As a more complete picture of the clinical phenotype of Parkinson's disease emerges, non-motor symptoms have become increasingly studied. Prominent among these non-motor phenomena are mood disturbance, cognitive decline and dementia, sleep disorders, hyposmia and autonomic failure. In addition, visual symptoms are common, ranging from complaints of dry eyes and reading difficulties, through to perceptual disturbances (feelings of presence and passage) and complex visual hallucinations. Such visual symptoms are a considerable cause of morbidity in Parkinson's disease and, with respect to visual hallucinations, are an important predictor of cognitive decline as well as institutional care and mortality. Evidence exists of visual dysfunction at several levels of the visual pathway in Parkinson's disease. This includes psychophysical, electrophysiological and morphological evidence of disruption of retinal structure and function, in addition to disorders of ‘higher’ (cortical) visual processing. In this review, we will draw together work from animal and human studies in an attempt to provide an insight into how Parkinson's disease affects the retina and how these changes might contribute to the visual symptoms experienced by patients.

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The retina in Parkinson's disease

Patients with Parkinson's disease have a number of specific visual disturbances. These include changes in colour vision and contrast sensitivity and difficulties with complex visual tasks such as mental rotation and emotion recognition. We review changes in visual function at each stage of visual processing from retinal deficits, including contrast sensitivity and colour vision deficits to higher cortical processing impairments such as object and motion processing and neglect. We consider changes in visual function in patients with common Parkinson's disease-associated genetic mutations including GBA and LRRK2 . We discuss the association between visual deficits and clinical features of Parkinson's disease such as rapid eye movement sleep behavioural disorder and the postural instability and gait disorder phenotype. We review the link between abnormal visual function and visual hallucinations, considering current models for mechanisms of visual hallucinations. Finally, we discuss the role of visuo-perceptual testing as a biomarker of disease and predictor of dementia in Parkinson's disease.

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Visual dysfunction in Parkinson's disease.

Visual deficits related to dopamine deficiency in experimental animals and parkinson's disease patients

Visual hallucinations (VH) in Parkinson's disease (PD) are a chronic complication in 30 to 60% of treated patients and have a multifaceted phenomenology. Flickering, faultive impressions, and illusionary misperceptions precede the core syndrome of stereotyped, colorful images. The patient variably recognizes these images as hallucinations, being rarely irritated or frightened and more often amused as a bystander. Although studies on VH in PD focus on several research domains, no comprehensive, unified theory has been developed to study their pathophysiology. We have adapted Hobson's work on the states of consciousness and propose a model integrating seemingly disparate data on VH. We suggest that VH should be considered as a dysregulation of the gating and filtering of external perception and internal image production. Contributive elements and anatomical links for the model include poor primary vision, reduced activation of primary visual cortex, aberrant activation of associative visual and frontal cortex, lack of suppression or spontaneous emergence of internally generated imagery through the ponto-geniculo-occipital system, intrusion of rapid eye movement dreaming imagery into wakefulness, errative changes of the brainstem filtering capacities through fluctuating vigilance, and medication-related overactivation of mesolimbic systems. Different etiologies likely produce different phenomenologies and the prognosis may not be uniform. This new conceptual framework permits an anatomical view of VH and suggests new, testable hypotheses regarding their pathophysiology and therapy.

Repeated visual hallucinations in Parkinson's disease as disturbed external/internal perceptions: Focused review and a new integrative model

Chapter 10 Functional roles of dopamine in the vertebrate retina

Visual contrast sensitivity was measured using 2 cycle/deg sinewave gratings of different orientations in 10 patients with Parkinson's disease and in 15 age-matched controls. Loss of visual contrast sensitivity was found in 6 patients, all of whom had normal visual acuity. Visual loss depended on grating orientation; in all cases the maximum sensitivity loss was for the horizontal. Sensitivity loss was most marked at a temporal frequency of 4 to 8 Hz. Visual fields gave no hint of the orientation selectivity. We conclude that orientation selectivity implicates visual cortical cells in Parkinson's disease. We tentatively suggest that a preferential loss of contrast sensitivity to horizontal gratings might be due to a functional abnormality in the striate cortex that relatively spares the extrastriate cortex. The dependence of visual loss on temporal frequency combined with the sparing of visual acuity might possibly be understood if Parkinson's disease preferentially affects the visual pathway leading from the retina to cortex via the magnocellular layer of the lateral geniculate nucleus. There is an intriguing similarity between the pattern of visual loss in Parkinson's disease and in multiple sclerosis.

C. Maxner

Papers

Orientation-selective visual loss in patients with parkinson's disease