Affiliations: [a] Department of Neurology, Case Western Reserve University, Cleveland, OH, USA | [b] Cole Eye Institute, The Cleveland Clinic, Cleveland, OH, USA
Correspondence:
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Address for correspondence: Aasef G. Shaikh, M.D., Ph.D., Department of Neurology, Case Western Reserve University, 11100 Euclid Avenue, Cleveland, OH 44106-5040, USA. Tel.: +1 313 850 8604; Fax: +1 216 983 0792; E-mail: aasefshaikh@gmail.com
Abstract: Introduction:Foveation is the fundamental requirement for clear vision. Saccades rapidly shift the gaze to the interesting target while gaze holding ensures foveation of the desired object. Purpose:We will review the pertinent physiology of saccades and gaze holding and their pathophysiology leading to saccadic oscillations, slow saccades, saccadic dysmetria, and nystagmus. Summary:Motor commands for saccades are generated at multiple levels of the neuraxis. The frontal and parietal eye field send saccadic commands to the superior colliculus. Latter then projects to the brain-stem saccadic burst generator. The brain-stem burst generators guarantee optimum signal to ensure rapid saccadic velocity, while the neural integrator, by mathematically integrating the saccadic pulse, facilitates stable gaze holding. Reciprocal innervations that ensure rapid saccadic velocity are prone to inherent instability leading to saccadic oscillations. In contrast, suboptimal function of the burst generators causes slow saccades. Impaired error correction, either at the cerebellum or the inferior olive, leads to impaired saccade adaptation and ultimately saccadic dysmetria and oculopalatal tremor. Impairment in the function of neural integrator causes nystagmus. Conclusion:Neurophysiology of saccades, gaze holding, and their deficits are well recognized. These principles can be implemented to define novel therapeutic and rehabilitation approaches.
