Disordered inhibition in internuclear ophthalmoplegia: analysis of eye movement recordings with computer simulations

High resolution infra-red oculographic recordings were obtained in 19 patients with clinically evident internuclear ophthalmoplegia. The major findings were attenuated phasic and tonic components of adducting saccades, fractionated phasic components of abducting saccades, equally long durations for phasic components of adducting and abducting saccades with refixation, and nasal drift of the abducting eye which initiated abducting nystagmus. Ipsilateral gaze paresis and abduction lag were occasionally associated with primarily unilateral cases of internuclear ophthalmoplegia. These findings were interpreted using available anatomical, electromyographic and oculographic data as well as computer simulations of internuclear ophthalmoplegia. We concluded that deficient excitation of the ipsilateral medial rectus was due to interruption of burst-tonic neurons within the medial longitudinal fasciculus which mediate horizontal eye movements. This resulted in a decreased pulse height and step of the agonist neural controller signal. We were also able to determine that variably slowed fractionated abducting saccades were caused by deficient intrasaccadic inhibition of the antagonist medial rectus. When medial rectus excitation was more deficient than medial rectus inhibition of the opposite eye, then a typical internuclear ophthalmoplegia resulted; when the amount of medial rectus excitation was equal to the amount of medial rectus inhibition of the opposite eye, then a gaze paresis occurred; and when medial rectus excitation was less deficiennt than medial rectus inhibition of the opposite eye, abduction lag resulted in the oculographic appearance of internuclear ophthalmoplegia of abduction. Abducting nystagmus appeared to be initiated by a tendency for the abducted eye to drift nasally from the increased level of tonic inhibition of the antagonist medial rectus. Some oculographic patterns were attributed to higher level adaptive changes in innervation. These changes were a consequence of disordered excitatory and inhibitory controller signals at the lower, internuclear level. Possible anatomical pathways which might carry these inhibitory controller signals were discussed. High resolution eye movement recordings of patients with internuclear ophthalmoplegia were interpreted directly and by computer simulations as being most consistent with disordered inhibitory and excitatory control of the medial rectus motor pool during rapid eye movements and eccentric gaze.