Neurophysiology, pathology and models of rapid eye movements.

Abstract

This chapter discusses the premotor neural mechanisms that control horizontal saccadic eye movements. Oculomotoneurons carry a pulse-step signal that underlies the pulse-step force driving the overdamped plant. The pulse and step are both generated by a common signal, arising from medium-lead burst neurons in the pons. Their burst signal encodes saccadic eye velocity, while the number of spikes in the burst relates to the saccade amplitude. The step component, which encodes the eye position, is obtained by neural integration of the burst. Several oculomotor neural disorders can be explained by impairments in the binocular push-pull organization of this pulse-step mechanism. Plasticity of the pulse-step control, e.g., in response to muscle weakening, is mediated by cerebellar vermis and flocculus. Saccadic offset may be controlled, either by active braking, or by an exponential slide signal. The neurophysiology is summarized by a quantitative model, in which the firing rate of burst neurons is controlled by a dynamic negative feedback loop that carries the instantaneous eye position signal from the neural integrator. This signal is compared with a desired eye-position command in the head from higher centers, and the resulting dynamic motor error drives the high-gain burst cells. Instability of the system is prevented by the mutual inhibitory interaction between burst cells and omnipause neurons. The model explains many features of normal saccades, but also accounts for pathologies and abnormalities like dynamic overshoots and saccade oscillations.