3. Ambidiestros Cuando no existe una predominancia de lateralización clara de un lado sobre el otro Puede producirse transitoriamente (Thoumi, 2003)
2.8 Importancia de la conciencia corporal
It has been shown that the subcortical network for the generation of fixational saccades involves burst neurons in the Paramedian Pontine Reticular Formation (Van Gisbergen et al. 1981) and in the rostral SC (Hafed et al. 2009). When the target image falls on the fovea, the activity in the two rostral ends of the SC is almost balanced, and fixational saccades would result from fluctuations in the equilibrium of this bilateral activity (Hafed et al. 2009). The variability in the direction of fixational saccades starting from some specific positions, outlined by analytical technique proposed in the present study, could result from these fluctuations occurring when a visual target is being foveated. When the activity in the SC is unbalanced because of a distance between the actual position of the eye and the “on-target” position, saccades are generated in order to reduce this distance and to restore the balance in bilateral collicular activity. Accordingly, when the gaze is in
the direction encoded by the system as “on target”, the activity in the rostral SC would be roughly at equilibrium, and saccades are generated with an unpredictable direction. After FOR inactivation, saccades move the eyes toward an aiming zone which has shifted. This shift does not reflect an inability to correct for a small residual retinal error, but presumably a new encoding of the (foveal) target position. Indeed, the results showed that after a certain time, the average effect of fixational saccades on eye position cancel out each other (fig. 4.2) after the gaze has reached the “new” target position. Both before and after the lesion, the directions of saccades generated from the area at which the neuronal activity would be at equilibrium clearly display two modes (up and down). The distribution around two modes could result from different noise levels of the burst generator for horizontal and vertical saccades. However, a recent study has estimated similar motor noise level for the generators of vertical and horizontal movements (van Beers 2007); thus, it seems unlikely that motor noise could be the source of bimodality of fixational saccades. Instead, the fact that the two modes are vertically oriented can be explained by the worst motor control on this meridian; indeed, values for the vertical component of fixational saccades are higher than the one computed for horizontal movements (compare figure 4.6 C and D). Considering the collicular origin of fixational saccades, it is also possible that in the rostral SC horizontal and vertical movements have different gradients of representation, and that the activity elicited from the foveation of the target simply involves a larger spread of the population of active neurons along the medio-lateral axis. Additional experiments are required to test this hypothesis; since a preferred direction is also observed in humans, but on the horizontal meridian (Engbert, 2006), it would be interesting to perform more detailed analysis on their motor generation to gather additional information
supporting or rejecting the proposed mechanisms underling the bimodality of fixational saccades. Cornsweet (1956) has hypothesized three functional systems for the control of saccades. These systems would control 1) the direction and 2) the magnitude of fixational saccades, and 3) their triggering. The present study shows that the fastigial oculomotor region participates in the first two
“foveal exploration” on the aiming zone (via the fastigio-tectal connections) and regulate the amplitude of saccades (via the fastigio-reticular connections). Instead, the saccade rate (median of
2.45 and 1 saccade/second in monkey B and E, respectively) was unaffected by FOR inactivation
(monkey B and E: 2.51 and 1.31 saccades/second). The absence of changes in the saccade triggering
mechanisms is consistent with the lack of significant changes in latencies after FOR inactivation in the monkey (Quinet and Goffart 2007); note that changes in latencies happen after muscimol injection in the feline caudal fastigial nucleus (Goffart and Pélisson 1998). Previous studies reported a dependency of triggering mechanisms on attentional factors (Barlow 1952; Engbert and Kliegl 2003; Hafed and Clark 2002). The presented results are therefore consistent with the
observation that while several cortical areas (corresponding in the monkey to the FEF, SEF and LIP-7a) are active during both oculomotor and attentional tasks, the medial cerebellum is activated only during oculomotor tasks (Corbetta et al. 1998). Accordingly, the observed shifts of fixation after unilateral FOR inactivation have a magnitude (never more than 2°), which is not comparable with the gaze deviations observed in patients suffering from neglect after right hemispheric lesions (often more than 20°, Leigh and Zee 2006).
In the analyzed experiment, monkeys were performing a task that was easy from a visual point of view. It is possible to hypothesize that the observed behaviour while the animals were looking at the target was completely driven by subcortical mechanisms. It is however likely that cortical activity influences the otherwise reflexive behaviour. Indeed, both humans (Steinman et al. 1973) and monkeys (Skavenski et al. 1975) can suppress the generation of fixational saccades. In the monkey, this result can be obtained after a special training, while a verbal instruction to humans suffices to prevent the generation of microsaccades (Kowler and Steinman 1980). How this is achieved would require more thorough studies; suppression in the collicular activity and a reinforcement of the activity of the omni-pause neurons are two non-mutually exclusive hypotheses. Also the neuronal basis of the slow control of the eyes to maintain the gaze (Steinman et al. 1973) has to be better studied in order to have a complete picture of this particular behaviour.