Photoelectric eye movement recording in 9 patients with cerebellar disorders defined three features of saccadic overshoot dysmetria: (i) saccades were hypermetric and successively diminished in amplitude; (ii) saccadic initiation interval averaged 173 ms: and (iii) eye position was constant during the intersaccadic period. These characteristics indicated that the visually evoked saccades subserving foveation had increased gain, and were modelled by computer simulations using a sampled-data control model with increased feed-forward gain. Eight patients with saccadic overshoot dysmetria had cerebellar neoplasms, vermis-splitting surgical procedures and mid-line cerebellar signs. This clinical evidence suggests that vermian dysfunction is responsible for saccadic overshoot dysmetria. Normally, the cerebellar vermis appears to play an adaptive role by continuously adjusting gain of the direct visual motor pathway. When cerebellar disorder exists, adaptive gain modulation is lost, and, if gain then increases, saccadic overshoot dysmetria is a result.