The Development of the Brooding Scale

OBJECTIVE: The purpose of this study was to develop a Brooding Scale (BS) and to confirm its psychometric properties. METHODS: A preliminary questionnaire was developed based on a literature review and face-to-face interviews with healthy subjects. To evaluate reliability and construct validity, a 15-item BS was administered to 124 healthy subjects. Convergent validity was tested by assessing the relationship between the BS and the Ruminative Response Scale (RRS). Discriminant validity was confirmed in 58 patients with schizophrenia. RESULTS: The internal consistency for the BS was excellent. An exploratory factor analysis yielded two factors: the emotional (six items) and cognitive (five items) domains, which explained 33.83% and 23.69% of the variance, respectively. The BS total score and scores for factors 1 and 2 showed significant positive correlations with the RRS. The total score and sub-factor scores of the BS were significantly higher in patients with schizophrenia than in healthy subjects. CONCLUSION: The BS can be used as a reliable and valid tool to assess brooding in healthy adults. In addition, it had good discriminant validity for patients with schizophrenia.

Neural Signature for Auditory Hallucinations in Schizophrenia: A High-Resolution Positron Emission Tomography Study with Fludeoxyglucose (¹⁸F)

OBJECTIVE: Auditory hallucinations (AHs) are a core symptom of schizophrenia. We investigated the neural signature of AHs by comparing hallucinating patients with schizophrenia with non-hallucinating patients with schizophrenia. METHODS: We recruited hallucinating patients with schizophrenia meeting the criteria for persistent, prominent, and predominant AHs (n=10) and non-hallucinating patients with schizophrenia (n=12). Various clinical assessments were performed incluing Psychotic Symptom Rating Scale for Auditory Hallucinations. Using fludeoxyglucose (¹⁸F) positron emission tomography, regional differences in neural activity between the groups were analyzed. RESULTS: The regions of interest analysis showed significantly lower standardized uptake value ratio (SUVR) in the superior, middle, and inferior frontal gyri, and higher SUVR in the putamen in patients with AHs versus patients without AHs. These findings were confirmed in the voxel-wise analysis. CONCLUSION: Our findings indicate that hypoactivity in the frontal and cingulate gyri, coupled with hyperactivity in the temporal gyrus and putamen, may contribute to the pathophysiology of AHs.

A Rural Dementia-Friendly Village Project and Dementia Awareness, Cognition, and Depressive Symptom : A Preliminary Study

OBJECTIVE: According to the 3rd Korean National Dementia Plan, the dementia-friendly community initiative was launched. The aim of this study was to evaluate the effects of a rural dementia-friendly village project on the participants. METHODS: Jeollabukdo Provincial Dementia Center designated Sosu-maeul, located in Buan-gun Jeollabuk-do, as a rural dementia-friendly village. We conducted dementia partnership education, youth-elder matching activity, and cognitive enhancing program. The efficacy of this project was evaluated by the changes in dementia awareness, cognitive function, and depressive symptoms. We used dementia awareness questionnaire, Mini-Mental Status Examination for Dementia Screening (MMSE-DS), and Korean version of Short form of Geriatric Depression Scale (SGDS-K). RESULTS: This study was carried out with 24 residents in this community. There was no significant change in dementia awareness score between pre- and post-intervention (p=0.25). MMSE-DS score was significantly increased from 24.5 to 25.5 (p < 0.001) and SGDS-K score was statistically improved from 3.5 to 2.5 (p=0.04) after interventions. CONCLUSION: We Jeollabukdo Provincial Dementia Center carried out a pilot study of a rural dementia-friendly village project. This project led to improvements on cognitive functions and depressive symptoms in the participants. But the improvement of dementia awareness was not achieved. More direct and experiencing interventions for people with dementia are necessary to improve dementia awareness.

Efficacy and Tolerability of Paliperidone Extended-release in the Treatment of First-episode Psychosis: An Eight-week, Open-label, Multicenter Trial

OBJECTIVE: We investigated the efficacy and tolerability of paliperidone extended-release (ER) tablets in patients with first-episode psychosis (n=75). METHODS: This was an 8-week, open-label, multicenter trial. The primary outcome variable was scores on the Positive and Negative Syndrome Scale (PANSS); secondary measures included the Scale for the Assessment of Negative Symptoms (SANS), the Cognitive Assessment Interview (CAI), and the Global Assessment of Functioning (GAF). To assess safety, we measured drug-related adverse events, weight, lipid-related variables, and prolactin and administered the Simpson–Angus Rating Scale (SARS), the Abnormal Involuntary Movement Scale (AIMS), the Barnes Akathisia Scale (BAS), the Arizona Sexual Experiences Scale (ASEX), and the Udvalg for Kliniske Undersogelser side effect rating scale (UKU). RESULTS: The administration of paliperidone ER resulted in significant improvement in the PANSS, SANS, CAI, and GAF scores (p<0.001) over time. This improvement was evident as early as 1 week. The most frequent adverse events were akathisia, somnolence, anxiety, and sedation, which were well tolerated. Modest increases in weight and lipid profiles were also noted. Prolactin levels were substantially increased at the endpoint in both male and female patients. CONCLUSION: These results indicate that paliperidone ER is effective and is characterized by good tolerability in the treatment of positive and negative symptoms and cognitive functioning in first-episode psychosis.

Decreased Plasma BDNF Levels of Patients with Somatization Disorder

OBJECTIVE: Brain-derived neurotrophic factor (BDNF), one of the most abundant and important neurotrophins, is known to be involved in the development, survival, maintenance, and plasticity of neurons in the nervous system. Some studies have suggested that BDNF may play a role in the pathophysiology of several psychiatric illnesses such as depression and schizophrenia. Similarly, it is likely that the alteration of BDNF may be associated with the neuro-modulation that contributes to the development of somatization disorder. METHODS: The purpose of this study was to determine whether there is an abnormality of plasma BDNF levels in patients with somatization disorder, and to analyze the nature of the alteration after pharmacotherapy using an enzyme-linked immunosorbent assay (ELISA). RESULTS: The plasma BDNF levels of the patients with a somatization disorder were significantly lower compared with those of the control volunteers (83.61±89.97 pg/mL vs. 771.36±562.14 pg/mL); moreover, the plasma BDNF levels of those patients who received an antidepressant were significantly increased after the treatment (118.13±91.45 pg/mL vs. 72.92±88.21 pg/mL). CONCLUSION: These results suggest that BDNF may play a role in the pathophysiology of somatization disorder.

Alteration of Brain-Derived Neurotrophic Factor Levels in Panic Disorder / 신경정신의학

OBJECTIVES: Brain-derived neurotrophic factor (BDNF), a neurotrophin involved in neurogenesis and synaptic plasticity, has been implicated in the pathophysiology of several neuropsychiatric disorders. However, there have been no consistent findings regarding BDNF levels in panic disorder. In this study, we investigated plasma BDNF levels in panic disorder, and evaluated whether there is an association between plasma BDNF levels and severity of symptoms of panic disorder. METHODS: Plasma BDNF levels were measured in 110 panic disorder patients and 110 normal control subjects using the enzyme-linked immunosorbent assay. The severity of symptoms of panic disorder was determined using the Panic Disorder Severity Scale, Acute Panic Inventory, Agoraphobic Cognition Questionnaire, and Hamilton Anxiety Rating Scale. RESULTS: The mean plasma BDNF levels of patients with panic disorder were significantly lower compared with those of control subjects (192.50 pg/mL vs. 693.75 pg/mL). No significant association was observed between plasma BDNF levels and the severity of symptoms of panic disorder. CONCLUSION: These results suggest that BDNF may play a potential role in the pathophysiology of panic disorder.

A Case of Clinical Application of Covert Sensitization in a Patient with Kleptomania / 신경정신의학

Kleptomania is a well-known impulse-control disorder. Although it is a rare disease, it exerts a greater influence on the social and economic. There are a variety of treatments for kleptomania, however case reports of its specific treatment techniques are extremely rare. In this case, covert sensitization was applied to a 44-year-old hospitalized patient with kleptomania, which can facilitate a specific treatment method through case presentation.

Characteristics of Subsyndromal Anxiety Disorder and Its Clinical Importance

Subsyndromal anxiety disorder indicates mental states of having anxiety symptoms not fulfilling criteria for anxiety disorders. Despite of the lack of previous objective findings of the subsyndromal anxiety disorder, its clinical importance has increased. It can cause many kinds of clinical anxiety symptoms and functional disabilities. But the early intervention and early treatment make it possible not only to attenuate the anxiety symptoms and functional disabilities but also to prevent disease progression to a full syndromal anxiety disorder. In this article, we will review the previous studies about the subsyndromal anxiety disorder and discuss its clinical characteristics and importance.

Anti-IgE mAb Suppresses Systemic Anaphylaxis through the Inhibitory IgG Receptor FcgammaRIIb in Mice: Interaction between Anti-IgE and FcgammaRIIb

BACKGROUND: Anti-IgE mAb which binds circulating but not receptor-bound IgE has been shown to be effective in treatment for asthma and other allergic diseases. However, the mechanisms by which anti-IgE mAb influences the pathophysiological responses are remained to be illustrated. This study was undertaken to examine the therapeutic efficacy of non-anaphylactogenic anti-mouse IgE mAb using murine models of IgE-induced systemic fatal anaphylaxis. METHODS: Active systemic anaphylaxis was induced by either penicillin V (Pen V) or OVA and passive systemic anaphylaxis was induced by either anaphylactogenic anti-mouse IgE or a mixture of anti-chicken gamma globulin (CGG) IgG1 mAb and CGG. The binding of the Fc portion of anti-IgE to CHO-stable cell line expressing mouse FcgammaRIIb was examined using flow cytometry. Fc fragments of anti-IgE mAb were prepared using papain digestion. The expression of phosphatases in lungs were assessed by Western blotting and immunohistochemistry. RESULTS: Anti-IgE mAb prevented IgE- and IgG-induced active and passive systemic fatal reactions. In both types of anaphylaxis, anti-IgE mAb suppressed antigen-specific IgE responses, but not those of IgG. Anti-IgE mAb neither prevented anaphylaxis nor suppressed the IgE response in FcgammaRIIb-deficient mice. The Fc portion of anti-IgE mAb was bound to murine FcgammaRIIb gene-transfected CHO cells and inhibited systemic anaphylaxis. Anti-IgE mAb blocked the anaphylaxis-induced downregulation of FcgammaRIIb-associated phosphatases such as src homology 2 domain-containing inositol 5-phosphatase (SHIP) and phosphatase and tensin homologue deleted on chromosome ten (PTEN). CONCLUSION: Anti-IgE mAb prevented anaphylaxis by delivering nonspecific inhibitory signals through the inhibitory IgG receptor, FcgammaRIIb, rather than targeting IgE.

Dexamethasone Does Not Inhibit Airway CXC Chemokine Expression and Neutrophilia in a Murine Model of Asthma - Mechanism of Steroid Resistance in Asthma

BACKGROUND: Although glucocorticoids (GCs) are effective in controlling asthma in the majority of patients, a subset of asthmatics fails to demonstrate a satisfactory response, even to systemic GC therapy. This population is referred to as being "steroid-resistant". The actual mechanism underlying steroid resistance in asthma remains to be elucidated. METHODS: We have investigated how dexamethasone (DEX) regulates asthmatic phenotypes in a murine model of asthma, in which mice received i.p. immunization twice, followed by two bronchoprovocations with aerosolized OVA with a one-week interval, which we have recently described. RESULTS: Pretreatment with DEX resulted in an inhibition of NF-kappaB activation in asthmatic lungs, and also inhibited bronchoalveolar lavage (BAL) levels of NF-kappaB-dependent cytokines such as TNF-alpha and CC chemokines [eotaxin and monocyte chemotactic protein (MCP)-1]. DEX was effective in suppressing airway hyperresponsiveness (AHR) at 10 h, Th2-dependent asthmatic phenotypes such as airway eosinophilia, BAL levels of Th2 cytokines (IL-5 and IL-13), and mucin production. However, DEX failed to suppress BAL levels of CXC chemokines [macrophage inflammatory protein-2 (MIP-2) and keratinocyte-derived chemokine (KC)] and airway neutrophilia. CONCLUSION: Airway neutrophilia is among the phenomena observed in patients with severe GC-resistant asthma. This study will provide insight into the molecular basis for airway neutrophila seen in steroid-resistant asthma. Further studies are required to delineate the underlying mechanism of CXC chemokine expression in asthma.