The Mood-Improving Effect of Viewing Images of Nature and Its Neural Substrate.

It has been recently suggested that contact with nature improves mood via reducing the activity of the prefrontal cortex. However, the specific regions within the prefrontal cortex that underlie this effect remain unclear. In this study, we aimed to identify the specific regions involved in the mood-improving effect of viewing images of nature using a 52-channel functional near-infrared spectroscopy (fNIRS). Specifically, we focused on the orbitofrontal cortex (OFC) and dorsolateral prefrontal cortex (dlPFC), two regions associated with affective processing and control. In a randomized controlled crossover experiment, we assigned thirty young adults to view images of nature and built environments for three minutes each in a counterbalanced order. During image viewing, participants wore a fNIRS probe cap and had their oxyhemoglobin (oxy-Hb) measured. Immediately following each image viewing, participants indicated their mood in terms of comfortableness, relaxation, and vigor. Results showed that viewing images of nature significantly increased comfortableness and relaxation but not vigor compared to viewing images of built environments, with a large effect size. Meanwhile, the concentration of oxy-Hb in only the right OFC and none of the other regions significantly decreased while viewing the images of nature compared to built environments, with a medium effect size. We speculate that viewing images of nature improves mood by reducing the activity of or calming the OFC. Since the OFC is hyperactive in patients with depression and anxiety at rest, contact with nature might have therapeutic effects for them.

[Clinical examination of 3 patients with delayed neuropsychiatric encephalopathy induced by carbon monoxide poisoning, who recovered from severe neurocognitive impairment by repetitive hyperbaric oxygen therapy].

We performed hyperbaric oxygen (HBO) therapy for 3 patients with delayed neuropsychiatric encephalopathy induced by carbon monoxide (CO) poisoning. All patients were male and around 50 years old, and they had not received HBO therapy within 24 h after CO poisoning, even though they showed severe consciousness disturbance. In these patients, delayed neuropsychiatric encephalopathy appeared about 25 days after acute CO poisoning, and HBO therapy was initiated within 8 days after disease onset. Although the condition of 2 of the patients worsened initially, they showed significant improvement of neurocognitive impairment after 30 sessions of HBO therapy. The clinical courses of these patients suggest that the effect of HBO therapy can be evaluated after 30 sessions. To evaluate the validity of the indices of the clinical effect of HBO therapy, we performed brain magnetic resonance imaging, single photon emission computed tomography, electroencephalography (EEG), and neurocognitive tests (HDS-R, and Wechsler Adult Intelligence Scale-Revised or III). Our results showed that changes in EEG signals and neurocognitive tests were closely correlated with the patients' clinical courses.