In acute stages of unilateral vestibular deficit, the imbalanced tonic activity on vestibular afferents evokes spontaneous nystagmus. The slow-phase velocity of this nystagmus varies with eye position, such that it is smaller when looking in the direction of slow-phases. The neural mechanism for this behavior is still not understood. Here, using a simple control system model, we show that plausible changes in the neural responses within the central vestibulo-ocular reflex pathway are adequate to cause eye position dependent effects in the nystagmus pattern. The proposed transformations in population response functions could happen immediately following a lesion and can be useful to stabilize gaze in part of the gaze field.