| Literature DB >> 34902680 |
Abstract
The size of brain lesions is a variable that is frequently considered in cognitive neuropsychology. In particular, lesion-deficit inference studies often control for lesion size, and the association of lesion size with post-stroke cognitive deficits and its predictive value are studied. In the present article, the role of lesion size in cognitive deficits and its computational or design-wise consideration is discussed and questioned. First, I argue that the commonly discussed role or effect of lesion size in cognitive deficits eludes us. A generally valid understanding of the causal relation of lesion size, lesion location, and cognitive deficits is unachievable. Second, founded on the theory of causal inference, I argue that lesion size control is no generally appropriate covariate control. Instead, it is identified as a procedure with only situational benefits, which is supported by empirical data. This theoretical background is used to suggest possible research practices in lesion-deficit inference, post-stroke outcome prediction, and behavioural studies. Last, control for lesion size is put into a bigger historical context - it is identified to relate to a long-known association problem in neuropsychology, which was previously discussed from the perspectives of a mislocalisation in lesion-deficit mapping and the symptom complex approach.Entities:
Keywords: Covariate control; Lesion volume; Lesion–deficit prediction; Stroke; Voxel-based lesion symptom mapping
Mesh:
Year: 2021 PMID: 34902680 DOI: 10.1016/j.cortex.2021.11.005
Source DB: PubMed Journal: Cortex ISSN: 0010-9452 Impact factor: 4.027