132 Chapter 5 our findings, since we could relate eloquent functions to areas with an established role in that function. Tumor patients in lesion-symptom mapping Different factors could explain the minimal overlap in critical areas, even in brain areas with adequate lesion coverage in both groups. Some factors are inherent to lesion studies in general, others are etiology specific. First, both tumor and stroke have a systematic bias in lesion anatomy. For example, if region A and region B get blood supply from the same artery, a stroke in this artery will likely damage both regions. Suppose that only region A is causally related to the function under investigation, a lesion-symptom association for region B can be found as a mere side-effect.11,65,66 The possibility of collateral damage is higher when lesion size increases, irrespective of etiology. Thus, it is possible that some regions are associated with the behavioral deficit in one population but not the other, because of correlated damage occurring in one population only. Hence, the lesion-symptom association in question (region B) is not a causal relation. Second, several tumor-related factors could cause over- or underestimation of affected tissue. These include the possibility of functional reorganization, tumor invasion of apparently healthy tissue, and vice versa the possibility of functional tissue within the area demarked by abnormal MRI signal. Both temporal and spatial differences in activity have been observed in glioma-infiltrated cortex compared to healthy cortex during language tasks.15 This could indicate that glioma-infiltrated cortex also negatively impacts cognitive performance. Since our results indicated that on group level larger tumor lesions did not lead to worse cognitive performance compared to the smaller stroke lesions, this increases the likelihood of functional reorganization in our tumor group. However, in the current tumor sample a large proportion of patients had high-grade gliomas (38.7%), while the chance of functional reorganization or function preservation within the tumor area is highest in slowgrowing lesions, like low-grade glioma.18 Last, mass effect, shift and infiltration of white matter pathways, and increased intracranial pressure may cause noise in lesion-symptom associations. These effects do not always lead to destruction of structures, but impact lesion-symptom associations through spatial displacements that are specific for brain tumors, and may change over time.67 These tumor-related factors have been used as arguments against the use of tumor series in function localization. On the other hand, our study also clearly illustrates the advantage of using multiple etiologies. Firstly, the ability to investigate a broader range of brain structures unconstrained by the nonrandom lesion distribution inherent to
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