Modelling the role of the cerebellar fastigial nuclei in producing accurate saccades: the importance of burst timing.

Clinical and experimental data indicate that damage to the cerebellar vermis results in permanent loss of saccadic accuracy. Models of saccade production therefore need to provide a role for the cerebellum. It has been proposed that the vermis adjusts the gain of the saccadic internal feedback loop in response to information about the amplitude of the intended saccade. A model of how the fastigial nuclei (through which vermal output is channelled) influence brainstem saccadic circuitry to achieve this effect was constructed in three stages. (1) The brainstem was represented by a version of Robinson's internal feedback model, which relates excitatory burst neuron discharge to horizontal saccade dynamics. (2) The original model was lesioned to simulate the effects of bilateral inactivation of the fastigial nuclei, namely slow hypermetric saccades. This required reducing the synaptic weight of the internal feedback pathway, and lowering the gain of the excitatory burst neurons. The resultant brainstem-only model served as a preparation for testing the effects of neuronal discharge patterns within the fastigial nuclei. (3) These discharge patterns were simulated using measurements from recent electrophysiological studies. It was found that saccadic accuracy and normal dynamics were restored in the model if the simulated burst from neurons in the contralateral fastigial nucleus were subtracted from the feedback signal (i.e. added to the command signal) early in the saccade, and the burst from neurons in the ipsilateral fastigial nucleus were added to the feedback signal later in the saccade. This pattern corresponds to the observed timing of neuronal bursts in the fastigial nuclei, and accounts qualitatively for the effects of unilateral stimulation and inactivation of both the fastigial nuclei and the cerebellar vermis. This method of producing accurate saccades also contributes to time optimal control, by increasing both saccadic acceleration and deceleration. Appropriate timing of burst onset and duration in the fastigial nuclei is essential for these roles. Evidence concerning the effects of cerebellar damage on fast movements of other parts of the body suggests that the cerebellum may use similar strategies for controlling a wide range of simple movements.