105 research outputs found

    Rule violation errors are associated with right lateral prefrontal cortex atrophy in neurodegenerative disease

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    Good cognitive performance requires adherence to rules specific to the task at hand. Patients with neurological disease often make rule violation errors, but the anatomical basis for rule violation during cognitive testing remains debated. The current study examined the neuroanatomical correlates of rule violation (RV) errors made on tests of executive functioning in 166 subjects diagnosed with neurodegenerative disease or as neurologically healthy. Specifically, RV errors were voxel-wisely correlated with gray matter volume derived from high-definition MR images using voxel-based morphometry implemented in SPM2. Latent variable analysis showed that rule violation errors tapped a unitary construct separate from repetition errors. This analysis was used to generate factor scores to represent what is common among rule violation errors across tests. The extracted rule violation factor scores correlated with tissue loss in the lateral middle and inferior frontal gyri and the caudate nucleus bilaterally. When a more stringent control for global cognitive functioning was applied using Mini Mental State Exam scores, only the correlations with the right lateral prefrontal cortex remained significant. These data underscore the importance of right lateral prefrontal cortex in behavioral monitoring and highlight the potential of rule violation error assessment for identifying patients with damage to this region

    Visuospatial Functioning In The Primary Progressive Aphasias

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    Objectives: The aim of this study was to identify whether the three main primary progressive aphasia (PPA) variants would show differential profiles on measures of visuospatial cognition. We hypothesized that the logopenic variant would have the most difficulty across tasks requiring visuospatial and visual memory abilities. Methods: PPA patients (n = 156), diagnosed using current criteria, and controls were tested on a battery of tests tapping different aspects of visuospatial cognition. We compared the groups on an overall visuospatial factor; construction, immediate recall, delayed recall, and executive functioning composites; and on individual tests. Cross-sectional and longitudinal comparisons were made, adjusted for disease severity, age, and education. Results: The logopenic variant had significantly lower scores on the visuospatial factor and the most impaired scores on all composites. The nonfluent variant had significant difficulty on all visuospatial composites except the delayed recall, which differentiated them from the logopenic variant. In contrast, the semantic variants performed poorly only on delayed recall of visual information. The logopenic and nonfluent variants showed decline in figure copying performance over time, whereas in the semantic variant, this skill was remarkably preserved. Conclusions: This extensive examination of performance on visuospatial tasks in the PPA variants solidifies some previous findings, for example, delayed recall of visual stimuli adds value in differential diagnosis between logopenic variant PPA and nonfluent variant PPA variants, and illuminates the possibility of common mechanisms that underlie both linguistic and non-linguistic deficits in the variants. Furthermore, this is the first study that has investigated visuospatial functioning over time in the PPA variants

    Altered topology of the functional speech production network in non-fluent/agrammatic variant of PPA

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    Non-fluent/agrammatic primary progressive aphasia (nfvPPA) is caused by neuro-degeneration within the left fronto-insular speech and language production network (SPN). Graph theory is a branch of mathematics that studies network architecture (topology) by quantifying features based on its elements (nodes and connections). This approach has been recently applied to neuroimaging data to explore the complex architecture of the brain connectome, though few studies have exploited this technique in PPA. Here, we used graph theory on functional MRI resting state data from a group of 20 nfvPPA patients and 20 matched controls to investigate topological changes in response to focal neuro-degeneration. We hypothesized that changes in the network architecture would be specific to the affected SPN in nfvPPA, while preserved in the spared default mode network (DMN). Topological configuration was quantified by hub location and global network metrics. Our findings showed a less efficiently wired and less optimally clustered SPN, while no changes were detected in the DMN. The SPN in the nfvPPA group showed a loss of hubs in the left fronto-parietal-temporal area and new critical nodes in the anterior left inferior-frontal and right frontal regions. Behaviorally, speech production score and rule violation errors correlated with the strength of functional connectivity of the left (lost) and right (new) regions respectively. This study shows that focal neurodegeneration within the SPN in nfvPPA is associated with network-specific topological alterations, with the loss and gain of crucial hubs and decreased global efficiency that were better accounted for through functional rather than structural changes. These findings support the hypothesis of selective network vulnerability in nfvPPA and may offer biomarkers for future behavioral intervention

    Visuospatial and visual object cognition in early Parkinson's disease

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    Recent evidence suggests that Parkinson's disease (PD) may be associated with greater impairment in visuospatial working memory as compared to visual object working memory. The nature of this selective impairment is not well understood, however, in part because successful performance on working memory tasks requires numerous cognitive processes. For example, the impairment may be limited to either the encoding or maintenance aspects of spatial working memory. Further, it is unknown at this point whether PD patients' selective impairment in spatial working memory generalizes to other tasks of spatial cognition. The present study investigated these issues by comparing the performance of nondemented patients with PD and normal control participants on a series of experiments that were designed to independently evaluate visuospatial and visual object cognition. Experiment 1 was composed of working memory conditions that differed only in what the participant was instructed to remember: locations or shapes. Encoding and maintenance aspects of performance were investigated by measuring accuracy over variable delays. Experiment 2 used an inhibition of return (IOR) task that has been demonstrated to measure spatial- and object-based components of inhibitory attention. Experiment 3 was composed of analogous location and shape discrimination conditions that did not have a working memory component. Group differences on the individual experiments were analyzed using repeated measures analysis of variance designs to test the overarching hypothesis that spatial-based cognition is more impaired than object- based cognition in PD. In Experiment 1, the patients demonstrated impairment in the encoding of spatial-based information, but were able to normally maintain that information over a 10-second delay. The reverse pattern was observed on the object working memory condition in that only maintenance processes were impaired. In Experiment 2, the patients also demonstrated a selective spatial impairment in that they showed reduced spatial- based IOR, while object-based IOR was intact. The results of Experiment 3 revealed that spatial-based visual discrimination was not more impaired than object-based visual discrimination, indicating that selective spatial deficits on higher-level visuocognitive tasks cannot be entirely attributed to a general impairment in spatial cognition. Rather, the selective spatial deficit appears to be limited to encoding and inhibitory attentional processe
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