Structural Disconnection of the Tool Use Network after Left Hemisphere Stroke Predicts Limb Apraxia Severity.
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ABSTRACT:
SUBMITTER: Garcea FE
PROVIDER: S-EPMC7573742 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:ObjectiveTo investigate the role of multiple distributed brain networks, including the default mode, fronto-temporo-parietal, and cingulo-opercular networks, which mediate domain-general and task-specific processes during speech production after aphasic stroke.MethodsWe conducted an observational functional MRI study to investigate the effects of a previous left hemisphere stroke on functional connectivity within and between distributed networks as patients described pictures. Study design included various baseline tasks, and we compared results to those of age-matched healthy participants performing the same tasks. We used independent component and psychophysiological interaction analyses.ResultsAlthough activity within individual networks was not predictive of speech production, relative activity between networks was a predictor of both within-scanner and out-of-scanner language performance, over and above that predicted from lesion volume, age, sex, and years of education. Specifically, robust functional imaging predictors were the differential activity between the default mode network and both the left and right fronto-temporo-parietal networks, respectively activated and deactivated during speech. We also observed altered between-network functional connectivity of these networks in patients during speech production.ConclusionsSpeech production is dependent on complex interactions among widely distributed brain networks, indicating that residual speech production after stroke depends on more than the restoration of local domain-specific functions. Our understanding of the recovery of function following focal lesions is not adequately captured by consideration of ipsilesional or contralesional brain regions taking over lost domain-specific functions, but is perhaps best considered as the interaction between what remains of domain-specific networks and domain-general systems that regulate behavior.
| S-EPMC4826341 | biostudies-literature
Project description:Left hemispheric cerebral stroke can cause apraxia, a motor cognitive disorder characterized by deficits of higher-order motor skills such as the failure to accurately produce meaningful gestures. This disorder provides unique insights into the anatomical and cognitive architecture of the human praxis system. The present study aimed to map the structural brain network that is damaged in apraxia. We assessed the ability to perform meaningful gestures with the hand in 101 patients with chronic left hemisphere stroke. Structural white matter fibre damage was directly assessed by diffusion tensor imaging and fractional anisotropy mapping. We used multivariate topographical inference on tract-based fractional anisotropy topographies to identify white matter disconnection associated with apraxia. We found relevant pathological white matter alterations in a densely connected fronto-temporo-parietal network of short and long association fibres. Hence, the findings suggest that heterogeneous topographical results in previous lesion mapping studies might not only result from differences in study design, but also from the general methodological limitations of univariate topographical mapping in uncovering the structural praxis network. A striking role of middle and superior temporal lobe disconnection, including temporo-temporal short association fibres, was found, suggesting strong involvement of the temporal lobe in the praxis network. Further, the results stressed the importance of subcortical disconnections for the emergence of apractic symptoms. Our study provides a fine-grain view into the structural connectivity of the human praxis network and suggests a potential value of disconnection measures in the clinical prediction of behavioural post-stroke outcome.
| S-EPMC8833454 | biostudies-literature
Project description:When pantomiming the use of tools, patients with limb apraxia after left hemisphere stroke (LCVA) produce more spatiotemporal hand action errors with tools associated with conflicting actions for use versus grasp-to-pick-up (e.g., corkscrew) than tools having a single action for both use and grasp (e.g., hammer). There are two possible accounts for this pattern of results. Reduced performance with 'conflict' tools may simply reflect weakened automaticity of use action activation, which is evident only when the use and grasp actions are not redundant. Alternatively, poor use performance may reflect a reduced ability of appropriate tool use actions to compete with task-inappropriate action representations. To address this issue, we developed a Stroop-like experiment in which 21 LCVA and 8 neurotypical participants performed pantomime actions in blocks containing two tools that were similar ("neighbors") in terms of hand action or function, or were unrelated on either dimension. In a congruent condition, they pantomimed the use action associated with the visually presented tool, whereas in an incongruent condition, they pantomimed the use action for the other tool in the block. Relative to controls and other task conditions, LCVA participants showed reductions in hand action errors in incongruent relative to congruent action trials; furthermore, the degree of reduction in this incongruence effect was related to the participants' susceptibility to grasp-on-use conflict in a separate test of pantomime to the sight of tools. Support vector regression lesion-symptom mapping analyses identified the left inferior frontal gyrus, supramarginal gyrus, and superior longitudinal fasciculus as core neuroanatomical sites associated with abnormal performance. Collectively, the results indicate that weakened activation of tool use actions in limb apraxia gives rise to reduced ability of these actions to compete for task-appropriate selection when competition arises within single tools (grasp-on-use conflict) as well as between two tools (reduced neighborhood effects).
| S-EPMC6951425 | biostudies-literature
Project description:Increasing evidence indicates that focal lesions following stroke cause alterations in connectivity among functional brain networks. Functional connectivity between hemispheres has been shown to be particularly critical for predicting stroke-related behavioral deficits and recovery of motor function and attention. Much less is known, however, about the relevance of interhemispheric functional connectivity for cognitive abilities like praxis that rely on strongly lateralized brain networks. In the current study, we examine correlations between symptoms of apraxia-a disorder of skilled action that cannot be attributed to lower-level sensory or motor impairments-and spontaneous, resting brain activity in functional MRI in chronic left hemisphere stroke patients and neurologically-intact control participants. Using a data-driven approach, we identified 32 regions-of-interest in which pairwise functional connectivity correlated with two distinct measures of apraxia, even when controlling for age, head motion, lesion volume, and other artifacts: overall ability to pantomime the typical use of a tool, and disproportionate difficulty pantomiming the use of tools associated with different, competing use and grasp-to-move actions (e.g., setting a kitchen timer versus picking it up). Better performance on both measures correlated with stronger interhemispheric functional connectivity. Relevant regions in the right hemisphere were often homologous to left hemisphere areas associated with tool use and action. Additionally, relative to overall pantomime accuracy, disproportionate difficulty pantomiming the use of tools associated with competing use and grasp actions was associated with weakened functional connectivity among a more strongly left-lateralized and peri-Sylvian set of brain regions. Finally, patient performance on both measures of apraxia was best predicted by a model that incorporated information about lesion location and functional connectivity, and functional connectivity continued to explain unique variance in behavior even after accounting for lesion loci. These results indicate that interhemispheric functional connectivity is relevant even for a strongly lateralized cognitive ability like praxis and emphasize the importance of the right hemisphere in skilled action.
| S-EPMC6319198 | biostudies-literature
Project description:The neural mechanisms underlying recovery of language after left hemisphere stroke remain elusive. Although older evidence suggested that right hemisphere language homologues compensate for damage in left hemisphere language areas, the current prevailing theory suggests that right hemisphere engagement is ineffective or even maladaptive. Using a novel combination of support vector regression-based lesion-symptom mapping and voxel-based morphometry, we aimed to determine whether local grey matter volume in the right hemisphere independently contributes to aphasia outcomes after chronic left hemisphere stroke. Thirty-two left hemisphere stroke survivors with aphasia underwent language assessment with the Western Aphasia Battery-Revised and tests of other cognitive domains. High-resolution T1-weighted images were obtained in aphasia patients and 30 demographically matched healthy controls. Support vector regression-based multivariate lesion-symptom mapping was used to identify critical language areas in the left hemisphere and then to quantify each stroke survivor's lesion burden in these areas. After controlling for these direct effects of the stroke on language, voxel-based morphometry was then used to determine whether local grey matter volumes in the right hemisphere explained additional variance in language outcomes. In brain areas in which grey matter volumes related to language outcomes, we then compared grey matter volumes in patients and healthy controls to assess post-stroke plasticity. Lesion-symptom mapping showed that specific left hemisphere regions related to different language abilities. After controlling for lesion burden in these areas, lesion size, and demographic factors, grey matter volumes in parts of the right temporoparietal cortex positively related to spontaneous speech, naming, and repetition scores. Examining whether domain general cognitive functions might explain these relationships, partial correlations demonstrated that grey matter volumes in these clusters related to verbal working memory capacity, but not other cognitive functions. Further, grey matter volumes in these areas were greater in stroke survivors than healthy control subjects. To confirm this result, 10 chronic left hemisphere stroke survivors with no history of aphasia were identified. Grey matter volumes in right temporoparietal clusters were greater in stroke survivors with aphasia compared to those without history of aphasia. These findings suggest that the grey matter structure of right hemisphere posterior dorsal stream language homologues independently contributes to language production abilities in chronic left hemisphere stroke, and that these areas may undergo hypertrophy after a stroke causing aphasia.
| S-EPMC4990653 | biostudies-literature
Project description: Not available
| S-EPMC9217871 | biostudies-literature
Project description:This study aimed to quantify dynamic structural changes in the brain after subcortical stroke and identify brain areas that contribute to motor recovery of affected limbs. High-resolution structural MRI and neurological examinations were conducted at five consecutive time points during the year following stroke in 10 patients with left hemisphere subcortical infarctions involving motor pathways. Gray matter volume (GMV) was calculated using an optimized voxel-based morphometry technique, and dynamic changes in GMV were evaluated using a mixed-effects model. After stroke, GMV was decreased bilaterally in brain areas that directly or indirectly connected with lesions, which suggests the presence of regional damage in these "healthy" brain tissues in stroke patients. Moreover, the GMVs of these brain areas were not correlated with the Motricity Index (MI) scores when controlling for time intervals after stroke, which indicates that these structural changes may reflect an independent process (such as axonal degeneration) but cannot affect the improvement of motor function. In contrast, the GMV was increased in several brain areas associated with motor and cognitive functions after stroke. When controlling for time intervals after stroke, only the GMVs in the cognitive-related brain areas (hippocampus and precuneus) were positively correlated with MI scores, which suggests that the structural reorganization in cognitive-related brain areas may facilitate the recovery of motor function. However, considering the small sample size of this study, further studies are needed to clarify the exact relationships between structural changes and recovery of motor function in stroke patients.
| S-EPMC6869928 | biostudies-literature
Project description:Depending on the lesion site, a stroke typically affects various aspects of cognitive control. While executing a task, the performance monitoring system constantly compares an intended action plan with the executed action and thereby registers inaccurate actions in case of any mismatch. When errors occur, the performance monitoring system signals the need for more cognitive control, which is most efficient when the subject notices errors rather than processing them subconsciously. The current study aimed to investigate performance monitoring and error detection in a large sample of patients with left hemisphere (LH) stroke. In addition to clinical and neuropsychological tests, 24 LH stroke patients and 32 healthy age-matched controls performed a Go/Nogo task with simultaneous electroencephalography (EEG) measurements. This set-up enabled us to compare performance monitoring at the behavioral and the neural level. EEG data were analyzed using event-related potentials [ERPs; e.g., the error-related negativity (Ne/ERN) and error positivity (Pe)] and additionally more sensitive whole-brain multivariate pattern classification analyses (MVPA). We hypothesized that LH stroke patients would show behavioural deficits in error detection when compared to healthy controls, mirrored by differences in neural signals, in particular reflected in the Pe component. Interestingly, despite clinically relevant cognitive deficits (e.g., aphasia and apraxia) including executive dysfunction (trail making test), we did not observe any behavioral impairments related to performance monitoring and error processing in the current LH stroke patients. Patients also showed similar results for Ne/ERN and Pe components, compared to the control group, and a highly similar prediction of errors from multivariate signals. ERP abnormalities during stimulus processing (i.e., N2 and P3) demonstrated the specificity of these findings in the current LH stroke patients. In contrast to previous studies, by employing a relatively large patient sample, a well-controlled experimental paradigm with a standardized error signaling procedure, and advanced data analysis, we were able to show that performance monitoring (of simple actions) is a preserved cognitive control function in LH stroke patients that might constitute a useful resource in rehabilitative therapies for re-learning impeded functions.
| S-EPMC7306623 | biostudies-literature
Project description: Not available
| S-EPMC11338304 | biostudies-literature
Project description:Trans-neuronal propagation of mutant huntingtin protein contributes to the organised spread of cortico-striatal degeneration and disconnection in Huntington's disease (HD). We investigated whether the network diffusion model, which models transneuronal spread as diffusion of pathological proteins via the brain connectome, can determine the severity of neural degeneration and disconnection in HD. We used structural magnetic resonance imaging (MRI) and high-angular resolution diffusion weighted imaging (DWI) data from symptomatic Huntington's disease (HD) (N = 26) and age-matched healthy controls (N = 26) to measure neural degeneration and disconnection in HD. The network diffusion model was used to test whether disease spread, via the human brain connectome, is a viable mechanism to explain the distribution of pathology across the brain. We found that an eigenmode identified in the healthy human brain connectome Laplacian matrix, accurately predicts the cortico-striatal spatial pattern of degeneration in HD. Furthermore, the spread of neural degeneration from sub-cortical brain regions, including the accumbens and thalamus, generates a spatial pattern which represents the typical neurodegenerative characteristics in HD. The white matter connections connecting the nodes with the highest amount of disease factors, when diffusion based disease spread is initiated from the striatum, were found to be most vulnerable to disconnection in HD. These findings suggest that trans-neuronal diffusion of mutant huntingtin protein across the human brain connectome may explain the pattern of gray matter degeneration and white matter disconnection that are hallmarks of HD.
| S-EPMC6865500 | biostudies-literature