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This study evaluated the association between metabolic syndrome as defined by Japanese criteria and its diagnostic components (visceral obesity, dyslipidemia, hypertension, and impaired glucose tolerance) and acute cerebral infarction in younger elderly (age 50-74 years) and the older elderly (age ≥75 years) persons living in the Japanese city of Kurashiki. We studied 73 patients aged ≥50 years (44 of them aged ≥75 years) admitted to our hospital with acute cerebral infarction and 323 control subjects aged ≥50 years (52 aged ≥75 years) who underwent medical checkup of the brain in our hospital. Types of cerebral infarction included atherothrombotic (27 patients), lacunar (24 patients), cardioembolic (19 patients), and other types (3 patients). Metabolic syndrome was defined based on the Japanese criteria. In multiple logistic regression analysis, among the 29 younger elderly patients aged 50-74 years, dyslipidemia, hypertension, and impaired glucose tolerance as diagnostic components of metabolic syndrome, and metabolic syndrome itself were significantly related to acute cerebral infarction (adjusted odds ratio [OR], 5.664, 4.869, 3.390, and 3.214, respectively). Among the 44 older elderly patients aged ≥75 years, dyslipidemia was significantly related to acute cerebral infarction (OR, 4.193). However, metabolic syndrome was not a significant risk factor for acute cerebral infarction, even when patients with cardioembolic and other types of infarction were excluded. These data suggest that metabolic syndrome as defined by Japanese criteria is an independent risk factor for acute cerebral infarction in the younger elderly, but not the older elderly, Kurashiki population.

pocampus. Apo e4 carrier state was known in 11 AD (ApoE3/ApoE4: 3/8) and 38 controls (ApoE3/ApoE4: 29/14). Entorhinal cortex (ERC), subiculum, CA1, CA1-CA2 transition zone (CA1-2 transition), CA3-4& dentate gyrus (CA3&DG) and total hippocampal volume were manually marked. Statistical analysis was done with multiple regression and stepwise discriminant analysis. Results: Compared to controls, AD had significantly smaller volumes of ERC (-28.4%), subiculum (-23.0%), CA1 (-20.2%), CA1-2 transition (-31.4%) and total hippocampal volumes (-19.1%). MCI had smaller CA1 (-14%) and CA1-2 transition (-26.1%) volumes. CA1-2 transition discriminated best between controls and MCI (Wilks’ Lambda 0.68, p 0.0001) and CA1-2 transition and ERC (Wilks’ Lambda 0.63, p 0.0001) between AD and control. ApoE4 exerted a negative effect on CA3&DG volumes in healthy controls (p 0.036) and in a mixed group of AD and controls (p 0.0003). In the latter group we also found a significant interaction between AD and ApoE4 (p 0.029). Conclusions: The patterns of subfield atrophy in AD and MCI were consistent with patterns of neuronal cell loss/ reduced synaptic density described in histopathologcal studies. ApoE4 effects were restricted to CA3&DG, i.e., the subfield capable of neurogenesis throughout adult life. These preliminary findings suggest that hippocampal subfield volumetry might be a better measure for diagnosis of early AD and for detection of other disease effects than measurement of total hippocampal volume.

Among Parkinson's disease (PD) patients complaining of pain, 10 with pain not associated with a motor fluctuation or L-dopa therapy were evaluated. The controls were 14 PD without pain and eight with thalamic pain syndrome. The threshold of pain and neurotransmitters in CSF were measured in the three groups. In PD with pain, the maximum tolerance level and tourniquet pain ratio decreased significantly. In PD with pain, the score on the self-depression scale increased significantly and S-hydroxy-indole acetic acid (5-HIAA) among the neurotransmitters decreased significantly. These results suggest that decreases in the threshold of pain and changes of serotonin in CSF are involved in the development of specific pain in PD who do not respond to L-dopa.