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  In this Article
  Introduction
  Pathophysiology
  Conclusion
   References

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Table of Contents    
NI FEATURE: THE EDITORIAL DEBATE I-- PROS AND CONS
Year : 2019  |  Volume : 67  |  Issue : 1  |  Page : 53-55

Visual perceptual abnormalities in Parkinson's disease


Department of Neurology, Govind Ballabh Pant Postgraduate Institute of Medical Education and Research, New Delhi, India

Date of Web Publication7-Mar-2019

Correspondence Address:
Dr. Sanjay Pandey
Department of Neurology, Academic Block, Room No 507, Govind Ballabh Pant Postgraduate Institute of Medical Education and Research, New Delhi
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.253588

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How to cite this article:
Panda AK, Pandey S. Visual perceptual abnormalities in Parkinson's disease. Neurol India 2019;67:53-5

How to cite this URL:
Panda AK, Pandey S. Visual perceptual abnormalities in Parkinson's disease. Neurol India [serial online] 2019 [cited 2019 May 23];67:53-5. Available from: http://www.neurologyindia.com/text.asp?2019/67/1/53/253588





  Introduction Top


Patients with Parkinson's disease (PD) frequently report visual perceptual problems, including visual misrepresentations (VM) and visual hallucinations (VH).[1] The failure to successfully integrate the available physical stimuli denotes VM. For example, a pile of clothes might be misinterpreted as an animal. VH are perceptions in the absence of any stimulus. The hallucinations seen or experienced by PD patients are complex, bizarre, involve animate objects, usually nonfrightening, but can become frightening or distressful over time. This phenomenon has been reported to be experienced by 9-44% patients with PD.[1] This percentage increases with the duration of the disease and as many as 74% of PD patients have reported VH after 20 years of suffering from the disease. Interestingly, PD patients not only experience and report VM and VH, but also report visual symptoms in the form of difficulty in reading, double vision, misjudging the distance, as well as difficulty in navigation and using maps.[2] These were commonly described in PD dementia and  Lewy body dementia More Details but are now being reported in the early stages of the PD too. These visual phenomena, rather than occurring because of a single discrete lesion, are supposed to arise from the retina, the visual pathway, cortical-subcortical regions such as the frontal, parietal, occipital cortices, and limbic regions, cholinergic and dopaminergic systems, and the disruptions of neuronal circuitry.[2],[3]


  Pathophysiology Top


Changes in visual perception and attention deficits form the substrates necessary for the formation of VH. The models, which explain VM and VH, such as the “perception and attention deficit” model by Collerton and colleagues in 2005, the “activation--input--modulation” model by Hobson et al., or the neural network failure theory by Shine et al., in 2011, are based on them. Visual perception is the integration of visual input (for example, visual acuity, colour, and contrast sensitivity) and visual processing in the cortices. Within the visual input pathway, the information passes from the retina, via the optic nerve and optic tract to the lateral geniculate nucleus (LGN) in the thalamus. From there, the signals project via the optic radiation to the primary visual cortex (V1). Visual processing then starts by processing of simple local attributes such as the orientation of lines and edges in the V1, after which the information is organized as two parallel processing streams, the ventral and the dorsal stream. The ventral stream identifies features of the objects and passes this information from V1 through areas V2 and V4 to the inferior temporal cortex. The dorsal stream processes spatial relations between objects and projects this information through areas V2 and V3 to the superior temporal and parietal cortices. There are reciprocal connections between the regions connected by these pathways, which are subjected to feedback from areas outside of these streams.[2] Any defect in this stream can lead to an impaired visual perception.

Amacrine cells, which contain dopamine as the neurotransmitter, are present in the inner border of the inner nuclear layer (INL) of the retina. Autopsy findings have shown this layer to be thinner in PD patients and that the patients also have decreased dopaminergic innervation in the parafoveal region. α syn-nuclein is also found to be deposited in this inner nuclear layer, pointing towards a possible role of retinal dysfunction in decreased visual acuity, colour perception, and contrast sensitivity.[2],[4] It is interesting to note that the PD patients have a decreased contrast sensitivity at the middle range of spatial frequencies.

Visual processing also has a role in contrast sensitivity, colour perception, line orientation, depth perception, and pattern perception, as early cortical processing involves discrimination of local attributes. This early processing paves the way for object recognition, motion perception, and visuospatial construction in the higher levels of cortical processing. It is found that PD patients have a difficulty in horizontal line orientation, poor motion sensitivity, and difficulty in face and emotion recognition, especially the negative emotions, because of decreased contrast sensitivity. These primary processing errors lead to further deficits in the higher order processing. “Object processing” refers to the ability to identify common objects by their silhouettes. It occurs in V2, V4, and the lateral occipital complex, especially in the right hemisphere. Hence, PD patients with left-sided symptoms tend to have a difficulty in processing overlapping objects leading to misrecognition of objects. PD patients also have impaired visuospatial construction in terms of copying intersecting pentagons and clock drawings.

These deficits of contrast sensitivity, difficult facial recognition, and inability to identify patterns lead to VM and VH. These are mostly seen in dim light, with difficulty in recognizing faces or silhouettes, “passage hallucinations” because of illusions of objects in the peripheral vision, or complex hallucinations because of defective interactions between networks such as the dorsal attention network (DAN), the ventral attention network (VAN), and the default mode network (DMN). The hypothesis of attentional network states that faulty interaction of these networks leads to hallucinations.[2] According to this hypothesis, DAN is concerned with the external attention, DMN is associated with the resting state of the mind, whereas VAN is used for the salience stimulus monitoring and for switching between the DAN and the DMN. For proper interpretation of stimuli, DAN needs to keep a check on the DMN and VAN, as uninhibited VAN and DMN may lead to an ambiguous perception. In simple terms, when a stimulus is perceived and the DAN cannot filter the stimulus, DMN, which is the default network, wrongly retrieves an aberrant pre-recorded percept from the episodic or semantic knowledge. The impaired visual processing leads to misperception of a salient stimulus by the VAN. The wrong retrieval of knowledge combined with the improper perception of the stimulus leads to hallucination if the DAN, which directs attention and encodes neural signals according to the behavioral significance of the stimulus, does not check it. For example, a garden hose can be forgotten by the DMN and perceived as a snake by the VAN because of an ambiguous visual perception, when left unchecked by DAN.[3] Lenka et al., reviewed the literature focusing on structural and functional neuroimaging in patients of PD having hallucinations. In structural voxel-based imaging, they found that areas corresponding to visuospatial processing, attention, and memory had reduction in the grey matter volume rather than in a single distinct area. Furthermore, functional imaging in the form of positron emission tomography (PET) and single-photon emission-computed tomography (SPECT) revealed abnormalities in both the streams of visual pathways and the processing of occipital cortex. These findings support the theory that networking deficits and improper perception of visual stimuli lead to the hallucinations.[5] The presence of visual dysfunction is seen concurrently with the increased duration of disease, rapid eye movement (REM) behavioral disorders (RBD), postural instability with gait disorder, cognitive impairment, and side effects of dopaminergic medications. Also, it has now been reported that oculovisual features can be seen not only in the early and middle stages of PD but also in the prodromal stage of PD.[4] The presence of color vision deficit and contrast sensitivity have been shown to have a better discriminatory power in the diagnosis of PD than other non-motor features in the prodromal stage. Similarly, defects in color vision, impaired visuospatial construction, and hallucinations are harbingers of PD-related dementia.[2],[4]

Tests to detect visual perceptual abnormalities

Complex paradigms of serial grey scale images with constant noise, appearing slowly over a time period, have been used to test image recognition in patients with VH in PD.[6] Shine et al.,[7] in 2012, reported that a novel bistable percept paradigm helps to identify people who have VH and VM. The bistable perception is an interesting phenomenon in visual illusions, wherein an ambiguous picture is given, that is, a picture, which has two or more possible views or images. The illusion can be of “within-category” or “between-category.” The classic examples of each would be the Necker's cube and the Eskimo-Indian picture, respectively. At a given point of time, a person can see one image at a time and needs to flip his “view” to visualize another view-point or another image. It has been reported by the functional magnetic resonance imaging (fMRI) studies that when a person moves from one viewpoint to another, like in the case of a Necker's cube, the frontal and the parietal areas are activated. On the other hand, when a person switches between one image and the other, the frontal and the temporal area are activated, underlying the concept of dorsal and ventral imagery of visual processing. As we know that the visual processing is impaired in PD, this bistable percept can help in diagnosing VM. In this issue, Wadhwa and colleagues have published a paper titled “Assessment of visual misperceptions in patients with Parkinson's disease using the single and bistable percept as testing tools.”[8] They have also used the bistable percept to test VM in PD patients. They point out that these misrepresentations are common in PD and correlate with attention deficits tested by the trail making test. This correlation of attention deficits with visual misrepresentations bolsters the theory that decreased attention forms a necessary substrate for generation of these visual phenomena.


  Conclusion Top


Visual misrepresentations and hallucinations in a PD patient signify an improper perception of stimulus because of various oculovisual dysfunctions and also attention deficits. It is also seen that they can be present in the early and middle stages of PD and may also be present in the prodromal phase of the disease. These visual phenomena are also related to specific subtypes such as postural instability with gait disorder and PD dementia. An early detection of these misrepresentations by tests like the bistable percept can help in the prognosticating and future management of the patient.



 
  References Top

1.
Barnes J, David AS. Visual hallucinations in Parkinson's disease: A review and phenomenological survey. J Neurol, Neurosurg Psychiatry 2001;70:727-33.  Back to cited text no. 1
    
2.
Weil RS, Schrag AE, Warren JD, Crutch SJ, Lees AJ, Morris HR. Visual dysfunction in Parkinson's disease. Brain 2016;139:2827-43.  Back to cited text no. 2
    
3.
Shine JM, Halliday GM, Naismith SL, Lewis SJ. Visual misperceptions and hallucinations in Parkinson's disease: Dysfunction of attentional control networks? Mov Disord 2011;26:2154-9.  Back to cited text no. 3
    
4.
Armstrong RA. Oculo-visual dysfunction in parkinson's disease. J Parkinsons Dis 2015;5:715-26.  Back to cited text no. 4
    
5.
Lenka A, Jhunjhunwala KR, Saini J, Pal PK. Structural and functional neuroimaging in patients with Parkinson's disease and visual hallucinations: A critical review. Parkinsonism Relat Disord 2015;21:683-91.  Back to cited text no. 5
    
6.
Meppelink AM, de Jong BM, Renken R, Leenders KL, Cornelissen FW, van Laar T. Impaired visual processing preceding image recognition in Parkinson's disease patients with visual hallucinations. Brain 2009;132:2980-93.  Back to cited text no. 6
    
7.
Shine JM, Halliday GH, Carlos M, Naismith SL, Lewis SJ. Investigating visual misperceptions in Parkinson's disease: A novel behavioral paradigm. Mov Disord 2012;27:500-5.  Back to cited text no. 7
    
8.
Wadhwa A, Bajaj BK, Pandey S. Assessment of visual misperceptions in patients with Parkinson's disease using single and bistable percept as testing tools. Neurol India 2019;67:123-8.  Back to cited text no. 8
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