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1 ization, as they were evoked only in the non-dominant hemisphere.
2 iability in language localization within the dominant hemisphere.
3 in the effect of cTBS on the dominant or non-dominant hemisphere.
4 pread and marked cortical decreases over the dominant hemisphere.
5 erall accelerated degradative process in the dominant hemisphere.
6 rocessing is strongly lateralized to the non-dominant hemisphere.
7 nd the primary motor cortex (M1) of the left-dominant hemisphere.
8 and asymmetric predilection for the language-dominant hemisphere?
9 by perisylvian cortex in the left (language-dominant) hemisphere, and thus, left anterior temporal l
10 suggest that networked brain regions in the dominant hemisphere are critical for maintaining an adap
12 cortical metabolism in a pilot study of the dominant hemisphere in 9 control subjects and provide es
14 es showed lower values of NAA and Glx in the dominant hemisphere in all three groups but values of cr
15 es of creatine were selectively lower in the dominant hemisphere of only the presymptomatic patients.
16 ere, we show that resections in the language dominant hemisphere of patients with epilepsy reduce lym
18 ion of the perisylvian areas of the language-dominant hemisphere) offers novel insights into the rela
21 adult patient with low grade glioma (LGG) in dominant hemisphere suggest brain plasticity process wit
22 y pathology was more intense in the language-dominant hemisphere, the Braak pattern of hippocampo-ent
23 ated with asymmetric atrophy in the language-dominant hemisphere (usually left), and differs from typ
24 ent polarities of cTBS over dominant and non-dominant hemisphere we delivered AP-PA and postero-anter
25 mporal cortex, these encoding changes in the dominant hemisphere were more likely to be polymodal, wh
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