Walsh & Hoyt: Slow Saccades from Pontine Lesions

Slow saccades are characteristic of many degenerative and metabolic diseases. Horizontal saccades may be slowed in patients with spinocerebellar degenerations; vertical saccades are often relatively less affected in such patients. In diseases that principally affect the midbrain, such as progressive supranuclear palsy, vertical saccades are the first to become slow. In some patients with slow saccades, blinks of the eyelids may actually speed up the movements. The explanation for this phenomenon is uncertain, but it probably reflects the effects of blinks upon pause and burst neurons rather than a momentary deprivation of vision. Some patients with slow saccades can generate smooth-pursuit movements of up to about 20 degrees/sec. It is difficult to distinguish a considerably slowed saccade from pursuit, however, so that whether pursuit function is truly intact in such patients is not established. Conversely, if the saccades are so slow that they cannot bring the eye to the moving target, then even if pursuit is intact, it may not appear so because the eye seems to lag the target. Vestibular stimulation elicits normal compensatory slow phases, but quick phases of nystagmus are slow and show approximately the same abnormal relationship between amplitude and peak velocity, as do voluntary saccades. Patients with SCA2 usually make saccades of normal amplitude despite their low velocity. Progressive supranuclear palsy, however, causes both slow and small horizontal saccades. Patients with slow saccades may use a variety of strategies of combining eye and head movements to move their gaze more quickly to the target.