Kang E, et al. J Korean Med Sci. 2020 Dec;36(3):e33. https://doi.org/10.3346/jkms.2021.36.e33

To examine the resting-state functional connectivity (FC) between subcortical regions in relation to whole-brain activity in patients with psychophysiological insomnia (PI) and changes following cognitive-behavioral therapy for insomnia (CBTi). The FC between subcortical seed regions (caudate, putamen, pallidum, amygdala, thalamus, and hippocampus) and whole-brain voxels were compared between the PI group (n = 13, mean age: 51.0 ± 10.2 years) and good sleepers (GS, n = 18, mean age: 42.7 ± 12.3 years). Also, in the PI group, FC was compared before and after 5 weeks of CBTi. Compared to the GS group, the PI group exhibited stronger FC between the thalamus and prefrontal cortex and between the pallidum and precuneus but weaker FC between the pallidum and angular gyrus, the caudate and orbitofrontal cortex, and the hippocampus and fusiform gyrus. After CBTi, the PI group exhibited decreased FC between the thalamus and parietal cortex, the putamen and motor cortices, and the amygdala and lingual gyrus, but increased FC between the caudate and supramarginal gyrus, the pallidum and orbitofrontal cortex, and the hippocampus and frontal/parietal gyri. The present findings demonstrate different FC in PI patients compared to GS and provide insight into the neurobiological rationale for CBTi.

There has been a growing interest in the relationship between sedative-hypnotics use and the risk of Alzheimer’s dementia (AD) risk. This study aimed to evaluate the risk of AD associated with the use of sedative-hypnotics. A retrospective cohort study was conducted with randomly selected 5% samples from ≥50 years old beneficiaries of National Health Insurance Service (NHIS) of Korea from January 2002 to December 2015. The exposure to sedative-hypnotics was defined when prescribed over 30 defined daily dose (DDD) after January 2004 and it was categorized by prescribed dosage, types and half-lives of benzodiazepines. Time-dependent Cox regression model with a lag period of 5-years was used to evaluate the association between use of sedative-hypnotics and the risk of subsequent AD. Sensitivity analysis was performed for restricting sedative-hypnotics only when prescribed with insomnia. A total of 268,170 subjects were identified and subjects exposed to sedative-hypnotics showed a higher risk of AD (HR: 1.79; 95% CI: 1.72–1.86) than those who were not. There was an increased risk of AD among subjects exposed to benzodiazepines or zolpidem (HR: 1.75; 95% CI: 1.67–1.82) and antidepressants or low-dose antipsychotics (HR: 1.63; 95% CI: 1.42–1.87). The risk of AD was increased regardless of dose of sedative-hypnotics and half-life among benzodiazepines, especially in exposure to more than 360 DDD of sedative-hypnotics (HR: 1.78; 95% CI: 1.60–1.99) and the long-acting benzodiazepine (HR:1.77; 95% CI: 1.65–1.89).

Kim HH, et al. Psychiatry Investig. 2011 Sep;8(3):179-185. http://dx.doi.org/10.4306/pi.2011.8.3.179