Akira Osone

Introduction: Two reserve hypotheses have been proposed to account for the observed disjunction between the degree of brain pathology and its clinical manifestations. This study investigated whether cognitive reserve (CR), taken here as educational attainment and premorbid IQ, or brain reserve (BR; i.e., brain volume) is associated with progression and regression in patients with mild cognitive impairment (MCI) over a 12-month follow-up. Method: Patients with MCI (n = 123) were prospectively enrolled. The Mini-Mental State Examination, the Japanese version of the Cognitive subscale of the Alzheimer’s Disease Assessment Scale, the Clinical Dementia Rating (CDR), the Frontal Assessment Battery, the Neuropsychiatric Inventory, magnetic resonance imaging (MRI), and quantitative single-photon emission computed tomography were performed at intake and again at 12-month follow-up. Patients were classified into three groups: no change, conversion, and reversion. Conversion was defined as a change in CDR from 0.5 to 1, and reversion as a change from 0.5 to 0. Results: Voxel-based morphometry MRI revealed no significant differences in entorhinal and hippocampal gray matter loss among the groups. Patients with reversion had higher premorbid IQ (p = .03, η_p² = .35) as measured by the Japanese version of the National Adult Reading Test, higher atrophy ratio (hippocampal volume/whole brain volume; p = .04, η_p² = .89) at baseline, and better cognitive performance (p < .001) during the 12-month follow-up than those with conversion did. There were no statistically significant differences among the three groups in terms of years of education. Conclusion: Multinomial logistic regression analysis revealed that higher CR contributed to protecting against cognitive decline during the 12-month follow-up, whereas higher BR at baseline was the strongest predictor for reversion and conversion.

Objective: The objective of the study is to investigate whether the lifestyle‐related disease (LSRD) hypertension, type II diabetes mellitus, and lipid abnormality are associated with conversion and reversion in patients with mild cognitive impairment (MCI) over 12 months of follow‐up.Methods: One hundred and thirteen patients with MCI were prospectively enrolled and longitudinally assessed. Methods used include mini‐mental state examination, the Japanese version of the cognitive subscale of the Alzheimer's Disease Assessment Scale, the Clinical Dementia Rating, the Frontal Assessment Battery, the Neuropsychiatric Inventory, magnetic resonance imaging, and quantitative single‐photon emission computed tomography. In addition, laboratory examinations of glucose and lipids were also performed. All measurements were performed at first intake and again at the end of the 12‐month follow‐up. Conversion was identified as a change in Clinical Dementia Rating from 0.5 to 1 and reversion as a change from 0.5 to 0.Results: Patients with MCI with reversion had lower comorbid lipid abnormality at baseline and higher cognitive and behaviour function across the 12‐month follow‐up compared with those with no change or conversion. Patients without comorbid LSRD had lower systolic pressure and lower glucose and triglyceride levels at baseline, as well as less cognitive decline compared with other groups across the follow‐up period.Conclusions: The absence of lipid abnormality at baseline may contribute to reversion in patients with MCI. The presence of multiple LSRD was associated with cognitive decline. Our results highlight the contribution of multiple LSRD on increasing conversion and decreasing reversion in patients with MCI. Copyright © 2015 John Wiley & Sons, Ltd.

Aim: The present study aimed to investigate whether cognitive reserve (CR), referring here to education and premorbid intelligence (IQ), is associated with the risk for progression from mild cognitive impairment (MCI) to Alzheimer's disease (AD).Methods: A total of 51 patients with MCI and 59 patients with AD were prospectively enrolled for assessment with the Mini‐Mental State Examination, the Japanese version of the cognitive subscale of the Alzheimer's Disease Assessment Scale, the Japanese version of the Nelson Adult Reading Test (JART), magnetic resonance imaging (MRI) and single‐photon emission computed tomography (SPECT), adjusting for sex, age at diagnosis, age at onset and duration of illness.Results: SPECT findings showed hypoperfusion in the posterior cingulate gyri and precunei, suggesting that the participants were in the early or mild stage of AD or MCI. Voxel‐based morphometry MRI showed no statistical differences between the two groups in gray matter loss in the entorhinal and hippocampal areas; however, multiple logistic regression analysis showed a significant difference in premorbid IQ measured with JART.Conclusion: Despite the limitations of the cross‐sectional design, the findings suggest that premorbid intellectual function might explain the discrepancy in clinical status between MCI and AD patients with a similar magnitude of brain pathology and comorbid medical disorders. Geriatr Gerontol Int 2015; 15: 428–434.

Cases of acute pancreatitis caused by sodium valproate (VPA) have been reported by many authors thus far. However, most of these were cases with epilepsy. Chronic renal failure is also regarded as a risk factor for acute pancreatitis. Here, we report a case of acute pancreatitis development due to VPA in a patient with bipolar disorder on hemodialysis for chronic renal failure. The patient was a 52-year-old Japanese male who was diagnosed as bipolar disorder on hemodialysis for renal failure. He was treated with VPA and manic symptoms gradually stabilized. However, the patient complained of severe abdominal pain. Blood amylase was found to be markedly high, and computed tomography revealed pancreatomegaly and an increased amount of peripancreatic fat. Hence, we diagnosed the case as acute pancreatitis caused by VPA. We discontinued oral medication, and he was started on a pancreatic enzyme inhibitor, antibiotics, and transfusion, and he showed improvement. It has been reported that acute pancreatitis induced by VPA is caused by intermediate metabolites of VPA. We consider that patients with renal failure are prone to pancreatitis caused by VPA because of the accumulation of these intermediate metabolites. We need close monitoring for serious adverse effects such as pancreatitis when we prescribe VPA to patients with bipolar disorder on hemodialysis for chronic renal failure, although VPA is safer than other mood stabilizers.