Norio Yasui-Furukori

Sarcoidosis is a systemic disease of unknown etiology, in which granulomas develop in various organs, including the skin, lungs, eyes, or heart. It has been reported that patients with sarcoidosis are more likely to develop panic disorder than members of the general population. However, there are many unknown factors concerning the causal relationship between these conditions. We present the case of a 57-year-old woman who appeared to have panic disorder, as she experienced repeated panic attacks induced by transient complete atrioventricular block, associated with cardiac sarcoidosis. Psychotherapy and pharmacotherapy were not effective in the treatment of her panic attacks. However, when we implanted a permanent pacemaker and initiated steroid treatment for cardiac sarcoidosis, panic attacks were ameliorated. Based on these findings, we diagnosed the patient’s symptoms as an anxiety disorder associated with cardiac sarcoidosis, rather than panic disorder. This report highlights the importance of considering cardiac sarcoidosis in the differential diagnosis of panic disorder. This cardiac disease should be considered especially in patients have a history of cardiac disease (e.g., arrhythmia) and atypical presentations of panic symptoms. Panic disorder is a psychiatric condition that is typically diagnosed after other medical conditions have been excluded. Because the diagnosis of sarcoidosis is difficult in some patients, caution is required. The palpitations and symptoms of heart failure associated with cardiac sarcoidosis can be misdiagnosed as psychiatric symptoms of panic disorder. The condition described in the current case study appears to constitute a physical disease, the diagnosis of which requires significant consideration and caution.

Previous studies have reported changes in the dimensions of the Temperament and Character Inventory (TCI) after patients with major depressive disorder are treated. We aimed to investigate the changes in the TCI dimensions after paroxetine treatment in patients with major depressive disorder. Forty‐eight patients were enrolled in this study and were treated with 10–40 mg/day of paroxetine for 6 weeks. The TCI was completed twice, at weeks 0 and 6. We used the Montgomery–Asberg Depression Rating Scale (MADRS) to evaluate patients. The participants were divided into three groups (responders, non‐responders, and early responders) based on treatment response. The scores of each dimension of the TCI were compared before and after treatment using repeated‐measures two‐way analyses of variance. In the responders group (n = 24), no TCI dimension scores changed significantly during treatment, but the interaction between sex and MADRS score change was significantly associated with the results. In the non‐responders group (n = 15), the self‐directedness score increased significantly during the treatment period (p = 0.000), and the change in MADRS score significantly affected the results. In the early responders group (n = 9), no TCI dimension scores changed significantly during treatment. The results of the present study may reveal a possible correlation between paroxetine treatment and changes in personality traits. Copyright © 2015 John Wiley & Sons, Ltd.

Introduction: Screening tools for dementia should be valid and easy to complete and have a low psychological burden. Consistent with these principles, the Yamaguchi fox/pigeon-imitation test (YFPIT) has been developed. However, there is little information on the utility of the YFPIT for preclinical populations, although the detection of proven prodromal and preclinical states is important. Materials and methods: We recruited 392 volunteers who were at least 60 years old (139 men and 253 women) and had participated in the Iwaki Health Promotion Project. The YFPIT was administered to all participants. Results: Most subjects succeeded in imitating the fox gesture regardless of their cognitive function impairment, while the success rates for the pigeon gesture were 75.3% in the normal group and 56.3% in the cognitive impairment group. The sensitivity, specificity, positive predictive value (PV⁺), and negative predictive value (PV^-) were 43.8%, 75.3%, 7.0%, and 97.0%, respectively. The greatest significant difference between the imitation of the pigeon gesture and cognitive impairment was found in females with subjective memory impairments (P=0.001). In that group, the sensitivity, specificity, PV⁺, and PV^- were 100%, 81.9%, 18.8%, and 100%, respectively. Conclusion: This study suggests that the utility of the YFPIT is limited in the general population, but that it is a useful tool in females with subjective memory impairments in a community-dwelling population.

Hyperprolactinemia is a frequent consequence of treatment with antipsychotics. Earlier studies have indicated that terguride, which is a partial dopamine agonist, reduces the prolactin levels that are induced by prolactinemia. Thus, we examined the dose effects of adjunctive treatment with terguride on the plasma concentrations of prolactin in patients with elevated prolactin levels resulting from antipsychotic treatment. Terguride was concomitantly administered to 20 schizophrenic patients (10 males and 10 females) receiving paliperidone and risperidone. The dose of terguride was 1.0 mg/day. Sample collections for prolactin were conducted before terguride (baseline) and 2–4 weeks after administration. The samples were obtained after the morning dose of terguride. The average (± standard deviation) plasma prolactin concentration during terguride coadministration was significantly lower than the baseline concentration in females (82.3±37.1 ng/mL versus 56.5±28.5 ng/mL, Pr_s=−0.638, Pr_s=−0.152, not significant). Many patients complained of various adverse events following terguride administration, such as insomnia, agitation, and/or the aggravation of hallucinations. This study suggests that additional treatment with terguride decreases the prolactin concentrations in females experiencing high prolactin levels as a result of antipsychotic treatment. However, its utility for schizophrenia may be diminished because of its low tolerability.

Background: We investigated the relationship between plasma concentrations of paroxetine and the therapeutic effect of the drug, and we evaluated the therapeutic reference range for plasma concentration of paroxetine in patients with major depressive disorders (MDD). Methods: In this study, 120 patients with MDD were treated with 10–40 mg/d of paroxetine for 6 weeks, and 89 patients completed the protocol. The Montgomery–Asberg Depression Rating Scale (MADRS) was used to evaluate the patients at 0, 1, 2, 4, and 6 weeks. At the 6-week treatment time point, the patients were divided into 7 groups according to their paroxetine plasma concentrations in increments of 20 ng/mL. We used an analysis of variance and a χ² test to define the therapeutic reference range for plasma paroxetine concentrations. Results: We used 50% as the cutoff values for the percentage of MADRS improvement to determine the responder rates, and we defined remitters as patients with MADRS scores 2 test. According to the results of the χ² test in the responder rates, the 20–60 ng/mL plasma paroxetine group showed the highest effect size. Conclusions: The results of this study suggested that a range of 20–60 ng/mL is the therapeutic reference range for concentrations of paroxetine in plasma in patients with MDD.