None of the patients or the control persons developed headache or motion sickness or reported individual symptoms associated with MA during or immediately after the study. Data analysis of the study population (n = 36) showed a bilateral activation (P ≤ .05; FWE-corrected; total of 24,974 voxels; max T value 17.37) of the striate and extrastriate visual cortex and the lateral geniculate body including complete regions corresponding to V1, V2, V3, V4, and V5 bilaterally. In the normal control group (n = 18), the Lumacaftor main cluster of activation was found in V1, V2, and V3 bilaterally as well as in the right V4 and V5 region (P ≤ .05; FWE-corrected; total of 4544 voxels; max T value 14.48; see Fig. 2 —a).

A separate cluster was also identified in the left V4 and V5 regions. Activation pattern showed a significant lateralization (P = .008) to the right hemisphere with a laterality index (SD) of 0.26 (±0.30). In the group consisting of MA patients, the pattern

of activation included a cluster corresponding to V1–V5 bilaterally (P ≤ .05; FWE-corrected; total of 11,401 voxels; max T value 22.17; see Fig. 2 —b). Activation in the left hemisphere was more pronounced than in controls; thus, lateralization was significant (P = .02), but less prominent than in the control group with a laterality index (SD) of 0.13 (±0.23). The LI was not significantly different between the groups (P = .168). Group analysis of MA patients vs controls revealed significantly Nutlin-3 molecular weight increased activation in 7 clusters (P ≤ .001 uncorrected; see Table 2). The largest cluster was identified as

the left V5 area (118 voxels, coordinates of maximum: –42 –70 10). Other motion sensitive areas activated included the right V5 complex and the left V3 area as well as Brodmann area 7 (precuneus) in the right hemisphere (see Fig. 2 —c). No increased activation was found when comparing controls to MA. The characteristics of the responses during stimulation in both groups are summarized in Table 3. Org 27569 Neither the MA nor the control group showed a significant side-difference in the VEFR% or Vmax. Even though not statistically significant, the control group had a higher mean Vmax (54.26 cm/second) than the patient group (49.78 cm/second) and also a higher mean V0 (36.86 cm/second vs 34.73 cm/second). VEFR% in the control group was 47.37% on the left and 49.73% on the right side, while in the MA group, VEFR% was somewhat lower with 42.98% on the left and 45.34% on the right side. Controls as well as patients had higher mean VEFR% values on the right side compared with the left side, however, without statistical significance (laterality index MA 0.04 ± 0.21, controls 0.03 ± 0.12). The side-difference of the offset latency was significantly larger and the steepness of the decreasing slope on the left side was reduced when comparing the MA vs the control group.