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Clinical-instrumental algorithm for assessment visuospatial dysfunction in patients with Parkinson’s disease

K. Stepanchenko (Kharkiv, Ukraine)

Meeting: 2019 International Congress

Abstract Number: 1629

Keywords: Neurophysiology, Parkinsonism, Visuospatial deficits

Session Information

Date: Wednesday, September 25, 2019

Session Title: Non-Motor Symptoms

Session Time: 1:15pm-2:45pm

Location: Agora 3 West, Level 3

Objective: To study the features of visual spatial dysfunction (VSD) in patients with Parkinson’s disease (PD) using modern clinical-neuropsychological, ophthalmological and neuroimaging methods.

Background: Visual spatial dysfunction is often an early symptom of neurodegenerative disease, however, there is no single algorithm for both clinical and instrumental diagnosis of VSD in patients with PD.

Method: Two groups: 1st (79 pers., ages 65,8±8,5) – patients with PD, 2nd (34 pers., ages 64,2±4,7) – patients without PD (control group) were examined. Neurological and ophthalmological examination, neuropsychological examination: Yerkes test, mirror test “mirror numbers and letters” and “clock hands” (AR Luria, 1969), “noisy” images (R. Sells, 2011), reduced test of Raven’s progressive matrices (J. Raven et all, 2000), Poppelreuter test (W. Poppelreuter, 1925)); cognitive functions (MMSE, FAB (Frontal assessment battery, B. Dubois, 2000), CDR (Clinical Dementia Rating, JS. Morris, 1993)); optical coherence tomography (OCT, protocols – Ganglion Cell Complex (GCC), Retinal Nerve Fiber Layer (RNFL), Macular Map 5 (MM5)); MRI morphometry were performed.

Results: The thinning of the retinal sections of the eye assessed by OCT (thickness of the lower part of the retinal ganglion cell complex (89,1±7,2 μm versus 96,1±7,6 μm, p<0,01), lower quadrant of the layer of nerve fibers of the retina (121,3±17,5 μm versus 124,9±15,6 μm, p<0,05), the central fossa (278,5±17,2 μm versus 286,8±18,8 μm, p<0,05) and the upper hemisphere of the paracentral zone (319,9±14,4 μm versus 328,6±15,1 μm, p<0,01)) and the cerebral cortex atrophy assessed by MRI morphometry (calcarine sulcus (р<0,01), parietal-occipital sulcus, inferior occipital gyrus and sulcus (p<0,05)) were the most significant for the development of VSD in PD. The risk of VSD (visual agnosia, illusory optic-spatial phenomena, hallucinatory optic-spatial phenomena) increased with the development of dementia (p<0,05).

Conclusion: VSD in PD can be caused by changes in the light-transmitting systems of the eye, morphological changes in certain layers of the retina and degeneration of the neurons of the parietal and occipital cortex of the brain. Diagnostics of VSD in PD should be carried out clinical-neuropsychological tests (Poppelreuter test, reduced test of Raven’s progressive matrices, Yerkes test, MMSE, FAB), OCT (GCC, RNFL, MM5) and, in some cases, Brain MRI.

To cite this abstract in AMA style:

K. Stepanchenko. Clinical-instrumental algorithm for assessment visuospatial dysfunction in patients with Parkinson’s disease [abstract]. Mov Disord. 2019; 34 (suppl 2). https://www.mdsabstracts.org/abstract/clinical-instrumental-algorithm-for-assessment-visuospatial-dysfunction-in-patients-with-parkinsons-disease/. Accessed May 10, 2025.
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