Rapid eye movement generation in the primate. Physiology, pathophysiology, and clinical implications.

The trajectories of rapid eye movements are usually described in a Cartesian coordinate frame with a horizontal, vertical and torsional component. The sensory to motor coordinate transformations for horizontal components of rapid eye movements can be localized to neurons of the paramedian pontine reticular formation (PPRF), where long-lead and short-lead burst neurons are found. The equivalent area for recoding of vertical and torsional movement components is situated in the rostral interstitial nucleus of the MLF (rostral iMLF). Pause cells in caudal midline structures of the PPRF help to coordinate the various movement components. Experimental inactivation of these different neuron population lead to palsies of rapid eye movement generation. A unilateral PPRF lesion leads to a loss of all horizontal rapid eye movements towards the ipsilateral side. A bilateral PPRF lesion involving caudal midline structures leads to a bilateral horizontal gaze palsy in addition to a severe disruption of vertical and torsional eye movements. A bilateral rostral iMLF lesion leads to a loss of all rapid eye movements with a vertical or torsional movement component. A unilateral iMLF lesion leads to a loss of all rapid eye movements with an ipsilateral torsional component.