Aberrant Resting-state Functional Connectivity in Complex Regional Pain Syndrome: A Network-based Statistics Analysis

Complex regional pain syndrome (CRPS) is a chronic neuropathic pain disorder. Pain catastrophizing, characterized by magnification, rumination, and helplessness, increases perceived pain intensity and mental distress in CRPS patients. As functional connectivity patterns in CRPS remain largely unknown, we aimed to investigate functional connectivity alterations in CRPS patients and their association with pain catastrophizing using a whole-brain analysis approach. Twenty-one patients with CRPS and 49 healthy controls were included in the study for clinical assessment and resting-state functional magnetic resonance imaging. Between-group differences in whole-brain functional connectivity were examined through a Network-based Statistics analysis. Associations between altered functional connectivity and the extent of pain catastrophizing were also assessed in CRPS patients. Relative to healthy controls, CRPS patients showed higher levels of functional connectivity in the bilateral somatosensory subnetworks (components 1~2), but lower functional connectivity within the prefronto-posterior cingulate (component 3), prefrontal (component 4), prefronto-parietal (component 5), and thalamo-anterior cingulate (component 6) subnetworks (p<0.05, family-wise error corrected). Higher levels of functional connectivity in components 1~2 (β=0.45, p=0.04) and lower levels of functional connectivity in components 3~6 (β=-0.49, p=0.047) were significantly correlated with higher levels of pain catastrophizing in CRPS patients. Higher functional connectivity in the somatosensory subnetworks implicating exaggerated pain perception and lower functional connectivity in the prefronto-parieto-cingulo-thalamic subnetworks indicating impaired cognitive-affective pain processing may underlie pain catastrophizing in CRPS.

A Review of Clinical Applications of Hyperbaric Oxygen Therapy in Psychiatric Disorders / 생물치료정신의학

Hyperbaric oxygen therapy (HBOT) is a noninvasive method that supplies pure oxygen under a pressure greater than normal atmospheric pressure to increase the partial pressure of oxygen in the plasma and tissue. Based on the potential mechanisms of HBOT, including neuroprotection and neurological recovery, HBOT has been suggested as a promising therapeutic option for neurological and psychiatric disorders. This review specifically focused on the clinical trials applying HBOT for psychiatric disorders published during the recent decade. We critically reviewed the efficacy and safety of HBOT in psychiatric disorders, and cautiously suggested the future directions for further research.

Now and Future of Data Sharing : Brain Magnetic Resonance Imaging Repositories / 생물치료정신의학

Over the past decade, practice of sharing brain magnetic resonance imaging (MRI) data is increasing given significance of reproducibility and transparency in human neuroscience. Larger multimodal brain MRI databases are needed for more robust research findings considering potential possibilities of large variability in human neuroscience. There are currently more than tens of thousands of shared brain MRI datasets across multiple conditions and hundreds of neuroimaging studies using multimodality through shared brain MRI data repositories. This article critically reviews aims, procedures, and current state of brain MRI data sharing. This review focuses on projects and research findings using structural and functional MRI open databases and is further divided into T1- and diffusion-weighted images for structural MRI as well as resting-state and task-based functional MRI. The challenges and directions are finally discussed. Advances in brain MRI data sharing will lead to more rapid progression in human neuroscience by fostering effective longitudinal, multi-site, multimodal neuroimaging research.

Molecular Neuroimaging in Posttraumatic Stress Disorder

Over the past decade, an increasing number of neuroimaging studies have provided insight into the neurobiological mechanisms of posttraumatic stress disorder (PSTD). In particular, molecular neuroimaging techniques have been employed in examining metabolic and neurochemical processes in PTSD. This article reviews molecular neuroimaging studies in PTSD and focuses on findings using three imaging modalities including positron emission tomography (PET), single photon emission computed tomography (SPECT), and magnetic resonance spectroscopy (MRS). Although there were some inconsistences in the findings, patients with PTSD showed altered cerebral metabolism and perfusion, receptor bindings, and metabolite profiles in the limbic regions, medial prefrontal cortex, and temporal cortex. Studies that have investigated brain correlates of treatment response are also reviewed. Lastly, the limitations of the molecular neuroimaging studies and potential future research directions are discussed.

Reduced Gray Matter Density in the Posterior Cerebellum of Patients with Panic Disorder: A Voxel-Based Morphometry Study

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.