Effects of occipital lobectomy upon eye movements in primate

Abstract

1. Eye movements were recorded before and after bilateral occipital lobectomy in six rhesus monkeys trained to fixate and to follow small targets. Striate cortex was completely removed in two animals; small islands islands remained in the others. In all animals portions of extrastriate cortex were also removed but the medial superior temporal area in the superior temporal sulcus was largely spared. Optokinetic nystagmus (OKN) was markedly altered but not abolished in all animals. The immediate pursuit component of OKN was eliminated leading to a poor response to stimuli comprised of high frequencies. The velocity-storage component of OKN was present, but the maximum value of OKN that could be achieved was decreased to 6 and 16 degrees/s in the two most severely affected animals (preop, 65-116 degrees/s). The residual OKN was similar to that of afoveate animals with a diminished response to high velocities of retinal-image motion and a temporal to nasal predominance during monocular viewing. 2. In the initial postoperative period all animals appeared completely blind. Within 1-6 mo, however, they regained an ability to make visually guided saccades to, and smooth pursuit of, small targets. Saccades were nearly as accurate as preoperatively, but saccade amplitudes were more variable and saccade latencies increased. In the two animals with a complete removal of striate cortex, gains (eye velocity/target velocity) of smooth pursuit during sinusoidal tracking (60 degrees/s, 0.5 Hz) were 0.9 and 0.95. During tracking of step-ramp (Rashbass) stimuli with 60 degrees/s ramps, the average acceleration of the eyes during the first 120 ms of smooth pursuit was 189-278 degrees.s-1.s-1 (preop range, 154-418 degrees.s-1.s-1). In other respects, though, smooth pursuit was not normal. Latencies were increased two- to threefold, and tracking was more variable. 3. Paradoxically, as visually guided saccades and pursuit recovered, some other ocular motor functions deteriorated. Spontaneous and gaze-evoked nystagmus developed 3-6 mo after occipital lobectomy; the time constant of the neural eye-position integrator dropped to values as low as 2.6-4.8 s. The maximum slow-phase velocity of OKN also decreased. 4. The findings immediately after occipital lobectomy indicate that in normal primates occipital cortex is necessary for visually guided saccades and smooth pursuit as well as for the immediate component of OKN. Occipital cortex also makes the predominant contribution toward the generation of the velocity-storage component of OKN.(ABSTRACT TRUNCATED AT 400 WORDS)

Long-Term Retention Explained by a Model of Short-Term Learning in the Adaptive Control of Reaching

“…For example, the eye velocity of optokinetic nystagmus (involuntary eye movements in response to continuous movement of the visual field) is also characterized by two components: a rapid rise followed by a slower increase to steady state (Cohen et al 1977). Interestingly, the rapid rise in eye velocity has been shown to be affected by particular neural lesions (Zee et al 1987). The ability to disrupt specific time scales in the learning of motor adaptation tasks similar to that used in this study has been demonstrated (Della-Maggiore et al 2004).…”

Visual Pathway for the Optokinetic Reflex in Infant Macaque Monkeys

“…Lesion studies in primates demonstrate the relevance of striate and extrastriate visual cortical areas for unperturbed slow eye movements and symmetric mhOKN (e.g., Ter Braak and Van Vliet, 1963;Lynch and McLaren, 1983;Zee et al, 1987;Dürsteler and Wurtz, 1988). As we failed to reveal a cortical input to the NOT-DTN at P9, binocularity in the NOT-DTN up to this age should indeed originate from the direct projections of retinal ganglion cells from both eyes (Ballas et al, 1981;Kourouyan and Horton, 1997;Telkes et al, 2000).…”

Error Correction, Sensory Prediction, and Adaptation in Motor Control

“…For example, eye velocity in optokinetic nystagmus (involuntary eye movements in response to continuous movement of the visual field) is characterized by two components: a rapid rise followed by a slower increase to steady state (Cohen et al, 1977). Interestingly, the rapid rise in eye velocity has been shown to be specifically affected by particular neural lesions (Zee et al, 1987), suggesting that these time scales may have distinct neuroanatomical bases. This idea is supported by data indicating that during saccade adaptation in patients with cerebellar cortical damage, there is a profound loss in the fast timescales of adaptation but less impairment in the slower adaptive processes (Xu-Wilson et al, 2009a).…”