Evidence for cortical coding of saccade velocity in memory-guided saccadesin patients with CADASIL

Saccadic eye movements were elicited in ten patients with CADASIL (an autos omal dominant cerebral angiopathy) and ten age-matched controls under six d ifferent conditions: 1) the gap paradigm, which tests visually guided, refl exive saccades; 2) the overlap paradigm; 3 and 4) the anti-gap and anti-ove rlap paradigms, which are thought to test especially the function of the fr ontal cortex; 5) the memory paradigm, which tests internally guided, intent ional saccades; and 6) the sequential memory-guided saccades. Eye movements were recorded by means of DC electro-oculography, and the saccade latency, gain, duration, and peak eye velocity were estimated. The amplitude-to-dur ation as well as the amplitude-to-peak velocity ratios were calculated for both groups and conditions 1 and 5. There were no significant differences i n the gains of the primary saccades in the gap, overlap, and memory paradig ms. In general, the CADASIL patients showed a tendency toward longer saccad e latencies and a larger number of unwanted saccades in the antitask saccad e and memory saccade paradigms (suppression errors). Our main finding was t hat the patients had a highly significant reduction in peak velocity and a corresponding prolongation of the duration of the memory-guided saccades co mpared to the controls. In contrast, the duration and the peak velocity of the visually guided saccades did not differ between controls and patients. Thus, we observed a specific change in he dynamic properties of memory-guid ed saccades in CADASIL patients. The observed pattern of saccade abnormalit ies in the CADASIL patients does not allow localization to a specific corti cal side; however, it might reflect the presence of a mostly frontal type o f lesion. This finding contradicts the view that information passed from th e cortex to the brainstem codes only the saccade vector and not saccade dyn amics.