The main findings in unilateral INO are paresis of adduction in the eye on the side of the lesion (for conjugate but not vergence eye movements) and abduction nystagmus in the eye on the side opposite to the lesion. A skew deviation (eye usually higher on the side of the lesion) or a dissociated, mixed vertical-torsional nystagmus, with the eye beating down on the side of the lesion, may also occur. The main findings in bilateral INO are paresis of adduction in both eyes, bilateral abduction nystagmus and, in the vertical plane, impaired gaze-holding, vestibular responses and smooth tracking. Abduction nystagmus in INO may have a number of causes; probably most common are a gaze-evoked nystagmus superimposed on adduction weakness and adaptation to adduction weakness. Most of the findings in INO can be explained by interruption of projections from abducens internuclear neurones, mediating adduction, and from the vestibular nuclei, mediating both canal- and otolith-induced reflexes as well as vertical gaze holding and pursuit. Extension of the lesion to structures near but outside the MLF, or involvement of cell bodies intermixed with MLF fibres, may also be important in the pathogenesis of the abduction nystagmus and the occasional slowing of abducting saccades.