Pathophysiology of slow vertical saccades in progressive supranuclear palsy

Objectives: To investigate the relative roles of burst neurons (which generate the saccadic command) and omnipause neurons (which gate the activity of burst neurons) in the pathogenesis of slow saccades in progressive supranuclear palsy (PSP) Background: Experimental inactivation of mesencephalic burst neurons impairs vertical but not horizontal saccades. Experimental inactivation of omnipause neurons causes slowing of both horizontal and vertical saccades. Combining saccadic with vergence movements in healthy subjects induces small, high-frequency, conjugate oscillations, which indicate that omnipause neurons are inhibited. Methods: The authors studied seven patients with PSP, six patients with other parkinsonian syndromes, and seven age-matched control subjects. They compared vertical saccades of similar sizes made with or without associated vergence movements. They compared the speed of vertical and horizontal saccades. Results: Five patients with PSP and the six patients with other parkinsonian made vertical saccades in combination with horizontal vergence; all showed conjugate horizontal oscillations (29 to 41 Hz) during 27%, to 93% of saccade-vergence trials. Vertical saccades made in conjunction with vergence movements were not speeded up or increased in size compared with saccades made between equidistant targets for the PSP or parkinsonian groups. Vertical saccades were slowed more than horizontal saccades in the PSP group (p < 0.005) but not in the parkinsonian group. Conclusions: Dysfunction of omnipause neurons (gate dysfunction) is unlikely to be the primary cause of slow vertical saccades in progressive supranuclear palsy. Deficient generation of the motor command by midbrain burst neurons is the more likely cause.