Insomnia is a common sleep-related symptom which occurs in many populations, however, the neural mechanism underlying insomnia is not yet known. The hyperarousal model explains the neural mechanism of insomnia to some extent, and the frontal cortex dysfunction has been known to be related to primary insomnia. In this review, we discuss studies that applied resting state and/or task-related functional magnetic resonance imaging to demonstrate the deficits/dysfunctions of functional activation and network in primary insomnia. Empirical evidence of the hyperarousal model and proposed relation between the frontal cortex and other brain regions in primary insomnia are examined. Reviewing these studies could provide critical insights regarding the pathophysiology, brain network and cerebral activation in insomnia and the development of novel methodologies for the diagnosis and treatment of insomnia.

Objectives This study intended to identify the deficits of cognitive control among patients with bipolar I disorder and their first-degree relatives, and identify the possibility of cognitive control as an endophenotype of bipolar disorder. Methods The study included three groups: euthymic states patients with bipolar I disorder (n = 55), unaffected first-degree relatives of probands with bipolar I disorder (n = 30), and a healthy control group (n = 51), that was matched on age, sex, and years of education. The AX version of the continuous performance test (CPT) was used to examine cognitive control. Error rate, correct response times of each subsets (AX, BX, AY, BY), and d' as an indication of accuracy sensitivity index were calculated. Psychopathology, intelligence, and psychomotor speed were also assessed. Results Patients with bipolar I disorder showed significantly worse error rates in the AX (p = 0.01) and BX (p = 0.02) subsets and d' (p = 0.05) than the others. They also showed more delayed correct response times than the healthy control group and first-degree relatives in all subsets (p < 0.01). But first-degree relatives showed neither high error rates nor delayed correct response times than healthy control group. Conclusions These findings suggest that cognitive control is impaired in bipolar I disorder but less likely to be an endophynotype of bipolar I disorder.

Objectives Psychological resilience is the ability to cope with stress. The genetic background behind psychological resilience is not much known. The serotonin transporter and dopamine transporter are implicated in stress related psychology and emotional processing. The aim of this study is to investigate a possible genetic role of functional polymorphisms of serotonin and dopamine transporters for psychological resilience. Methods A total of 951 healthy adult subjects were included. Psychological resilience was measured using Connor-Davidson Resilience Scale (CD-RISC). Genotyping was performed for serotonin transporter gene(SERT) promoter variable number tandem repeat (VNTR) and dopamine transporter gene(DAT1) 3'-untranslated region (UTR) VNTR. Genetic association analysis was conducted between genotypes and the CD-RISC score. Results No genetic association was observed for SERT promoter VNTR or DAT1 3'-UTR VNTR with CD-RISC score. No genetic interaction between SERT promoter VNTR and DAT1 3'-UTR VNTR with CD-RISC score was detected. Conclusions Either serotonin or dopamine transporter did not seem to play a significant role for psychological resilience in this sample.