Publications (2)5.11 Total impact
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Article: Silent neurological involvement in biopsy-defined coeliac patients.
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ABSTRACT: Coeliac disease (CD) is an autoimmune disease of small intestine associated with sensitivity to gluten. The clinical manifestations are often of gastrointestinal nature, although the disease may be present asymptomatically as well. It is a chronic disease and in the absence of overt neurological involvement, extended gluten exposure may give rise to silent or subtle morphological and white-matter changes in central nervous system. The present study investigates such changes using brain volumetry and the assessment of white-matter tissue in CD patients without neurological symptoms. Seventeen CD patients without any neurological involvement were included in the study and went under neurological evaluation and anatomical MRI. Individual gray- and white-matter, and subcortical structure volumes were acquired for using automated volumetric analyses. The observed white-matter hyperintensities (WMH) evaluated using Age-Related White-Matter Changes scale. Findings show a bilateral decrease in cortical gray-matter and caudate nuclei volumes in CD compared to controls. Negative correlations were found between the duration of the disease and the volumes of the affected regions. Cerebellum was seemingly unaffected. In addition, significantly higher proportion of WMH was found in CD patients, specifically in bilateral frontal and occipitoparietal cortices. We observed a significant gray-matter and caudate nucleus atrophy in the CD patients in the absence of marked neurological symptoms. Present findings point out to a need for histopathological investigations potentially focusing on anti-TG2 antibodies, and serial volumetric analyses on the CD-related cortical and subcortical changes.Neurological Sciences 04/2013; · 1.32 Impact Factor -
Article: Differentiating symptomatic Parkin mutations carriers from patients with idiopathic Parkinson's disease: contribution of automated segmentation neuroimaging method.
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ABSTRACT: Parkin (PARK2) gene mutations are the predominant cause of autosomal recessive parkinsonism. Characteristic features include: early onset symptoms with slow clinical course, good response to low doses of levodopa, and frequently treatment-induced dyskinesia. Studies using a voxel-based morphometry approach showed a decrease in the gray matter volume of the basal ganglia in mutation carriers during the symptomatic stages. A bilateral, presumably compensatory increase of basal ganglia gray matter value was recently demonstrated in asymptomatic Parkin mutation carriers. Behavioral disorders including: anxiety, psychosis, panic attacks, depression, disturbed sexual, behavioral and obsessive-compulsive disorders have been reported in these patients. A total of 28 Parkinson's Disease (PD) patients consisting of 10 Young-Onset without Parkin mutations (YOPD), 9 Young-Onset with Parkin mutations (YOPD-p), 9 Late-Onset without Parkin mutations (LOPD) and 32 healthy control subjects were studied with an automated volumetric assessment method to quantify subcortical atrophy. Patients but not controls also underwent a neuropsychological and neuropsychiatric assessment. Results revealed a reduction of bilateral caudate nuclei volumes in YOPD-p patients compared to the YOPD patients while there were no statistically significant differences between other groups. YOPD-p patients showed similar results to other patient groups on neuropsychiatric and neuropsychological evaluation measures. YOPD-p and YOPD patients showed a different pattern of volume changes in basal ganglia. Despite its relatively benign clinical course, carrying the Parkin mutation seems to be associated with greater atrophy in subcortical structures. Failure of compensatory mechanisms, different mutation types and pathophysiologic processes may underlie this diverse pattern of subcortical brain changes.Parkinsonism & Related Disorders 03/2012; 18(5):562-6. · 3.80 Impact Factor
