<p>See-saw nystagmus (SSN), and the possibly related hemi-see-saw nystagmus (hSSN), occur in certain forms of visual loss and in some brainstem lesions. These disparate lesions have made it challenging for investigators to arrive at a unified mechanism. Here we propose a model involving detection of peripheral retinal disparity in the superior colliculi (SC), which send inhibitory projections to the interstitial nucleus of Cajal (INC) that maintain calibration, and how loss of such calibration may provoke INC neurons (which are already mutually inhibitory with contralateral INC neurons) to develop self-inhibitory axo-dendritic autapses, resulting in a network configuration from which a pathologic Matsuoka oscillator can emerge and drive the alternating vertical and torsional movements characteristic of SSN and hSSN.</p>