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Differentiating posterior cortical atrophy (PCA) from other diseases can be difficult and time‐consuming, and there is a particularly high possibility of misdiagnosis when psychiatrists diagnose complaints related to visual perception. Here, a case of PCA involving prominent visual perceptual disorders is reported; PCA was difficult to distinguish from psychogenic disturbance of vision in this case. For a year, a 59‐year‐old woman had had visual perceptual disorders, including a distorted view and prosopagnosia. She underwent examinations at multiple clinical departments at several medical institutions before receiving a definitive diagnosis of PCA. This PCA diagnosis was based on clinical symptoms, including Gerstmann syndrome, Bálint's syndrome, and transcortical sensory aphasia, and hypoperfusion in the occipital lobe observed on single‐photon emission computed tomography. This case was initially misdiagnosed as a psychogenic disease partly because characteristic clinical manifestations of PCA include visual agnosia with a disjunctive component. This patient displayed a disordered perception of stationary objects but an intact perception of moving objects. For example, she had to grope her way through a room at home, but she could visit a familiar hair salon on foot without hindrance. Behaviours like claiming to be blind while inexplicably moving without colliding with surrounding objects may lead to the misdiagnosis of PCA as a psychogenic or dissociative disorder involving histrionic or neurologically irrational symptoms with an expectation of sympathy or personal gain. It is critical to make every effort to exclude organic diseases, even in cases provisionally diagnosed as psychogenic disease. Despite its low prevalence, PCA should be considered a syndrome caused by Alzheimer's disease, dementia with Lewy bodies, or other dementias.

Aim It remains unclear how functional connectivity (FC) may be related to specific cognitive domains in neuropsychiatric disorders. Here we used simultaneous resting-state functional magnetic resonance imaging (rsfMRI) and electroencephalography (EEG) recording in patients with schizophrenia, to evaluate FC within and outside the default mode network (DMN). Methods Our study population included 14 patients with schizophrenia and 15 healthy control participants. From all participants, we acquired rsfMRI data, and simultaneously recorded EEG data using an MR-compatible amplifier. We analyzed the rsfMRI-EEG data, and used the CONN toolbox to calculate the FC between regions of interest. We also performed between-group comparisons of standardized low-resolution electromagnetic tomography-based intracortical lagged coherence for each EEG frequency band. Results FC within the DMN, as measured by rsfMRI and EEG, did not significantly differ between groups. Analysis of rsfMRI data showed that FC between the right posterior inferior temporal gyrus and medial prefrontal cortex was stronger among patients with schizophrenia compared to control participants. Conclusion Analysis of FC within the DMN using rsfMRI and EEG data revealed no significant differences between patients with schizophrenia and control participants. However, rsfMRI data revealed over-modulated FC between the medial prefrontal cortex and right posterior inferior temporal gyrus in patients with schizophrenia compared to control participants, suggesting that the patients had altered FC, with higher correlations across nodes within and outside of the DMN. Further studies using simultaneous rsfMRI and EEG are required to determine whether altered FC within the DMN is associated with schizophrenia.

Aim To evaluate the safety, tolerability and pharmacokinetic profile of bapineuzumab after a single intravenous injection in Japanese patients with mild to moderate Alzheimer's disease. Methods Participants received either a placebo (n = 8), or bapineuzumab 0.15 (n = 6), 0.5 (n = 6), 1.0 (n = 6) or 2.0 (n = 6) mg/kg. Serum concentrations of bapineuzumab, antibapineuzumab antibody and total plasma β-amyloidx-40 were assayed. Results Adverse events for bapineuzumab and placebo groups were 71% and 88%, respectively. Treatment-emergent adverse events (cataract, injection site hemorrhage, nasopharyngitis, pneumonia and muscle twitching) reported for ≥2 participants were mild or moderate in severity and unrelated to bapineuzumab dose. No deaths, serious adverse events or withdrawals were reported. Mean peak concentration for bapineuzumab increased with dose, from 3.3 ± 0.9 μg/mL with the 0.15 mg/kg dose to 61.0 ± 32.8 μg/mL with 2.0 mg/kg. Mean bapineuzumab exposure (area under the curve from time 0 to last measurable concentration; μg·h/mL) increased in a linear manner with increasing dose (mean 1260 for 0.15 mg/kg, 4264 for 0.5 mg/kg, 7818 for 1.0 mg/kg, 15 313 for 2.0 mg/kg). Mean half-life ranged from 15 to 28 days, and clearance was similar across dose groups (range 0.12–0.17 mL/h/kg). Conclusions Plasma β-amyloidx-40 levels increased with increasing doses of bapineuzumab. Bapineuzumab was safe and well tolerated at all doses in Japanese patients with mild to moderate Alzheimer's disease. Geriatr Gerontol Int 2016; 16: 644–650.

Herein, we report on a patient with spinocerebellar degeneration who exhibited subclinical rhythmic electrographic discharge of adults (SREDA). Thyrotropin-releasing hormone (TRH) improved the clinical symptoms and SREDA was observed only when administration of thyrotropin-releasing hormone was discontinued and the symptoms worsened. Furthermore, after resuming administration of taltirelin hydrate, a TRH analog, the improvement in motor function was accompanied by a decrease in delirium. It is plausible that taltirelin hydrate improved the distorted cerebral blood flow, which has been reported previously as the mechanism underlying SREDA, as a consequence of the functional improvement in neurotransmitter systems.