Saccade dynamics in peripheral vs central sixth nerve palsies

To investigate differences between peripheral idiopathic and central sixth nerve palsies from brainstem damage by comparing peak velocities and durations of horizontal saccades. Fourteen patients with unilateral incomplete sixth nerve palsies caused by idiopathic, presumed ischemic, peripheral damage, 5 with incomplete central (fascicular) palsy caused by brainstem lesions, and 10 controls were studied. Palsies under 1 month in duration were designated as acute and those of longer duration were chronic. Among peripheral palsies, five were acute, nine were chronic. Among central palsies, two were acute, three were chronic. Subjects made +/- 10 deg horizontal saccades while wearing search coils. Serial recordings were made in seven patients with acute palsy (five peripheral, two central). Centrifugal abducting saccadic velocities in the paretic eye were subnormal in both central and peripheral acute palsies, as anticipated from lateral rectus weakness. In chronic central palsies, abducting velocities in the paretic eye remained reduced. However, in chronic peripheral palsies, velocities became normal in the tested range of excursion, within 2 months of onset, despite persisting abduction deficit. Saccade peak velocities are reduced and their durations are prolonged in the field of action of acutely palsied peripheral and central nerves. Speeds remain reduced in chronic central (fascicular) palsies, consistent with limited regeneration within the brain. Saccade speeds are repaired in chronic peripheral palsies, probably by remyelination and axonal regeneration, and perhaps also by central monocular adaptation of innervation selectively to the paretic eye, in order to drive both eyes rapidly and simultaneously into the paretic field of motion.