Dysfunctional mode switching between fixation and saccades: collaborative insights into two unusual clinical disorders.

Voluntary rapid eye movements (saccades) redirect the fovea toward objects of visual interest. The saccadic system can be considered as a dual-mode system: in one mode the eye is fixating, in the other it is making a saccade. In this review, we consider two examples of dysfunctional saccades, interrupted saccades in late-onset Tay-Sachs disease and gaze-position dependent opsoclonus after concussion, which fail to properly shift between fixation and saccade modes. Insights and benefits gained from bi-directional collaborative exchange between clinical and basic scientists are emphasized. In the case of interrupted saccades, existing mathematical models were sufficiently detailed to provide support for the cause of interrupted saccades. In the case of gaze-position dependent opsoclonus, existing models could not explain the behavior, but further development provided a reasonable hypothesis for the mechanism underlying the behavior. Collaboration between clinical and basic science is a rich source of progress for developing biologically plausible models and understanding neurological disease. Approaching a clinical problem with a specific hypothesis (model) in mind often prompts new experimental tests and provides insights into basic mechanisms.

Case Studies in Neuroscience: Instability of the visual near triad in traumatic brain injury-evidence for a putative convergence integrator.

Deficits of convergence and accommodation are common following traumatic brain injury, including mild traumatic brain injury, although the mechanism and localization of these deficits have been unclear and supranuclear control of the near-vision response has been incompletely understood. We describe a patient who developed profound instability of the near-vision response with inability to maintain convergence and accommodation following mild traumatic brain injury, who was identified to have a structural lesion on brain MRI in the pulvinar of the caudal thalamus, the pretectum, and the rostral superior colliculus. We discuss the potential relationship between posttraumatic clinical near-vision response deficits and the MRI lesion in this patient. We further propose that the MRI lesion location, specifically the rostral superior colliculus, participates in neural integration for convergence holding, given its proven anatomic connections with the central mesencephalic reticular formation and C-group medial rectus motoneurons in the oculomotor nucleus, which project to extraocular muscle nontwitch fibers specialized for fatigue-resistant, slow, tonic activity such as vergence holding.NEW & NOTEWORTHY Supranuclear control of the near-vision response has been incompletely understood to date. We propose, based on clinical and anatomic evidence, functional pathways for vergence that participate in the generation of the near triad, "slow vergence," and vergence holding.

The nodulus and uvula: source of cerebellar control of spatial orientation of the angular vestibulo-ocular reflex.

The nodulus and rostral-ventral uvula of the vestibulo-cerebellum play a critical role in orienting eye velocity of the slow component of the angular vestibulo-ocular reflex (aVOR) to gravito-inertial acceleration (GIA). This is done by altering the time constants of "velocity storage" in the vestibular system and by generating "cross-coupled" eye velocities that shift the eye velocity vector from along the body yaw axis to the yaw axis in a spatial frame. In this report, we show that eye velocity generated through the aVOR by constant velocity centrifugation in the monkey orients to the GIA in space, regardless of the position of the head with respect to the axis of rotation. We also show that, after removal of the nodulus and rostral-ventral uvula, the spatial orientation of eye velocity to the GIA is lost and that eye velocity is then purely driven by the semicircular canals in a body frame of reference. These findings are further confirmation that these regions of the vestibulo-cerebellum control spatial orientation of the aVOR.