Pathophysiology of slow vertical saccades in progressive supranuclear palsy

Objectives: To investigate the relative roles of burst neurons (which gener ate the saccadic command) and omnipause neurons (which gate the activity of burst neurons) in the pathogenesis of slow saccades in progressive supranu clear palsy (PSP) Background: Experimental inactivation of mesencephalic bu rst neurons impairs vertical but not horizontal saccades. Experimental inac tivation of omnipause neurons causes slowing of both horizontal and vertica l 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 patient s with PSP, six patients with other parkinsonian syndromes, and seven age-m atched control subjects. They compared vertical saccades of similar sizes m ade with or without associated vergence movements. They compared the speed of vertical and horizontal saccades. Results: Five patients with PSP and th e six patients with other parkinsonian made vertical saccades in combinatio n with horizontal vergence; all showed conjugate horizontal oscillations (2 9 to 41 Hz) during 27%, to 93% of saccade-vergence trials. Vertical saccade s made in conjunction with vergence movements were not speeded up or increa sed in size compared with saccades made between equidistant targets for the PSP or parkinsonian groups. Vertical saccades were slowed more than horizo ntal saccades in the PSP group (p < 0.005) but not in the parkinsonian grou p. Conclusions: Dysfunction of omnipause neurons ("gate dysfunction") is un likely to be the primary cause of slow vertical saccades in progressive sup ranuclear palsy. Deficient generation of the motor command by midbrain burs t neurons is the more likely cause.