Cognitive and anatomical correlates of anosognosia in amnestic mild cognitive impairment and early-stage Alzheimer's disease.

BACKGROUND: Anosognosia is a common feature in Alzheimer's disease (AD). The brain substrates of anosognosia are not fully understood, and less is known about the cognitive substrates of anosognosia in prodromal and early stages of AD. METHODS: Fourty-seven patients with amnestic-type mild cognitive impairment (aMCI) (n = 26) and early-stage AD (n = 21) were included, and Clinical Insight Rating Scale and Anosognosia Questionnaire for Dementia (AQ-D) were used to assess anosognosia. A detailed neuropsychological battery was administered; each patient underwent a structural magnetic resonance imaging (MRI). Correlation between anosognosia and performance in individual cognitive domains as well as correlation between anosognosia and cortical thickness values in regions of interest were assessed. RESULTS: Performance of the anosognosic patients in Digit Ordering Test (DOT), Digit Span Backwards, and Clock Drawing Test (CDT) was significantly worse compared to non-anosognosic patients in the total study population and in the aMCI subgroup but not in AD group. AQ-D scores negatively correlated with Mini-Mental State Examination (MMSE), California Verbal Learning Test (CVLT), Digit Span Backwards and CDT scores in total group and MMSE, CVLT, DOT, and Digit Span Backwards scores in the aMCI group. No significant correlations were found between cortical thickness measurements and AQ-D scores in any of the patient populations. CONCLUSIONS: Anosognosia was associated with episodic memory, working memory, and executive functions in the total population and aMCI group, but no association was found in early-stage AD patients. Anosognosia in the early stages of AD may be related with non-structural changes such as hypoconnectivity rather than structural changes.

Volumetric differences suggest involvement of cerebellum and brainstem in chronic migraine.

BACKGROUND: Chronic migraine (CM) is a disabling neurologic condition that often evolves from episodic migraine. There has been mounting evidence on the volumetric changes detected by magnetic resonance imaging (MRI) technique in migraineurs. These studies mainly focused on episodic migraine patients and less is known about the differences in CM patients. METHOD: A total of 24 CM patients and 24 healthy control individuals (all females) were included in this study. All participants underwent neurological examination and MRI. High-resolution anatomical MRI images were processed with an automated segmentation method (FreeSurfer). White-matter abnormalities of the brain were also evaluated with the Age-Related White-Matter-Changes Scale. RESULTS: The volumes of the cerebellum and brainstem were found to be smaller in CM patients compared to healthy controls. White-matter abnormalities were also found in CM patients, specifically in the bilateral parieto-occipital areas. There was no correlation between the clinical variables and volume decrease in these regions. CONCLUSION: CM patients showed significant volume differences in infratentorial areas and white-matter abnormalities in the posterior part of the brain. It is currently unclear whether the structural brain changes seen in migraine patients are the cause or the result of headaches. Longitudinal volumetric neuroimaging studies with larger groups, especially on the chronification of migraine, are needed to shed light on this topic.

Silent neurological involvement in biopsy-defined coeliac patients.

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.

Differentiating symptomatic Parkin mutations carriers from patients with idiopathic Parkinson's disease: contribution of automated segmentation neuroimaging method.

BACKGROUND: 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. METHOD: 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: 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. CONCLUSION: 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.