Assessment of Mild Cognitive Impairment Using CogEvo: A Computerized Cognitive Function Assessment Tool.

INTRODUCTION/OBJECTIVES: To assess the utility of the computerized cognitive function assessment tool, CogEvo, as a screening tool for mild cognitive impairment in primary care, we explored the relationship between CogEvo performance, age, and the severity of cognitive dysfunction evaluated by the Mini-Mental State Examination (MMSE). METHODS: The observational cross-sectional study included 209 individuals' data (mean age 79.4 ± 8.9 years). We conducted a correlation analysis between CogEvo and MMSE scores, compared the performance among the 3 cognitive function groups (MMSE ≥ 28 group; MMSE24-27 group; MMSE ≤ 23 group) using the MMSE cut-off, and evaluated CogEvo's predictive accuracy for cognitive dysfunction through ROC analysis. RESULTS: Both total CogEvo and MMSE scores significantly decreased with age. A significant positive correlation was observed between total CogEvo and MMSE scores, but a ceiling effect was detected in MMSE performance. Significant differences were observed in the total CogEvo score, including orientation and spatial cognitive function scores, among the 3 groups. CogEvo showed no educational bias. ROC analyses indicated moderate discrimination between the MMSE ≥ 28 group and the MMSE24-27 and MMSE ≤ 23 groups. CONCLUSIONS: The computer-administered CogEvo has the advantage of not exhibiting ceiling effects or educational bias like the MMSE, and was found to be able to detect age-related cognitive decline and impairment.

Three-dimensional wall-thickness distributions of unruptured intracranial aneurysms characterized by micro-computed tomography.

Aneurysmal rupture is associated with wall thinning, but the mechanism is poorly understood. This study aimed to characterize the three-dimensional wall-thickness distributions of unruptured intracranial aneurysms. Five aneurysmal tissues were investigated using micro-computed tomography. First, the wall thickness was related to the aneurysmal wall appearances during surgery. The median wall thicknesses of the translucent and non-translucent walls were 50.56 and 155.93 µm, respectively (p < 0.05) with significant variation in the non-translucent wall thicknesses (p < 0.05). The three-dimensional observations characterized the spatial variation of wall thicknesses. Thin walls showed a uniform thickness profile ranging from 10 to 40 µm, whereas thick walls presented a peaked thickness profile ranging from 300 to 500 µm. In transition walls, the profile undulated due to the formation of focal thin/thick spots. Overall, the aneurysmal wall thicknesses were strongly site-dependent and spatially varied by 10 to 40 times within individual cases. Aneurysmal walls are exposed to wall stress driven by blood pressure. In theory, the magnitude of wall stress is inversely proportional to wall thickness. Thus, the observed spatial variation of wall thickness may increase the spatial variation of wall stress to a similar extent. The irregular wall thickness may yield stress concentration. The observed thin walls and focal thin spots may be caused by excessive wall stresses at the range of mechanical failure inducing wall injuries, such as microscopic tears, during aneurysmal enlargement. The present results suggested that blood pressure (wall stress) may have a potential of acting as a trigger of aneurysmal wall injury.

Association of bleb formation with peri-aneurysmal contact in unruptured intracranial aneurysms.

The mechanism of bleb formation in unruptured intracranial aneurysms (UIAs) remains unclear. This study aimed to investigate the association between peri-aneurysmal contact (PAC) and bleb formation. Forty-five aneurysms were classified depending on the presence of blebs and PAC using computed tomographic angiography and magnetic resonance imaging. Aneurysmal hemodynamics were assessed using computational fluid dynamics. The independent variables associated with bleb formation were statistically assessed. Fourteen aneurysms (31.1%) had blebs, all of which were located at the site of PAC (group A). Thirty-one aneurysms (68.9%) had no bleb, of which 13 had a PAC (group B) and 18 had no PAC (group C). PAC was the only independent variable associated with bleb formation (p < 0.05). Aneurysmal volumes were significantly higher in group A, followed by groups B and C in series. Aneurysmal wall shear stress (WSS) tended to be lowest in group A, followed by groups B and C in series. The maximum WSS at the blebs was only 17% of the maximum WSS at the aneurysmal domes. This study demonstrated that bleb formation in UIAs was associated with the establishment of PAC during their growth, which may have more detrimental effects on bleb formation than hemodynamics.

Impaired perception of illusory contours and cortical hypometabolism in patients with Parkinson's disease.

Neuroimaging evidence suggests that areas of the higher-order visual cortex, including the lateral occipital complex (LOC), are engaged in the perception of illusory contours; however, these findings remain unsubstantiated by human lesion data. Therefore, we assessed the presentation time necessary to perceive two types of illusory contours formed by Kanizsa figures or aligned line ends in patients with Parkinson's disease (PD). Additionally, we used 18F-fluorodeoxyglucose positron emission tomography (FDG-PET) to measure regional cerebral glucose metabolism in PD patients. Although there were no significant differences in the stimulus durations required for perception of illusory contours formed by aligned line ends between PD patients and controls, PD patients required significantly longer stimulus durations for the perception of Kanizsa illusory figures. Difficulty in perceiving Kanizsa illusory figures was correlated with hypometabolism in the higher-order visual cortical areas, including the posterior inferior temporal gyrus. These findings indicate an association between dysfunction in the posterior inferior temporal gyrus, a region corresponding to a portion of the LOC, and impaired perception of Kanizsa illusory figures in PD patients.

Attentional set-shifting deficit in Parkinson's disease is associated with prefrontal dysfunction: an FDG-PET study.

The attentional set-shifting deficit that has been observed in Parkinson's disease (PD) has long been considered neuropsychological evidence of the involvement of meso-prefrontal and prefrontal-striatal circuits in cognitive flexibility. However, recent studies have suggested that non-dopaminergic, posterior cortical pathologies may also contribute to this deficit. Although several neuroimaging studies have addressed this issue, the results of these studies were confounded by the use of tasks that required other cognitive processes in addition to set-shifting, such as rule learning and working memory. In this study, we attempted to identify the neural correlates of the attentional set-shifting deficit in PD using a compound letter task and 18F-fluoro-deoxy-glucose (FDG) positron emission tomography during rest. Shift cost, which is a measure of attentional set-shifting ability, was significantly correlated with hypometabolism in the right dorsolateral prefrontal cortex, including the putative human frontal eye field. Our results provide direct evidence that dysfunction in the dorsolateral prefrontal cortex makes a primary contribution to the attentional set-shifting deficit that has been observed in PD patients.

Illusory misidentifications and cortical hypometabolism in Parkinson's disease.

Idiopathic Parkinson's disease (PD) is associated with documented impairments in various visual functions. However, there have been only a limited number of studies that have reported on the brain regions responsible for impairment of visual recognition in PD. In our study, we evaluated the performance of PD patients and 24 healthy controls on the Poppelreuter-type overlapping figure identification test to investigate the impairment of visual recognition. We also measured the PD patients' resting cerebral glucose metabolism using (18) F-fluorodeoxyglucose positron emission tomography and investigated the relationship between the impairment of visual recognition and cortical hypometabolism. The PD patients had substantial and frequent illusory responses in the overlapping figure identification test, and their illusory misidentifications were correlated with hypometabolism in the visual cortices, including the right inferior temporal gyrus and the bilateral temporo-parieto-occipital junction. These findings suggest that PD patients have impaired visual recognition characterized by illusory misidentifications of visual stimuli, which could be attributed to dysfunction of the visual cortices.

Distinct patterns of regional cerebral glucose metabolism in Parkinson's disease with and without mild cognitive impairment.

There is no consensus with regard to the clinical and neuroimaging characteristics of prodromal dementia in Parkinson's disease (PD). To delineate functional neuroimaging features of PD with mild cognitive impairment (PDMCI) and with no cognitive impairment (PDNC), we compared regional cerebral glucose metabolism (CMRglc) amongst 13 patients with PDMCI, 27 with PDNC, and 13 healthy controls. The PDNC patients had limited areas of hypometabolism in the frontal and occipital cortices. In the PDMCI patients, there were extensive areas of hypometabolism in the posterior cortical regions, including the temporo-parieto-occipital junction, medial parietal, and inferior temporal cortices. The present results suggest that posterior cortical dysfunction is the primary neuroimaging feature of PD patients at risk for dementia.