Parkinson’s disease (PD), the second most common neurodegenerative disorder, affects around ten million people worldwide. Visual impairments in PD are more widespread than often recognized, with patients scoring significantly lower on visual function questionnaires compared to healthy controls. These deficits include a difficulty in shifting gaze (saccades), leading to disrupted reading and visual scanning, and impaired vergence, affecting depth perception and spatial navigation. Up to one-third of PD patients experience diplopia, and 23% report tired eyes or blurred vision during reading. Vergence issues in PD include increased latency, reduced speed, and reliance on alternative eye movements. Gaze-holding abnormalities in PD include excessive fixational eye movements like microsaccades and pendular movements, linked to abnormal basal ganglia function. Deep brain stimulation (DBS) of the subthalamic nucleus (STN) impacts these movements, with varying effects on saccade amplitude and intersaccadic intervals (ISIs). These abnormalities could serve as markers for PD progression. Strabismus in PD often presents with diplopia and blurred vision, linked to convergence insufficiency. This can improve with levodopa or DBS, but convergence ability fluctuates, complicating management. DBS can cause transient diplopia, requiring careful monitoring. PD also affects visually guided and memory-guided saccades, with greater impairment in the latter. This impacts reading and visual scanning. PD patients have higher anti-saccadic error rates, linked to cognitive dysfunction. The superior colliculus and brainstem burst generators play key roles, with PD causing premature activation of colliculus fixation zones, leading to interrupted and irregular saccades. Understanding these mechanisms provides insights into PD’s motor and perceptual dysfunctions.