97; p < .001) than the controls (mean = 49.8 msec, SD = 4.06). In addition, there was also a significant difference between Cyclopamine the Incongruence Cost measures where KP (102 msec) demonstrated a 27 msec increased latency compared to the control group (mean = 75 msec, SD = 8.08; t = 3.35; p < .001). KP's accuracy in responding (97%) was not significantly different to the control group (mean = 94.2%, SD = 5; t = .56). We also calculated KP's ICV (4.49), but this was again not significantly different to the controls (mean = 3.98, SD = .89; t = .539). It is possible that the large increase in incongruence costs demonstrated

by KP in session 2 could have been a product of generalised slowing, rather than a specific impairment when responding to incongruent stimuli. To investigate this possibility, the ratio between neutral reaction time and the three incongruence measures was examined. If KP were to demonstrate a significant deviation from the controls on these measures, this might be evidence that her incongruence Fulvestrant supplier costs were not just

a product of increased reaction times. The analysis demonstrated that the ratio of neutral reaction time to Incongruence Cost (KP = .21; Controls = .18, SE = .022), Pure Cost (KP = .14; Controls = .12, SE = .014) or Benefit (KP = .068; Controls = .059, SE = .015) there was no significant difference between KP and the control group. Therefore it is likely that KP’s Cyclin-dependent kinase 3 higher incongruence costs in the first session were simply

a consequence of a general increased latency in responding following her lesion. In the following session (S3) KP’s reaction times improved and there was now no significant difference between her reaction time to congruent (422 msec), incongruent (495 msec) or neutral stimuli (440 msec), compared to the control group. Nor were there any significant differences between any of the incongruence measures and the controls. In this session KP again demonstrated no significant differences in accuracy (94%) to the control group, and her consistency (ICV) in responding to neutral stimuli increased relative to the previous session (4.91), but was not significantly higher than in the control group (mean = 3.98, SD = .89; t = .99). In summary, in the first session using the flanker task (S2), KP was consistently slower in responding to all three types of stimuli. KP also demonstrated significantly larger incongruence costs, but this is likely a product of generalised slowing. In the second Flanker session (S3), KP demonstrated no significant impairment compared to controls. In this study we explored the behavioural consequences of a lesion of the caudal right pre-SMA on three standard measures of cognitive control. Our aim was to identify whether KP’s behaviour had changed as a result of the lesion and how this could be integrated into contemporary accounts of pre-SMA function.