occurs in primary position should be observed for at least 2 minutes to be certain that the condition is not PAN. A patient with PAN may also demonstrate periodic alternating head turn to minimize the nystagmus, in accordance with Alexander’s law.

PAN is typically associated with dysfunction of the cerebellar nodulus and uvula, which play a role in the time constant of rotational velocity storage. An oscillatory shifting of the null point results. Common causes include multiple sclerosis, cerebellar degeneration, Arnold-Chiari type I malformation, stroke, use of anticonvulsant medication, and bilateral loss of vision. If the bilateral vision loss is reversible (eg, caused by a vitreous hemorrhage), PAN may be abolished. Baclofen can be effective for the acquired form of this nystagmus.

Acquired Pendular Nystagmus

Acquired pendular nystagmus includes pendular, slow-phase eye movements in the horizontal, vertical, and torsional planes (often forming elliptical waveforms). (In contrast, the much rarer congenital pendular nystagmus usually manifests with only horizontal movements.) Pendular nystagmus with both vertical and horizontal components produces oblique nystagmus (if the components are in phase) or circular or elliptical nystagmus (if the components are out of phase). The eye movements may be conjugate or disconjugate and are often dissociated.

The localizing value of acquired pendular nystagmus is poor. It is most commonly observed in patients with multiple sclerosis, who may exhibit asymmetric or monocular forms. This form of nystagmus can also develop after blindness occurs secondary to optic nerve disease, including that due to multiple sclerosis. Assuming reduced vision in both eyes, the nystagmus is typically larger in the eye with poorer vision.

Oculopalatal Myoclonus or Tremor

Acquired pendular nystagmus may accompany palatal myoclonus, an acquired oscillation of the palate. The eye movements are continuous and rhythmic, occur at a frequency of approximately 1 Hz, typically conjugate in the vertical plane, and persist during sleep. This eye movement disorder may also be associated with synchronous movements of the facial muscles, pharynx, tongue, larynx, diaphragm, trunk, and extremities. The condition usually arises several months (rarely, up to years) after a lesion occurs that involves the Guillain-Mollaret triangle—a region that encompasses pathways from the deep cerebellar nuclei through the superior cerebellar peduncle and the central tegmental tract to the contralateral inferior olive in the medulla. Lesions within this pathway (most often within the central tegmental tract) can disrupt transmission between the cerebellum, specifically the flocculus, and the inferior olive. The lesion produces inferior olivary hypertrophy, which is easily visualized with MRI as a T2 hyperintensity within 1 or both inferior olives.

See-Saw Nystagmus

See-saw nystagmus is a form of disconjugate nystagmus in which 1 eye elevates and intorts while the other eye depresses and extorts, movement reminiscent of that of a see-saw. The eye movements are