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Alzheimer's disease (AD) is clinically characterized by gradual onset over years with worsening of cognition. The initial and most prominent cognitive deficit is commonly memory dysfunction. However, a subset of AD cases has less hippocampal atrophy than would be expected relative to the predominance of cortical atrophy. These hippocampal-sparing cases have distinctive clinical features, including the presence of focal cortical clinical syndromes. Given that previous studies have indicated that severe hippocampal atrophy corresponds to prominent loss of episodic memory, it is likely that memory impairment is initially absent in hippocampal-sparing AD cases. Here, we report on a patient with an 8-year history of delusional jealousy with insidious onset who was clinically diagnosed as possible AD and pathologically confirmed to have AD with relatively preserved neurons in the hippocampus. This patient had delusional jealousy with a long pre-dementia stage, which initially was characterized by lack of memory impairment. Head magnetic resonance imaging findings showed preserved hippocampal volume with bilateral enlarged ventricles and mild-to-moderate cortical atrophy. Head single-photon emission computed tomography revealed severely decreased regional cerebral blood flow in the right temporal lobe. The resolution of the delusion was attributed to pharmacotherapy by an acetylcholinesterase inhibitor, suggesting that the occurrence of delusional jealousy was due to the disease process of AD. Although the neural basis of delusional jealousy remains unclear, this hippocampal-sparing AD case may be classified as an atypical presentation of AD.

Japan approved clozapine for treatment-resistant schizophrenia in June 2009. The aim of this study was to evaluate clozapine's efficacy and tolerability in Japanese patients. A twelve-week, single-arm clinical trial of clozapine in treatment-resistant schizophrenia inpatients, was conducted under real-world conditions using raters masked for type of antipsychotic. Thirty-eight patients were recruited, with 33 (86.8%) completing the trial. At week 12, clozapine was associated with significant improvement in the Positive and Negative Syndrome Scale (PANSS) total (p0.0001), PANSS positive (p0.0001), negative (p = 0.0055) and general subscale scores (p0.0001). Significant improvements occurred in all PANSS scores by week 4, the first post-baseline psychopathology rating. Altogether, 50.0% of patients showed ≥20% reduction in PANSS total score, 20.6% had ≥30% reduction and 14.7% had40% reduction. Eighteen patients (47.4%) were discharged before week 12. However, all patients experienced ≥1 adverse event. Two of 38 patients (5.2%) dropped out due to moderate leucopenia and one of them developed agranulocytosis after stopping clozapine. However, both patients recovered. Eight adverse events (hypersalivation, fatigue, sedation, constipation, insomnia, nausea/vomiting, chest pain and leucopenia) were observed in 34-79% of patients. These findings suggest that clozapine is beneficial in Japanese treatment-resistant schizophrenia patients. However, attention should be paid to patients' adverse events.

Aims: Previous studies have reported that the incidence of obstructive sleep apnea syndrome (OSAS) in patients with depression is higher than in the general population. We examined the risk factors to predict OSAS in mood disorder patients with depressive symptoms. Method: We conducted polysomnography for patients who satisfied the following criteria: (i) diagnosis of major depressive disorder or bipolar disorder according to the Mini-International Neuropsychiatric Interview (MINI); (ii) a score of ≥10 on the Hamilton Rating Scale for Depression (HAM-D); (iii) fulfillment of either (a) or (b) below: (a) at least one of the following: severe snoring, witnessed apnea during sleep, excessive daytime sleepiness; (b) at least one of the following plus an oxygen desaturation index of 4% ≥5 times/h by pulse oximeter: mild snoring, sleep disturbance, headache, high blood pressure. The patients with apnea hypopnea index ≥5 were diagnosed with OSAS. Results: Of the 32 mood disorder patients who met the subject conditions, 59.4% had OSAS. The diagnosis rate with our criteria was significantly higher than the previously reported incidence of OSAS in patients with depression. There was no significant difference among diagnosis rates as to individual risk factors or the number of risk factors. A multiple regression test showed no significant association between apnea–hypopnea index and other clinical factors including depression severity. Conclusion: The present results showed that OSAS can be detected at a remarkably higher rate by considering appropriate OSAS risk factors in mood disorder patients, and suggested that there is a high rate of undetected and therefore untreated OSAS among mood disorder patients.

The aim of this study was to examine the effects of negative cognition on PBI score before and after treatment for depression. Forty major depressive disorder outpatients were assessed with the PBI scale and Structured Interview Guide for Hamilton Rating Scale for Depression (SIGH-D) at the time of the first medical examination (baseline) and 8 weeks later. The SIGH-D scores decreased by about 50% from baseline to 8 weeks, but there was no significant change in the PBI scores of the depressed outpatients from baseline to 8 weeks. Analysis of covariance with the SIGH-D scores as covariate was conducted for PBI scores between baseline and 8 weeks to remove effects of MDD. No significant differences were found on any of the PBI scales. Even though the therapeutic values on the SIGH-D of the depressed patients indicated that depressive symptoms were reduced by about 50%, depression level did not influence the PBI scores. This study provides evidence for the stability of parental representations throughout treatment, as measured by the PBI.