NeuroImage. Clinical
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NeuroImage. Clinical · Jan 2020
ReviewWhy we should systematically assess, control and report somatosensory impairments in BCI-based motor rehabilitation after stroke studies.
The neuronal loss resulting from stroke forces 80% of the patients to undergo motor rehabilitation, for which Brain-Computer Interfaces (BCIs) and NeuroFeedback (NF) can be used. During the rehabilitation, when patients attempt or imagine performing a movement, BCIs/NF provide them with a synchronized sensory (e.g., tactile) feedback based on their sensorimotor-related brain activity that aims at fostering brain plasticity and motor recovery. The co-activation of ascending (i.e., somatosensory) and descending (i.e., motor) networks indeed enables significant functional motor improvement, together with significant sensorimotor-related neurophysiological changes. ⋯ This stresses the importance of also considering them and reporting them in the literature in BCI-based rehabilitation after stroke, especially since half of post-stroke patients suffer from somatosensory impairments. We argue that somatosensory abilities should systematically be assessed, controlled and reported if we want to precisely assess the influence they have on BCI efficiency. Not doing so could result in the misinterpretation of reported results, while doing so could improve (1) our understanding of the mechanisms underlying motor recovery (2) our ability to adapt the therapy to the patients' impairments and (3) our comprehension of the between-subject and between-study variability of therapeutic outcomes mentioned in the literature.
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NeuroImage. Clinical · Jan 2020
Computational quantification of brain perivascular space morphologies: Associations with vascular risk factors and white matter hyperintensities. A study in the Lothian Birth Cohort 1936.
Perivascular Spaces (PVS), also known as Virchow-Robin spaces, seen on structural brain MRI, are important fluid drainage conduits and are associated with small vessel disease (SVD). Computational quantification of visible PVS may enable efficient analyses in large datasets and increase sensitivity to detect associations with brain disorders. We assessed the associations of computationally-derived PVS parameters with vascular factors and white matter hyperintensities (WMH), a marker of SVD. ⋯ Computational measures reflecting individual PVS size, length and width were more strongly associated with WMH, stroke and hypertension than computational count or visual PVS score. Multidimensional computational PVS metrics may increase sensitivity to detect associations of PVS with risk exposures, brain lesions and neurological disease, provide greater anatomic detail and accelerate understanding of disorders of brain fluid and waste clearance.
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NeuroImage. Clinical · Jan 2020
Post-acute white matter microstructure predicts post-acute and chronic post-concussive symptom severity following mild traumatic brain injury in children.
Mild traumatic brain injury (TBI) is a global public health concern that affects millions of children annually. Mild TBI tends to result in subtle and diffuse alterations in brain tissue, which challenges accurate clinical detection and prognostication. Diffusion tensor imaging (DTI) holds promise as a diagnostic and prognostic tool, but little research has examined DTI in post-acute mild TBI. The current study compared post-acute white matter microstructure in children with mild TBI versus those with mild orthopedic injury (OI), and examined whether post-acute DTI metrics can predict post-acute and chronic post-concussive symptoms (PCS). ⋯ Post-acute white matter microstructure did not differ for children with mild TBI versus OI after correcting for multiple comparisons, but was predictive of post-acute and chronic PCS in both injury groups. These findings support the potential prognostic utility of this advanced DTI technique.
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Regional cortical thinning in dementia with Lewy bodies (DLB) and Parkinson disease dementia (PDD) may underlie some aspect of their clinical impairments; cortical atrophy likely reflects extensive Lewy body pathology with alpha-synuclein deposits, as well as associated Alzheimer's disease co-pathologies, when present. Here we investigated the topographic distribution of cortical thinning in these Lewy body diseases compared to cognitively normal PD and healthy non-PD control subjects, explored the association of regional thinning with clinical features and evaluated the impact of amyloid deposition. ⋯ The pattern of cortical thinning is similar in DLB and PD-associated cognitive impairment, overlapping with and extending beyond AD signature regions to involve fusiform, precentral, and paracentral regions. Cortical thinning in AD signature and fusiform regions in these diseases reflects cognitive impairment and is markedly accentuated by amyloid co-pathology. Further work will be required to determine whether the distinct topography of cortical thinning in DLB and PD-associated cognitive impairment might have value as a diagnostic and/ or outcome biomarker in clinical trials.
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Huntington's disease (HD) is a fatal genetic neurodegenerative disorder with no effective treatment currently available. Progressive basal ganglia and whole-brain atrophy and concurrent cognitive deterioration are prototypical aspects of HD. However, the specific patterns of brain atrophy underlying cognitive impairment of different severity in HD are poorly understood. The aim of this study was to investigate the specific structural brain correlates of major cognitive deficits in HD and to explore its association with neuropsychological indicators. ⋯ Major cognitive impairment in the range of dementia in HD is associated with brain and cognitive alterations exceeding the prototypical frontal-executive deficits commonly recognized in HD. The observed posterior-cortical damage identified by MRI and its association with memory, language, and visuoconstructive dysfunction suggest a strong involvement of extra-striatal atrophy in the onset of severe cognitive dysfunction in HD patients. Critically, major cognitive impairment in this sample was not associated with CAG repeat length, age or education. This finding could support a possible involvement of additional neuropathological mechanisms aggravating cognitive deterioration in HD.