Pathological nystagmus may be spontaneous, positional, or gaze-evoked. Peripheral vestibular nystagmus is usually rotatory, the horizontal component being most prominent. It is - in contrast to a central vestibular nystagmus - strongly inhibited by fixation. Spontaneous congenital nystagmus is also prominent with fixation, but it can usually be distinguished from acquired fixation nystagmus based on its long duration, atypical waveforms and high frequency. Two general types of positional nystagmus can be identified on the basis of nystagmus regularity: static and paroxysmal. The most common variety of positional nystagmus is the so-called benign paroxysmal positional nystagmus, which in the majority of cases occurs as an isolated symptom of unknown cause. Gaze-evoked nystagmus, prominent with fixation, includes dissociated, rebound and gaze-paretic nystagmus forms. Symmetrical gaze-evoked nystagmus is most commonly produced by ingestion of certain drugs. Phenomena related to nystagmus include: amblyopic, voluntary, and convergence-retraction nystagmus, ocular dysmetria, ocular flutter, opsoclonus, ocular bobbing, and ocular myoclonus.