ABSTRACT
Background@#and Purpose: Previous studies suggest that cognitive intervention can mitigate the development of dementia in patients with mild cognitive impairment (MCI). However, the previous cognitive intervention was mostly provided as a group session, in which MCI patients sometimes had difficulty in regularly attending sessions or were reluctant to participate in group-based classes. Additionally, experienced instructors for traditional cognitive intervention may be unavailable in some chronic-care facilities or community centers. Considering these reasons, we have developed 5 programs for home-based cognitive intervention using a personal robot for MCI patients. In this preliminary study, we aimed to demonstrate the effects of our newly developed home-based cognitive intervention with robots on cognitive function in MCI patients. @*Methods@#We conducted a single-blind randomized controlled trial enrolling 46 MCI patients. Participants were randomized into 2 groups: the robot cognitive intervention (robot) (n=24) group and without cognitive intervention (control) (n=22) group. The interventions comprised 60-min sessions per day for 4 weeks. The primary outcome was the change in cognitive function measured using the Cambridge Neuropsychological Test Automated Battery. @*Results@#There were no significant baseline demographic or clinical differences between the robot and control groups. After the 4-week cognitive intervention, the robot group showed greater improvement in working memory than did the control group. @*Conclusions@#Our home-based cognitive intervention with a personal robot improved the working memory in MCI patients. Further studies with larger samples and longer study periods are required to demonstrate the effects of these programs in other cognitive domains in MCI patients.
ABSTRACT
OBJECTIVES: It is increasingly thought that the human cerebellum plays an important role in emotion and cognition. Although recent evidence suggests that the cerebellum may also be implicated in fear learning, only a limited number of studies have investigated the cerebellar abnormalities in panic disorder. The aim of this study was to evaluate the cerebellar gray matter deficits and their clinical correlations among patients with panic disorder. METHODS: Using a voxel-based morphometry approach with a high-resolution spatially unbiased infratentorial template, regional cerebellar gray matter density was compared between 23 patients with panic disorder and 33 healthy individuals. RESULTS: The gray matter density in the right posterior-superior (lobule Crus I) and left posterior-inferior (lobules Crus II, VIIb, VIIIa) cerebellum was significantly reduced in the panic disorder group compared to healthy individuals (p < 0.05, false discovery rate corrected, extent threshold = 100 voxels). Additionally, the gray matter reduction in the left posterior-inferior cerebellum (lobule VIIIa) was significantly associated with greater panic symptom severity (r = -0.55, p = 0.007). CONCLUSIONS: Our findings suggest that the gray matter deficits in the posterior cerebellum may be involved in the pathogenesis of panic disorder. Further studies are needed to provide a comprehensive understanding of the cerebro-cerebellar network in panic disorder.