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The flocculus of cerebellum inhibits the vestibular nuclei and keeps the eyes steady during downward gaze. Disinhibition of the flocculus leads to slow upward drift of the eyes, followed by corrective downward saccade—the ‘downbeat’—hence the name ‘downbeat’ nystagmus. Asymmetry in the vertical smooth pursuit pathway or, imbalance in the neural tone of the central connections of the vertical semicircular canals and otoliths can cause downbeat nystagmus. Idiopathic downbeat nystagmus, however, is the most common form.
Historically, the therapeutic approach for downbeat nystagmus has focused on the compounds that affect serum pH or inhibitory neurotransmitters modulating the cell membrane function. Acetazolamide was traditionally used for the treatment of downbeat nystagmus in patients with episodic ataxia.1 Baclofen (reinforcing the function of inhibitory neurotransmitter gamma-amino butyric acid (GABA)) or gabapentin (blocking alpha-2-delta calcium channels) rarely improved …
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