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<p>Lesion-symptom mapping studies have generally focused on associations between behavioral deficits and grey matter damage, though there is also recognition that white matter damage contributes to language impairment following left hemisphere stoke. White matter damage can be measured with a continuous variable (i.e., percentage of the white matter tract that has been destroyed by the lesion, known as “lesion load”) or a binary variable – whether the lesion has severed the tract producing a structural disconnection. Recently, Hope et al (2016) demonstrated that high lesion load does not always lead to white matter tact disconnection, and vice versa. Further, Hope et al. found that a simple binary estimate of structural disconnection explained more of the variance in fluency and naming scores than did lesion load. In the current study, we attempt to replicate and extend this finding by examining lesion load and tract disconnection in three white matter tracts that have been implicated in language processing: arcuate fasciculus, uncinate fasciculus, and inferior fronto-occipital fasciculus (IFOF) using a different sample of stroke patients and language measures. </p>
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