Page 41 - AN-2-4

Advanced Neurology Evoked potential response in parkinsonian syndromes

tomography studies in Parkinson’s disease patients showed IPD patients exhibited more pronounced latency and
the thinning of the retinal nerve fiber layer, macula, and amplitude changes in P100 and N145, indicating bilateral
annular zone around the fovea [10-12] . The post-mortem study higher cortical involvement in occipital-temporal-parietal
of IPD patients showed a decrease in dopamine in retinal lobes. Our study corroborated findings of many studies by
cells . The possible mechanism of visual dysfunction in showing extensive bilateral involvement in visual pathways
[13]
Parkinson’s disease patients could be pathological changes correlating with the severity of the disease.
in the caudal nuclei, putamen nuclei, hypothalamus, and VEP N75, P100, and N145 latency were increased
[12]
pontine nucleus coeruleus . It could result in cholinergic bilaterally and N75-P100 amplitude was reduced
system dysfunction that diffusely affects the brainstem bilaterally in APS compared to HCs. So, there were both
auditory pathway. The degenerative pathology in these demyelinating and axonal changes in the visual cortical
regions causes dopaminergic neuron degeneration and a areas, as well as in anterior visual pathways in APS in our
decrease in dopamine production and secretion, which study. We noted a prolonged P100 latency in the MSA
may cause dysfunction of the inter-plexiform cells and group in our study, consistent with findings reported by
horizontal cells in the retina, contributing to the abnormal Abele et al. At present, the mechanisms underlying
[23]
changes of VEP . Long-term dopamine deficiency could the slowed conduction in the visual pathways remain
[14]
trigger a compensatory decrement of acetylcholine and unclear. The probable hypothesis of increased latency and
lead to changes in VEP latency. A retinal dopaminergic decreased amplitude may be related to the involvement
deficiency could also underlie some visual changes. of the nigrostriatal system, which leads to manifestations
Besides, the expression of alpha-synuclein (α-syn) in such as gliosis, vacuolation, and glial cytoplasmic inclusion
the vertebrate retina may shed light on the pathological (GCI) mainly in the putamen and substantia nigra, causing
mechanism behind the visual changes .
[15]
dopamine deficiency and possibly abnormal function of the
By investigating the structural changes in the retina retinal cells. In this study, CBD patients showed increased
using spectral-domain optical coherence tomography, latency. A previous study demonstrated that in CBD
Ma et al. found that the patterns of retinal involvement in patients, subcortical and deep gray matter involvement
of IPD, MSA, and PSP were different and also correlated leads to basal ganglia dysfunction, especially posterior
with disease duration . Another study showed that putamen, which causes visual dysfunction . An earlier
[16]
[24]
dopaminergic amacrine cell loss leads to activation of study by Bak et al. on APS using VOSP neuropsychological
the rod pathway, which subsequently results in reduced tests confirmed that visuospatial function was intact in
[25]
contrast sensitivity in IPD . Retinal thinning, which the MSA patients, whereas profound visuospatial deficits,
[17]
started in the early stage of IPD, correlated with disease not correlated with MMSE score, were detected in the
severity and might be related to dopaminergic degeneration CBD patients. On the contrary, PSP patients had milder
in the substantia nigra . Moreover, smaller thickness of visuospatial involvement, which was also correlated with
[18]
parafoveal ganglion cell-inner plexiform layer complex and the decline in MMSE scores.
peripapillary retinal nerve fiber layer in IPD constitutes an BAER wave I represented the auditory nerve compound
increased risk for cognitive decline at 3 years . In this
[19]
study, we found that the duration and severity of the disease action potential from the most distal portion of the auditory
had a positive correlation with greater extent of damage in nerve. Wave II was generated mainly in the proximal
the visual pathway. Both ventral and dorsal visual streams auditory nerve but probably included a contribution from
are involved in IPD. IPD patients with freezing of gait had the intra-axial part of the nerve and the cochlear nucleus.
The wave III potential was generated in the lower pons in the
significantly reduced dopamine levels in the nigrostriatal superior olive and trapezoid regions. Finally, the generators
system and low metabolism of primary visual cortex . of waves IV and V lay in the upper pons and the midbrain,
[20]
A recent functional connectivity study using functional
magnetic resonance imaging (fMRI) and Visual Object as high as the inferior colliculus. In this study, increased
and Space Perception battery (VOSP) by Kawabata absolute latency of waves I, III, and V and interpeak latency
et al. found that IPD patients had visual perceptual of I-III, III-V were noted on both sides in the patients with
[21]
disturbance due to decreased connectivity in the ventral IPD, MSA-C, DLB, and PDD. A decreased V/I amplitude
visual feedback pathway. Overall, visual abnormalities ratio was noted in patients with MSA-C.
[10]
in IPD encompass changes in visual acuity, contrast Liu et al. noted prolonged latency of waves III, V, III-V,
sensitivity, color vision, retinal function, eye movements, and I-V in IPD patients. In their respective studies, Hassan
[26]
[27]
cortical visual processing, peripheral vision, object et al. and Shalash et al. found prolonged latency of
perception, visuospatial construction, motion perception, waves V and I-V. Daniel et al. noted that waves II, III, IV,
[28]
facial neglect, and face and emotion recognition . The V, and III-V were bilaterally prolonged, and Shalash et al.
[27]
[22]
Volume 2 Issue 4 (2023) 10 https://doi.org/10.36922/an.1907