[Show abstract][Hide abstract]ABSTRACT: Background and purposeRecent studies have demonstrated an association between increased insulin secretion and cognitive impairment. However, there is no previous study that directly evaluates the association between increased insulin secretion and cortical thickness to our knowledge. Therefore, our aim was to evaluate the effect of hyperinsulinemia, as measured by C-peptide level, on cortical thickness in a large sample of cognitively normal individuals.Methods
Cortical thickness was measured in 1093 patients who visited the Samsung Medical Health Promotion Center and underwent brain magnetic resonance imaging (MRI) and a blood test to measure C-peptide concentration. Automated surface-based analyses of the MRI data were used to measure cortical thickness. C-peptide levels were divided into quartiles for comparison. Patients in the first to third quartiles were used as the reference category.ResultsPatients in the highest quartile group (Q4) of C-peptide levels showed cortical thinning, predominantly in both medial temporal lobes, the right inferior temporal gyrus, both medial prefrontal lobes and the right superior parietal lobule, compared with the lower quartile groups (Q1–Q3) after controlling for age, gender, body mass index, history of hypertension, hyperlipidemia, previous stroke, cardiovascular disease and fasting glucose level.ConclusionsA higher C-peptide level is associated with regional cortical thinning, even in cognitively normal individuals.
Full-text Article · Jul 2014 · European Journal of Neurology
[Show abstract][Hide abstract]ABSTRACT: Background:
In healthy elderly people, silent brain infarctions (SBIs) have been recognized as common lesions. In this study, we evaluated the association between SBI located outside the perforating artery territory (PAT) and paradoxical embolism detected by agitated saline transcranial Doppler (TCD) monitoring in healthy subjects.
This was a prospective observational study undertaken by a university health promotion center for healthy subjects and by a university stroke center for acute stroke patients. We defined SBI as evidence on fluid-attenuation inversion recovery (FLAIR) magnetic resonance imaging (MRI) of one or more infarcts, without history of corresponding stroke or transient ischaemic attack. We also evaluated in all subjects the neuroimaging indicator of microangiopathy leukoaraiosis (LA). This study is registered with ClinicalTrials.gov, number NCT01429948.
Amongst 1103 consecutive healthy adults who underwent MRI, 347 (31%) had one or more SBIs located outside the PAT, suggesting embolism. Amongst them, 253 subjects underwent agitated saline TCD monitoring and 128 (51%) had right-to-left shunts (RLS). The prevalence of RLS was similar to cryptogenic embolic stroke (62.0%, P = 0.056), but higher than in patients with other stroke subtypes (36.2%, P = 0.021). Amongst subjects with SBI, absence of LA was the only factor associated with RLS (OR 1.78; 95% CI 1.01-3.14; P = 0.046).
Our results suggest that paradoxical embolism may play an important role in the development of SBI outside the PAT in apparently healthy adults.
Full-text Article · Sep 2012 · European Journal of Neurology
[Show abstract][Hide abstract]ABSTRACT: Uric acid (UA), a product of purine metabolism, is known to be reduced in patients with various neurological disorders including multiple sclerosis (MS). However, it has still remained unclear whether there is a close relationship between UA and neuromyelitis optica (NMO). The aim of this study was to investigate the association between serum UA levels and disease activity in NMO.
Retrospective analysis was made of blood samples during relapses (n = 48) and during stable disease (n = 49) from 20 patients with NMO. As controls, 59 blood samples during relapses from 39 patients with MS and 90 samples from healthy subjects were obtained. Spine magnetic resonance images (MRIs) performed during relapses (n = 24) in NMO were analysed.
The results indicated that UA levels during relapses in NMO were significantly lower compared to healthy subjects (P < 0.01), but not different from those during relapses in MS, and that reduced UA levels during relapses in NMO were normalized during stable disease. However, UA levels during relapses were not correlated with Gd enhancement in spine MRI.
UA levels are associated with clinical disease status in patients with NMO. Further investigations are recommended to elucidate the role of UA as a biomarker of disease activity in NMO.
Article · Feb 2012 · Acta Neurologica Scandinavica