the AUD patients had decreased BOLD responses associated with cue reactivity to drinking juice in the left precuneus during the period from 15 to 18 s (p = 0.004, df = 37) and 18 to 21 s (p = 0.002, df = 37). Using the Spearman correlation, we found a significant negative correlation between BOLD responses in the left PCC of the AUD patients and Mini–Mental State Examination (MMSE) scores (r = −0.619, p = 0.001). Our findings suggest that HCs and severe AUD patients differ in their responses not to images of alcoholic beverages but those related to alcohol drinking behavior. Thus, these patients appear to have different patterns of brain activity. This information may aid clinicians in developing treatments for patients with AUD.

[This corrects the article DOI: 10.1371/journal.pone.0229187.].