Rightward attentional bias and left hemisphere dominance in a cue-target light detection task in a callosotomy patient.

Six normal subjects and a callosotomized man with a prefrontal lesion, mostly on the right side, were tested in a reaction time (RT) task involving a key-pressing response to an extrafoveal light target preceded by an extrafoveal light cue. Cues and targets were presented along the horizontal meridian at 4 degrees and 12 degrees on the right and left of fixation. Fixation was maintained throughout each trial. The cue signalled the occurrence of the target within a time window extending from 200 to 4000 misec from the cue, but did not predict target location. Normal controls responded faster to medial than to lateral targets in both fields, but showed no between-field difference, and their RT was not affected by cue location. Furthermore, they showed the so-called 'ipsilateral inhibition' or 'inhibition of return' effect, their RT being longer when cues and targets occurred in the same field than when they occurred in opposite fields. The RT of the callosotomized subject showed a left-right gradient for both cue location and target location, being longest for the leftmost location and shortest for the right locations. In addition, he showed a significant advantage for the right hand regardless of cue and target location, as well as a consistent ipsilateral inhibition in the left field, whereas in the right field there was ipsilateral inhibition only at the two longest stimulus onset asynchronies. These results suggest that, at least under these experimental conditions, there was a rightward orientational bias which reflected the taking over of the control of performance by the left hemisphere. This attentional bias was reminiscent of that seen in patients with hemi-inattention from right hemisphere damage, although the callosotomized patient showed no sign of such hemi-inattention in routine clinical tests. On the basis of several considerations the rightward bias could be attributed to the callosal interhemispheric disconnection rather than to the right prefrontal lesion.