Enduring Dysmetria and Impaired Gain Adaptivity of Saccadic Eye Movements in Wallenberg's Lateral Medullary Syndrome

Abstract

Saccadic eye movements and the adaptive control of their amplitudes were examined in patients with Wallenberg's lateral medullary syndrome. Half of the patients had permanent saccadic dysmetria. Their primary saccades had asymmetric amplitudes: those made in response to an ipsilateral target step (i.e. to the lesion side) tended to be hypermetric and saccades made in response to a contralateral target step were strongly hypometric. Multiple correction saccades were needed for target fixation. The adjustment of the amplitude of artificially induced hypermetric saccades, called gain adaptivity, was examined experimentally by using double target steps. The first target step elicited the primary saccade which triggered a further target displacement. This second, intra-saccadic target displacement was opposite to the first target step and caused the primary saccade to overshoot the final target position. In this way a post-saccadic target position error was generated which had to be corrected for foveal fixation. With repetition of this stimulus sequence the saccadic control system of normal subjects made an adjustment in amplitude of the main saccade such that the overshooting gradually diminished. After a few hundred trials primary saccades became orthometric with respect to the final target position; in respect to the first target step they were, however, strongly hypometric. The experimental data show that patients with Wallenberg's syndrome had a reduced capability to readjust saccadic amplitude. This observation together with the enduring saccadic dysmetria suggest that adaptive gain control of saccades is impaired in patients with lesions restricted to the dorsolateral medulla. It is speculated that these lesions most likely disrupt olivo-cerebellar pathways which are believed to be of paramount importance in visuo-motor adaptation of the cerebellum.

Theta-Burst Stimulation of the Cerebellum Interferes with Internal Representations of Sensory-Motor Information Related to Eye Movements in Humans

“…These results have all been attributed to transient inhibition of the cFN. An asymmetric pattern of saccadic dysmetria with contralateral hyopometria and ipsilateral hypermetria has been shown in patients with Wallenberg's lateral medullary syndrome, in which cerebellar signs have been attributed to lesion of the climbing fibers from the inferior olivary nucleus before they cross the midline and enter the inferior cerebellar peduncle [32][33][34]. However, we cannot exclude a bilateral effect of cTBS, because we did not detect a full asymmetric pattern; since ipsilateral saccade did not become hypermetric but, even if not significantly so, slightly hypometric, and this could support a bilateral effect on vermal and paravermal cerebellar areas.…”

Sensorimotor adaptation of saccadic eye movements

“…In humans, deficits of backward adaptation of reactive saccades were related to stroke or degenerative lesions affecting the cerebellum (Alahyane et al, 2008;Choi et al, 2008;Golla et al, 2008;Straube et al, 2001). Patients suffering from a Wallenberg syndrome consecutive to infarcts of the lateral medulla, which possibly interrupt an afferent cerebellar input from the inferior olive (see discussion in Tilikete et al, 2006), also showed adaptation deficits in one study (Waespe and Baumgartner, 1992) but not in another (Choi et al, 2008). In our own on-going study, we confirmed that adaptation deficits were found only in some Wallenberg syndrome patients (abstract by Pelisson et al, 2006).…”

“…This would suggest that cerebellar-dependent saccadic adaptation mechanisms can themselves be compensated in case of developmentalbut not of sudden onset -cerebellar dysfunction, a hypothesis meriting further consideration. On the other hand, several studies have now revealed an impaired adaptation without -or independently of -any marked decrease of saccadic accuracy (Takagi et al, 1998;Gaymard et al, 2001;Barash et al, 1999;Straube et al, 2001;Waespe and Baumgartner, 1992;Choi et al, 2008;Alahyane et al, 2008). Furthermore, longitudinal studies in the monkey (Takagi et al, 1998, Barash et al, 1999 have indicated that the maintenance of saccadic accuracy results from a progressive, long-term, functional restoration after the lesion.…”

Cerebellar Contributions to the Processing of Saccadic Errors

“…Finally, lesions of vermis V-VIII impair the gradual modification of saccadic amplitudes in a saccade adaptation task [27,28]. Similarly, patients with cerebellar lesions [30], cerebellar atrophy [34], or paraneoplastic cerebellar ataxia [35] showed impairments in or complete lack of saccadic adaptation capacities. In a functional imaging study using PET, cerebellar involvement during saccadic adaptation was confirmed [6,12].…”