Spontaneous nystagmus may occur due to a central impairment (usually up or down beating) or due to a vestibular imbalance (peripheral).
In the case of vestibular imbalance, spontaneous nystagmus generally occurs in the acute stage (vestibular neuritis, after vestibular schwannoma resection, etc.) with the fast phase beating toward the intact ear and would be expected to gradually fade away.
Gaze-evoked nystagmus is nystagmus that is only present for certain directions of gaze. Gaze-evoked nystagmus is considered normal with prolonged gaze holding or at end range of motion. Persistent gaze-evoked nystagmus for ocular displacement of 30 degrees or less are considered abnormal. Causes of abnormal gaze-evoked nystagmus include medications (especially sedatives and anti-convulsants), alcohol/recreational drugs, and brainstem/cerebellar disorders.
Screening for these types of nystagmus in the clinic is generally completed by observing eye movements at rest and during our oculomotor screen. I screen for gaze-evoked nystagmus by pausing at the end range of my assessment (not the patient’s maximal ocular excursion) in all directions during my smooth pursuit exam – keeping in mind that gaze-evoked nystagmus would be expected at maximal ocular excursion. Spontaneous nystagmus can also be observed with VNG.
Note that spontaneous and gaze-evoked nystagmus can also be congenital.