A triple distinction of cerebellar function for oculomotor learning and fatigue compensation
Fig 8
Simulation of long-term visuomotor behavior after disease onset.
(A) Oculomotor fatigue in the very early phase of the disease causes a loss of saccade peak velocity κ that can only be partially compensated by upregulation of saccade duration λ. Consequently, a decline of the saccadic motor command M leads to saccade hypometry, that, in turn, results in a rise of motor errors Epost. Preserved long-term learning at perceptual (αv) and motor level (αm)—that, yet, slowly decays throughout disease progression—counteracts to keep saccadic behavior calibrated. Hence, the visuomotor system stabilizes with an overestimation of the pre-saccadic target eccentricity (V1) and recovery from saccade hypometria (M), matching the baseline visuomotor gains measured in cerebellar patients (ωv and ωm; ωcd deviates; residual standard error RSEω = 0.05). Simulations started with the visuomotor gains ωv, ωm and ωcd, the learning rates αv, αm and αcd, the peak velocity decay rate γκ and the duration compensation rate γλ of healthy subjects; αv, αm, αcd, γκ and γλ change until they match the values of cerebellar patients. Progression rates were νκ = 0.012, νλ = 0.040 and να = 1.7*10−7. Please note that the different subplots show different timescales. (B) Residual standard error RSEω depending on how fast learning rates (scaled by να), peak velocity decay rate (scaled by νκ) and duration compensation rate (scaled by νλ) change towards patients’ values. Simulations with RSEω ≤ 0.05 are marked with a white dot.