I seem to be missing what possible use this is in getting survivors recovered.
Reclassifying stroke lesion anatomy
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Stroke is remarkable in the wide diversity of its cognitive and behavioural manifestations and the difficulty of predicting them from the contemporaneous clinical picture alone(Boyd et al., 2017; Stinear, 2017; Ward, 2017). This cardinal aspect impedes the management of individual patients, the identification of protective or exacerbating factors in the population, and the quantification of treatment doses and effects. Were this heterogeneity biologically impossible to capture, we could do no more than to accept it as an unalterable fact of life. But it arises from the interaction of two biological characteristics that are, at least in theory, accessible even if complex enough to appear suffused with randomness. The first is the functional anatomy of the brain focal ischaemic injury definitionally disrupts, now comprehensively established to be not only highly complex but also remarkably consistent across individuals: meta-analytic imaging databases would otherwise be filled with noise, not generalisable clusters of coherent activation (Biswal et al., 2010; Eickhoff et al., 2018; Glasser et al., 2016). The second is the structural anatomy of stroke: the product of pathological and anatomical factors that are plausibly both highly complex and non-random (Adams Jr et al., 1993; Amarenco et al., 2009; Mah, Husain, et al., 2014). The topology of the vascular tree, the mechanisms of occlusion or rupture, and the symptomatic eloquence2 of damaged brain will all combine to generate elaborate patterns of focal injury that will nonetheless conform to a potentially knowable spatial distribution (Figure 1). Since our knowledge of the functional anatomy of the brain depends to a great extent on the study of the functional consequences of stroke (Adolphs, 2016; Damasio & Damasio, 1989; Rorden & Karnath, 2004), the second of these characteristics is arguably of prior importance, and is our specific concern here.
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