In a recent review published in Brain Sciences, researchers reviewed existing data on visual impairments among Parkinson’s disease (PD) patients.
Background
Parkinson’s disease (PD), a widely prevalent neurodegenerative condition, affects people over the age of 60 and produces a variety of motor as well as non-motor symptoms. Because of the underlying neurodegenerative process, patients exhibit ocular, visuoperceptive, and visuospatial deficits.
Ocular impairments influence vision and eye movement, whereas visuoperceptual impairments affect visual perception and recognition. Visual impairments include problems recognizing and understanding spatial connections, evaluating distances, and navigating settings.
Visual hallucinations are prevalent in Parkinson’s disease sufferers. The neurological roots of visual-related problems in Parkinson’s disease are diverse and poorly understood.
About the review
In the present review, researchers described ocular disturbances in PD and their neuroanatomical, functional, and neurochemical correlates.
Visual disturbance in Parkinson’s disease
Lowered sensitivity of spatial contrast, decreased color discrimination, oculomotor control abnormalities, diplopia, dry eye illness, visual hallucinations (VHs), and open-angle glaucoma have been reported in PD. Inadequate performance in tests assessing high-order-type processing, including space perception, object mental rotation, successful navigation, visuospatial working memory, target localization, and spatial map representation, is associated with several visual disorders.
Macular retinal thickness, macular volume, retinal ganglion cell layer (RGC), retinal nerve fiber layer (RNFL), inner nuclear layer (INL), inner plexiform layer (IPL), outer nuclear layer (ONL), outer plexiform layer (OPL), photoreceptor layer, and retinal pigment epithelium all decrease in Parkinson’s disease.
Retinal alpha-synucleinopathy density scores correlate favorably with brain alpha-synucleinopathy density scores, pathology stage, and the motor sub-score of the Unified Parkinson’s Disease Rating Scale (UPDRS-III).
In Parkinson’s disease patients, ocular dysfunction encompasses anatomical changes, functional abnormalities, and cognitive and neurochemical changes affecting the serotoninergic, dopaminergic, and cholinergic systems.
Progressive dopamine depletion and -synuclein-mediated axonal degeneration may induce retinal degeneration. The density of -synucleinopathy in the retina correlates favorably with the density of -synucleinopathy in the brain, pathology stage, and the UPDRS-III motor sub-score.
In Parkinson’s disease patients, eyelid impairments such as decreased blink rate, apraxia in eyelid opening, blepharospasm, ptosis of the upper eyelid, and Meibomian gland illness occur. Contrast sensitivity has been found to be reduced, particularly at intermediate and high frequencies in central and peripheral regions. Color discrimination deficiencies may be an early dopaminergic sign of PD and a disease-specific characteristic.
VHs are prevalent signs of psychosis in PD patients and have been linked to fast cognitive deterioration. Visual cognition deficiencies in PD are caused by central processing dysfunction rather than specific visuospatial abnormalities, namely low-level perceptual deficits and executive function impairments.
Most patients initially appear with symptoms on one side of the body, indicating dopamine depletion largely in the contralateral hemisphere.
Neuroanatomical, functional, and neurochemical correlates of Parkinson’s disease
Gray matter shrinkage is seen in several brain areas in PD, including the main visual cortex and visual association cortices, cholinergic structures, and limbic areas. VHs in PD patients have been shown to exhibit extensive decreases in cortical thickness, especially in the cuneus and superior frontal gyrus.
Functional magnetic resonance imaging (fMRI) investigations have revealed abnormally elevated activity in anterior cortical areas and decreased activation in the parietal lobe and cingulate gyrus.
Position emission tomography (PET) investigations have found enhanced glucose metabolism in the frontal areas and reduced metabolism in the temporal-parietal-occipital region. A single-photon emission computed tomography (SPECT) research found higher perfusion in the right superior and middle temporal gyri of hallucinating PD patients. An imbalance of pedunculopontine acetylcholine projections onto various regions in the visual cortex leads to abnormal visuospatial processing in PD.
Hallucinations have been connected to the deterioration of the basalis nucleus of Meynert connecting the brainstem with frontal cortical regions, which disrupts visuospatial task execution. VHs have also been linked to lower occipital GABA levels in PD.
Visual-perceptual disorders have been reported in PD, as has a decrease in the serotonergic 5-hydroxytryptamine (5-HT2A) receptor in the dorsal and lateral prefrontal cortex bilaterally, and the orbitofrontal cortex, insula, fusiform gyrus, and temporal gyrus situated on the right side.
Conclusions
Based on the review findings, numerous perception and visual issues have been described in Parkinson’s disease patients, which are frequently poorly understood and under-recognized.
Visual deficiencies in PD are caused by a variety of networks and structures, including lower-level components like the retina and higher-level visual cognitive pathways. Cognitive skills like attention, which continually controls incoming visual data, may mitigate these issues.
Cortical thickness, structural changes in the white matter, and functional changes in the left putamen, right insula, right hippocampus, and bilateral caudate have also been reported in studies. Visuoperceptual and visuospatial abnormalities in PD have been linked to illness progression and have been recommended as an early indicator of cognitive decline.
Combining genetics with functional neuroimaging may give a useful technique for classifying and identifying possible biomarkers for therapeutic trials to prevent and treat PD.
