Impaired Representation of Saccadic Eye Displacement after Posterior Parietal Lesions: Is It a Craniotopic or a Directional Deficit?

Despite constant shifts of its retinal image, due to eye or head movements, we perceive space as stable. To maintain this amazing ability of spatial constancy,our brain cannot rely on retinal maps, but it needs nonvisual (extraretinal) information about eye or head movements. The most important source of this information is a copy of the motor signal ("efferencecopy") that is neuronallygeneratedprior to each movement, such as a saccade, and fed back into the cortical visual pathways to compensate for the retinal image shift caused by the saccadic eye displacement.l-l For saccadiceye movements, this can be investigatedusing the double-step task, where the locations of two successively flashed peripheral targets (for 140 and 100 ms, respectively)have to be fixated in darkness in the correct order.As there is a spatial dissonanceafter the first saccadebetween the retinal locationof the secondtarget and the required motor vector of the second saccade, the brain must update the spatial representationof the second target by using efferencecopy about currenteye position or about the preceding saccadic eye displacement to achieve spatial accuracy for the second saccade. Patients with right posterior parietal lesions are specifically impaired in this task: The second saccade is grossly dysmetric (followingthe retinal vector of the target) wheneverthe first saccade is directed into the contralesionalleft hemifield-'. Twoalternativeexplanationsmay hold for this finding.These patients have no reliable extraretinal information about eye positions in left contralesional craniotopic hemispace, thus exhibiting a craniotopic deficit of maintaining spatial constancy