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Fig. 3 | Neurological Research and Practice

Fig. 3

From: Anodal tDCS over left parietal cortex expedites recovery from stroke-induced apraxic imitation deficits: a pilot study

Fig. 3

Graphical illustration of the Cologne Apraxia Screening (KAS) total score (a, upper, left panel), the KAS imitation subscore (b, lower, left panel), the relative grip force of the contra-lesional, right hand (c, upper, right panel), and the scores of the short version of the Aphasia Check-List (ACL-K, d, lower, right panel) in the four patient groups with LH stroke across the three assessments (baseline assessment [T1, n = 30], post-stimulation assessment [T2, n = 30], and follow-up assessment [T3, n = 25]). LH stroke patients with apraxia (squares) undergoing anodal tDCS (green, A+ anodal) or sham tDCS (blue, A+ sham), LH stroke patients without apraxia (triangles) undergoing anodal tDCS (black, A- anodal) or sham tDCS (grey, A- sham). Displayed are the means and the standard error of the mean (SEM). a. Apraxic patients scored significantly lower on the KAS than patients without apraxia (§, significant main effects of APRAXIA F (1,26) = 6.6, p < .05). Furthermore, there was a significant interaction APRAXIA by TIME ($, F (1,26) = 6.7, p < .05), indicating that the KAS total scores of apraxic patients (KAS total score at baseline: 66.7 ± 12.1, KAS total score at post-stimulation: 71.6 ± 9.3) improved significantly more from baseline to post-stimulation than those of the non-apraxic patients (KAS total score at baseline: 78.1 ± 8.8, KAS total score at post-stimulation: 77.7 ± 2.2; t (28) = − 2.4, p < .05). b. For the scores of the imitation subtests of the KAS (KAS imi), the asterix (*) indicates the significant 3-way-interaction APRAXIA by TIME by STIMULATION (F (1,26) = 4.6, p < .05): The KAS imitation scores (maximum of 40 points) of apraxic patients who underwent anodal tDCS (green squares) improved significantly more from baseline to post-stimulation (from 31.6 ± 3.3 to 37.1 ± 2.3 points) than those of the apraxic patients undergoing sham tDCS (blue squares, from 32.4 ± 10.6 to 32.4 ± 7.9 points; t (18) = − 2.8, p < .05), while there was no significant modulation by stimulation nor relevant changes with time for the non-apraxic patients (non-apraxic, anodal [black triangles]: 39.6 ± 0.9 to 39.2 ± 1.8 points; non-apraxic, sham [grey triangles]: 38.8 ± 1.8 to 39.2 ± 1.1 points; t (8) = 0.65, p = 0.535). c. Independent of apraxia, there was a significant interaction TIME by STIMULATION (&, F (1,26) = 4.9, p < .05), indicating that the grip force levels of the contralesional, right hand significantly improved from baseline to post-stimulation in the stroke patients who underwent anodal tDCS, while no relevant changes were observed for the sham group (anodal tDCS group [green and black lines]: from 65.8 ± 37.9% to 73.5 ± 42.1%; sham tDCS group [blue and grey lines]: from 77.9 ± 29.7% to 75.6 ± 29.1%). Rel. GF_r = relative grip force of the contra-lesional right hand (in relation to the ipsi-lesional left hand, in %). d. There were no significant differential effects of tDCS on the ACL-K-scores, but a main effect of APRAXIA (#, F (1,26) = 4.6, p < .05), which indicated more severe aphasic deficits in the apraxic patients (squares, 25.5 ± 11.5) compared to patients without apraxia (triangles, 33.8 ± 6.3)

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