Downbeat nystagmus: a practical approach based on a clinical case

Spontaneous downbeat nystagmus (DBN) is the most common form of acquired nystagmus, characterized by a slow upward ocular drift and a corrective downward quick phase. The pathophysiology involves a final common pathway leading to decreased inhibition of the superior vestibular nucleus, often secondary to lesions in the flocculonodular lobes (flocculus/paraflocculus, FL/PFL), the paramedian tract (PMT), or the dorsal vermis. The clinical presentation generally includes chronic dizziness, gait unsteadiness, and oscillopsia. The causes are diverse, encompassing Chiari malformation, vascular and demyelinating lesions, hereditary and acquired cerebellar ataxias, and toxic-metabolic causes. Approximately 40% of DBN cases remain idiopathic. The treatment involves disease-specific management, prism glasses, and vestibular rehabilitation. Pharmacotherapy, such as clonazepam, gabapentin, or baclofen (with 4-aminopyridine being the most beneficial but often unavailable), is considered a second-line intervention.