The effects of refixation fatigue, maintained gaze fatigue, and intravenous edrophonium on saccadic waveform, gain, and velocity were studied in 10 patients with ocular myasthenia gravis. Refixation fatigue was minimal. Gaze maintenance had four separate but differing effects on waveform and gain; normalized peak velocities did not decrease. Edrophonium caused hypermetria and increased gain but normalized peak velocities were either unchanged or decreased. These effects represent, in part, selective impairment of the tonic, as distinct from phasic, fibers in the extraocular muscles and compensatory increase in central saccadic gain induced by the muscle weakness.

An analog computer model of the saccadic eye movement system was constructed with provisions for deficits in the extraocular muscles. The model included a fixing and patched (open looped) eye, either of which could be paretic. Simulating specific neuromuscular lesions, such as tonic fiber deficits and muscle pareses, with integrator leaks and saturation circuits, respectively, produced saccadic responses which duplicated those found in each eye of patients with ocular myasthenia gravis. Simulation of the compensatory central gain increase produced the typical eye movements of a high-gain saccadic system which matched those after edrophonium administration to the myasthenic patients. The model allowed the testing of hypotheses concerning the interrelationship between the primary neuromuscular deficit and the secondary central changes.

Saccadic eye movements exhibit a characteristic peak velocity vs. amplitude relationship. As with all quantifications of biological function, there exists and associated intra- and intersubject variability of this relationship. This paper documents this variability and demonstrates both the absence of a predictable short-term "muscle fatigue" effect and the presence of a generalized "mental fatigue" (i.e. tiredness) effect.

Bei Fixation mit dem paretischen Auge paßt das Zentralnervensystem den Bewegungsentwurf einer sakkadischen Augenbewegung der veränderten peripheren Situation an. So zeigten Kommerell und Mitarb. (1976), daß adaptive Veränderungen des sakkadischen Systems nach 3tägiger Okklusion des paretischen aber visuell besseren Auges auftraten. Über die Plastizität des sakkadischen Systems berichteten außerdem Optican u. Robinson (1977). Sie zeigten an Affen, daß ein paretischer Augenmuskel eine Zunahme der Verstärkung (Gain) aufwies, wenn Sakkaden ausgeführt wurden. Verstärkung (Gain) einer Sakkade bedeutet: das Verhältnis von ausgeführter Amplitudenhöhe zur erforderlichen Amplitude einer Sakkade.

A subject with a medial rectus paresis secondary to a partial third nerve palsy was forced to use the affected eye for six days while the good eye was constantly patched. Saccadic eye movements were carefully measured each day; the gain increased, with a time constant of 0.85 day. The patch was then switched to the paretic eye and the gain decreased, with a time constant of 1.54 days. This demonstrated central nervous system plasticity of the pulse and step of neural activity responsible for the generation of saccades in the adult human. In addition to gain changes, postsaccadic drift velocity and saccadic velocity/amplitude relationship alterations during the patching are reported. A major conclusion that can be drawn from analysis of these data is that the gain changing is accomplished by pulse width changes rather than pulse height (firing frequency), which was not markedly altered.