Lesion-Symptom Mapping: From Single Cases to the Human Disconnectome

Forkel, Stephanie J.

doi:10.1016/b978-0-12-819641-0.00056-6

Cited by 5 publications

(4 citation statements)

References 119 publications

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“…Our purpose was to depict which fiber tracts usually traverse the significant volume of voxels identified in the VLSM analysis as related to CPSP vs controls. This strategy to apply a lesion mask derived from lesion-symptom mapping into an atlas generated from healthy tractography reconstructions was used and validated 34 before to demonstrate WM disconnection 33 after stroke, including in patients with CPSP. 8 Therefore, significant voxels derived from the CPSP vs control VLSM comparison located in the WM were saved in an image (WM-Lesion) which was used as a seed to trace the fibers that normally cross that region.…”

Section: Methodsmentioning

confidence: 99%

Dissecting neuropathic from poststroke pain: the white matter within

Lemos¹,

Faillenot²,

Lucato³

et al. 2021

Pain

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Poststroke pain (PSP) is a heterogeneous term encompassing both central neuropathic (ie, central poststroke pain [CPSP]) and nonneuropathic poststroke pain (CNNP) syndromes. Central poststroke pain is classically related to damage in the lateral brainstem, posterior thalamus, and parietoinsular areas, whereas the role of white matter connecting these structures is frequently ignored. In addition, the relationship between stroke topography and CNNP is not completely understood. In this study, we address these issues comparing stroke location in a CPSP group of 35 patients with 2 control groups: 27 patients with CNNP and 27 patients with stroke without pain. Brain MRI images were analyzed by 2 complementary approaches: an exploratory analysis using voxel-wise lesion symptom mapping, to detect significant voxels damaged in CPSP across the whole brain, and a hypothesis-driven, region of interest-based analysis, to replicate previously reported sites involved in CPSP. Odds ratio maps were also calculated to demonstrate the risk for CPSP in each damaged voxel. Our exploratory analysis showed that, besides known thalamic and parietoinsular areas, significant voxels carrying a high risk for CPSP were located in the white matter encompassing thalamoinsular connections (one-tailed threshold Z . 3.96, corrected P value ,0.05, odds ratio 5 39.7). These results show that the interruption of thalamocortical white matter connections is an important component of CPSP, which is in contrast with findings from nonneuropathic PSP and from strokes without pain. These data can aid in the selection of patients at risk to develop CPSP who could be candidates to pre-emptive or therapeutic interventions.

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Section: Methodsmentioning

confidence: 99%

Dissecting neuropathic from poststroke pain: the white matter within

Lemos¹,

Faillenot²,

Lucato³

et al. 2021

Pain

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“…Predictive maps were visualized in a glass brain (using the niilearn Python library) and the positive Z-scores (which are associated to deficit) were also rendered as a mosaic of 2D slices using MRIcroGL 58 (http://www.nitrc.org/). An atlas-based approach 59 was used to label the clusters of predictive voxels. For the lesion map we used the Automated Anatomical Labeling (AAL) atlas (version 3) of gray matter structures 60 .…”

Section: Neuroimaging Data Analysismentioning

confidence: 99%

“…An atlas-based approach 59 was used to label the clusters of predictive voxels. For the lesion map we used the Automated Anatomical Labeling (AAL) atlas (version 3) of gray matter structures 60 .…”

Section: Multivariate Lesion and Structural Disconnection Symptom Map...mentioning

confidence: 99%

Susceptibility to multitasking in chronic stroke is associated to damage of the multiple demand system and leads to lateralized visuospatial deficits

Blini,

D’Imperio,

Romeo

et al. 2023

Preprint

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Functional impairment after stroke is related to the amount of brain damage but there is no strict correspondence between lesion and magnitude of the deficit or its recovery. Theoretical constructs such as cognitive or brain reserve have been invoked as unspecific protective factors to explain this mismatch. Here, we consider the opposite point of view, that is the instances in which this protection is lost or overturned. Several studies have shown - in domains encompassing sensory, motor, and cognitive deficits - that paradigms in which the inherent processing limits of the brain are stressed (e.g., by introducing multitasking and attentional load), are indeed capable to unveil the presence of deficits that are otherwise missed. We administered a computerized multitasking paradigm to a sample of 46 consecutive patients with first-ever unilateral subacute to chronic stroke and no sign of lateralized spatial-attentional disorders according to established diagnostic tests. We then used cluster analysis to classify patients, in a purely data-driven manner, according to their multivariate pattern of performance across different conditions (e.g., single- vs dual-tasking, ipsi- vs. contra-lesional stimuli). This enabled us to identify, within a group of putatively spared patients, a cluster of individuals presenting with stark contralesional biases of spatial awareness exclusively in conditions of concurrent attentional load, i.e. a phenotype characterised by high susceptibility to multitasking. This construct was also captured by a latent factor obtained from principal component analysis, providing a continuous susceptibility index across the whole sample. In spite of similar lesion volume, patients in the high susceptibility cluster presented worse performance in activities of daily living and neuropsychological tests evaluating domain-general abilities spanning attention, executive functions, and reasoning. Multivariate predictive modeling based on lesions location and structural disconnections revealed distinctive correlates of high sensitivity to multitasking in the Multiple-Demand (MD) System, a network of frontal and fronto-parietal areas subserving domain general processes. Damage in these areas may critically interact with domain-specific ones (e.g., devoted to spatial attention), resulting in subtle, but significant difficulties for patients in everyday life situations. In conclusion, the construct of susceptibility to multitasking has the promising potential to provide us a better understanding of what marks the passage, after brain damage, to clinically visible deficits.

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“…Advanced lesion-symptom mapping approaches allow for the identification of multiple regions (i.e., white and gray matter) that, when lesioned, are associated with lower performance in a particular domain. Importantly, voxel-based lesion-symptom mapping offers a more formal analysis of brain areas critical for a particular behavior when compared to other previously utilized lesion methods, such as the subtraction method, and use the same voxel-based procedures as functional neuroimaging data (e.g., Forkel, 2020). While original lesion-symptom mapping approaches utilized a mass-univariate approach (i.e., applying statistical methods on individual brain voxels), this approach has been shown to have several limitations, including an increased potential for false positives and variation in statistical values (e.g., Inoue et al, 2014;Mah et al, 2014;Nachev, 2015;Pustina et al, 2018;Sperber & Karnath, 2017).…”

Section: Factors Associated With Academic Skills Outcomesmentioning

confidence: 99%

Academic skills after brain injury: A lifespan perspective.

Sullivan¹,

Bowren²,

Bruss³

et al. 2022

Neuropsychology

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Objectives: This study investigated academic skills outcomes after brain injury and identified the influence of age and injury factors across the lifespan. Method: Our sample included 651 participants with focal brain lesions. Math, reading, and spelling data from the Wide Range Achievement Test (WRAT) were used as the academic skills outcomes. Age of lesion onset ranged from 0 to 85 years old. Linear regressions were conducted to identify the relation between age and injury factors and academic skills outcomes. Lesionsymptom mapping was conducted to identify the brain areas that, when lesioned, were associated with deficits in academic skills. Results: A quadratic model of age of lesion onset significantly predicted math (R 2 = .28, p < .001), reading (R 2 = .29, p < .001), and spelling outcomes (R 2 = .32, p < .001), while accounting for various covariates. Education, sex, lesion size and laterality, etiology, and seizure history were additional reliable predictors of academic skills outcomes across the lifespan. Academic skill deficits were associated with damage to various brain areas across the left-hemisphere frontal, temporal, and parietal lobes, the insular area, and left-and right-hemisphere white matter. Conclusions: This study supports age of lesion onset as a relevant predictor of academic skills after brain injury in a lifespan sample. Several other variables (e.g., education, sex, lesion characteristics, and seizure history) are notable in the prediction of outcomes across the lifespan. Future work could investigate more diverse samples and emphasize recruitment of early onset injuries to examine generalizability and potential critical periods for academic skills.

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Lesion-Symptom Mapping: From Single Cases to the Human Disconnectome

Cited by 5 publications

References 119 publications

Dissecting neuropathic from poststroke pain: the white matter within

Dissecting neuropathic from poststroke pain: the white matter within

Susceptibility to multitasking in chronic stroke is associated to damage of the multiple demand system and leads to lateralized visuospatial deficits

Academic skills after brain injury: A lifespan perspective.

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