Central Positional Nystagmus

Purpose of review Central positional nystagmus (CPN) is attributed to disease affecting the central vestibulo-cerebellar pathways. It can be associated with prominent vertigo, oscillopsia, and dysautonomia. Its treatment highly depends on the etiology, and response is fairly heterogenous. This review presents a critical appraisal of CPN therapies. Recent findings Anecdotal reports have stated efficacy of 3,4-diaminopyridine, 4-aminopyridine, and clonazepam in downbeating CPN secondary to structural lesions. In tumors, CPN may improve after tumoral resection and radiotherapy. In multiple sclerosis, intravenous steroids may abate CPN during a relapse. In paraneoplastic CPN, remission has been occasionally observed after tumoral excision, but relapses may follow. In autoimmune ataxia, intravenous immunoglobulin and oral baclofen have been shown to improve upbeating CPN. In genetic ataxia, acetazolamide seems to be more effective in resolving ictal episodes than non-ictal CPN and ataxia. In vestibular migraine, prophylactic treatment seems to provide long-term improvement of attacks manifesting with CPN. Non-invasive vagus nerve stimulation has abolished CPN in a vestibular migraine attack. CPN secondary to toxics not responding to drug discontinuation might need further treatment such as midazolam or clonazepam. Prospective randomized placebo-controlled treatment trials using objective baseline, short- and long-term assessments of CPN, and related symptoms are highly needed.

Automated summary

This review evaluates the treatment options for central positional nystagmus (CPN) and highlights the heterogeneity in treatment response. Various therapeutic approaches have been suggested for different etiologies of CPN.