Deep Brain Stimulation: A Window Into the Neural Mechanisms of Latent Nystagmus

Latent nystagmus is a condition marked by a nasal-ward drift of the eye that reverses depending on the fixating eye. It is commonly associated with early-onset strabismus and amblyopia and is hypothesized to result from disrupted horizontal binocular connections in the primary visual cortex (V1), leading to impaired cortical integration. This deficit extends to extrastriate areas, middle temporal (MT) and medial superior temporal (MST) regions, which are critical for coordinating conjugate gaze and vergence eye movements. The resulting imbalance in cortical processing creates a nasal-ward bias in eye movements and contributes to underdeveloped vergence and latent nystagmus.

We investigated a unique case of latent nystagmus in a patient with Parkinson's disease (PD) undergoing subthalamic nucleus deep brain stimulation (STN DBS). Although DBS addressed PD motor symptoms, the electrode placement also enabled modulation of visuomotor circuits implicated in latent nystagmus. Specifically, stimulation targeted Forel's field H2, influencing the lateral geniculate nucleus (upstream of V1), parietopontine pathway (visual cortex projections to ocular motor regions, emphasizing the role of cortical bias), and cerebellar projections via the zona incerta.

We assessed five key outcomes: reductions in slow-phase velocity and quick-phase amplitude, decreased strabismus angle, and reduced disconjugacy of quick and slow phases of nystagmus. DBS significantly improved nystagmus metrics across viewing conditions, particularly when the non-amblyopic eye was fixating, and effects were consistent in both near and far gaze.

These findings support a mechanism in which modulation of cortical bias and its downstream influence on brainstem ocular motor regions contributes to the pathogenesis of latent nystagmus.