RESUMEN
This paper questions the prominent role that the parietal lobe is thought to play in the processing of corollary discharges for saccadic eye movements. A corollary discharge copies the motor neurons' signal and sends it to brain areas involved in monitoring eye trajectories. The classic double-step saccade task has been used extensively to study these mechanisms: two targets (T1 and T2) are quickly (40-150 ms) flashed sequentially in the periphery. After the extinction of the fixation point, subjects are to make two saccades (S1 and S2), in the dark, to the remembered locations of the targets in the order they appeared. The success of S2 requires a corollary discharge encoding S1's vector. Patients with a parietal lobe lesion, particularly on the right, are impaired at generating an accurate S2 when S1 is directed contralesionally, but not ipsilesionally, thought due to an impaired contralesional corollary discharge. In contrast, we hypothesize that failure on the classic double-step task is due to visual processing and attentional deficits that commonly result from lesions of the parietal lobe and imperfect data analysis methods. Here, we studied parietal patients who fail in the classic double-step task when tested and data analysed according to previously published methods. We then tested our patients on two modified versions of the double-step task, designed to mitigate deficits other than corollary discharge that may have confounded previous investigations. In our 'exogenous' task, T2 was presented prior to T1 and for longer (T2: 800-1200 ms, T1: 350 ms) than in the classic task. S1 went to T1 and S2 to T2, all in the dark. All patients who completed sufficient trials had a corollary discharge for contralesional and ipsilesional S1s (5/5). In our 'endogenous' task, a single target was presented peripherally for 800-1200 ms. After extinction of target and fixation point, patients made first an 'endogenous' S1, of self-determined amplitude either to the left or right, before making S2 to the remembered location of the previously flashed target. To be successful, a corollary discharge of endogenous S1-generated in the dark-was required in the calculation of S2's motor vector. Every parietal patient showed evidence of using corollary discharges for endogenous S1s in the ipsilesional and contralesional directions (6/6). Our results support the hypothesis, based on our previous studies of corollary discharge mechanisms in hemidecorticate patients, and electrophysiological studies by others in monkey, that corollary discharges for left and right saccades are available to each cortical hemisphere.
Asunto(s)
Lateralidad Funcional/fisiología , Modelos Biológicos , Lóbulo Parietal/patología , Lóbulo Parietal/fisiopatología , Movimientos Sacádicos/fisiología , Estudios de Casos y Controles , Femenino , Humanos , Masculino , Lóbulo Parietal/fisiología , Estimulación Luminosa , Tiempo de Reacción/fisiología , Reproducibilidad de los Resultados , Percepción Visual/fisiologíaRESUMEN
Patients who have had a cerebral hemisphere surgically removed as adults can generate accurate leftward and rightward saccadic eye movements, a task classically thought to require two hemispheres each controlling contralateral saccades. Here, we asked whether one hemisphere can generate sequences of saccades, the success of which requires the use of corollary discharges. Using a double-step saccade paradigm, we tested two hemidecorticate subjects who, by definition, are contralesionally hemianopic. In experiment 1, two targets, T1 and T2, were flashed in their seeing hemifield and subjects had to look in the dark to T1, then T2. In experiment 2, only one target was flashed; before looking at it, the subject had first to saccade voluntarily elsewhere. Both subjects were able to complete the tasks, independent of first and second saccade direction and whether the saccades were voluntarily or visually triggered. Both subjects displayed a strategy, typical in hemianopia, of making multiple-step saccades and placing, at overall movement-end, the recalled locations of T1 and T2 on off-foveal locations in their seeing hemifield, in a retinal area typically spanning a 5-15° window, depending on the subject, trial type and target eccentricity. In summary, a single hemisphere monitored the amplitude and direction of the first multiple-step saccade sequence bilaterally, and combined this information with the recalled initial retinotopic location of T2 (no longer visible) to generate a correct target-directed second saccade sequence in the dark. Unexpectedly, our hemidecorticate subjects performed better on the double-step task than subjects with isolated unilateral parietal lesions, reported in the literature to have marked deficiencies in monitoring contralesional saccadic eye movements. Thus, plasticity-dependent mechanisms that lead to recovery of function after hemidecortication are different than those deployed after smaller lesions. This implies a reconsideration of the classical links between behavioural deficits and discrete cortical lesions.