Visual Dysfunction in Parkinson's Disease

Abstract

Non-motor symptoms in Parkinson's disease (PD) include ocular, visuoperceptive, and visuospatial impairments, which can occur as a result of the underlying neurodegenerative process. Ocular impairments can affect various aspects of vision and eye movement. Thus, patients can show dry eyes, blepharospasm, reduced blink rate, saccadic eye movement abnormalities, smooth pursuit deficits, and impaired voluntary and reflexive eye movements. Furthermore, visuoperceptive impairments affect the ability to perceive and recognize visual stimuli accurately, including impaired contrast sensitivity and reduced visual acuity, color discrimination, and object recognition. Visuospatial impairments are also remarkable, including difficulties perceiving and interpreting spatial relationships between objects and difficulties judging distances or navigating through the environment. Moreover, PD patients can present visuospatial attention problems, with difficulties attending to visual stimuli in a spatially organized manner. Moreover, PD patients also show perceptual disturbances affecting their ability to interpret and determine meaning from visual stimuli. And, for instance, visual hallucinations are common in PD patients. Nevertheless, the neurobiological bases of visual-related disorders in PD are complex and not fully understood. This review intends to provide a comprehensive description of visual disturbances in PD, from sensory to perceptual alterations, addressing their neuroanatomical, functional, and neurochemical correlates. Structural changes, particularly in posterior cortical regions, are described, as well as functional alterations, both in cortical and subcortical regions, which are shown in relation to specific neuropsychological results. Similarly, although the involvement of different neurotransmitter systems is controversial, data about neurochemical alterations related to visual impairments are presented, especially dopaminergic, cholinergic, and serotoninergic systems.

Keywords: Parkinson’s disease; dopamine; visual hallucinations; visual impairment; visuoperceptive deficit; visuospatial deficit.

Figure 1

Portion of a human retina. A: Amacrine cell; Bi: Bipolar cell; BM: Bruch’s membrane; C: Cone; GCL: Ganglion cell layer; H: Horizontal cell; INL: Inner nuclear layer; IPL: Inner plexiform layer; IS: Inner segment; M: Muller cell; ONL: Outer nuclear layer; OPL: Outer plexiform layer; OS: Outer Segment; P: Pigment epithelial cell; R: Rod; RPE: Retinal pigment epithelium; G: Ganglion cell; AX: Axons. Adapted from Hartmann and Schmid [43]. Image licensed under GFDL by the author. https://de.wikipedia.org/wiki/Datei:Retina.jpg (accessed on 19 June 2023).

Figure 2

The van Ommen [182] model of visual hallucinations. Complex VHs are the result of a dissociation of higher-order visual processing areas from the primary visual cortex. Simultaneously, a looping of brain activity across the outside-world-focused DAN, the inner-world-focused and memory-related DMN, and the saliency-focused VAN, bias conscious visual perception away from information coming from the outer world and towards internally generated percepts. Visual network (VIS). Modified from “Human Brain sketch with eyes and cerebrellum.svg”, work released into the public domain by Hankem. https://commons.wikimedia.org/wiki/File:Human_Brain_sketch_with_eyes_and_cerebrellum.svg (accessed on 11 July 2023).