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Advanced Neurology Evoked potential response in parkinsonian syndromes

also noted rigidity and bradykinesia correlating with BAER prolonged N13 and N20 latency in APS patients compared
abnormalities contralateral to the clinically more affected to IPD. However, the PIGD and tremor-predominant
side in IPD. In another study, a prolonged III-V latency on IPD do not differ in terms of SSEP. Regarding the sensory
the symptomatic brainstem side was found in IPD . In pathway abnormality in Parkinson’s disease, Conte et al.
[29]
the current study, we found that BAER increased latency of postulate that disease-related dopaminergic denervation
waves III, IV, V, I-III, III-V, I-V and decreased V/I amplitude in parkinsonian syndromes results in the transmission
in IPD compared to HCs with relative sparing of wave I, of noisy and poorly differentiated sensory information
corroborating a demyelination and axonal involvement to cortical regions and suggest that abnormalities in
of central brainstem pathways in IPD. The occurrence of the periaqueductal gray matter and non-dopaminergic
dysfunction of alpha-synuclein, which is expressed in the neurotransmitter systems also play a role in contributing
inner ear, could explain a peripheral mechanism of hearing to the pathway abnormality. Of note, the measurement
[46]
loss . Functional study of the brain by single-photon of CCT is well-validated and reproducible approach. [47]
[30]
emission computerized tomography (SPECT) and fMRI The VEP, BAER, and SSEP changes correlated well
showed basal ganglia involvement in auditory stimulation. in IPD, but a few parameters in APS exhibited a good
Dysfunctional outputs from basal ganglia to the inferior correlation with the duration and severity of the disease.
colliculus, medial geniculate nucleus, and temporal cortex Compared to IPD, APS has diverse findings, which can
may explain the probable abnormality observed in the probably be ascribed to the heterogenous etiologies. The
BAER study [31-34] .
progression of electrophysiologic changes with the disease
Several studies have reported BAER anomalies in duration denoted a probable degenerative pathology in
patients with MSA [35,36] . In our study, absolute and interpeak the diseases. A negative correlation between the latency
latency was increased along with a decreased amplitude of BAER wave I with disease duration and severity in IPD
ratio of V/I waves. In pathological studies on MSA patients, probably pointed out the relative sparing of peripheral
degenerative changes were found in several nuclei and connections of auditory pathways even in the late disease
tracts close to the brainstem auditory pathway, including course. A progressively increasing positive feedback in
the substantia nigra, locus coeruleus, pontocerebellar wave I in gradually deteriorating brainstem connections
tracts, pontine nuclei, dorsal vagal nuclei, and inferior in the later course of IPD may account for the relative
olivary nuclei [37-41] . This may explain the auditory sparing of peripheral connections of auditory pathways.
pathway abnormality in patients with MSA-C. Brainstem Overall, results from the correlation analysis indicated
neuropathology may underline BAER abnormality in DLB that progressive central nervous system degeneration is a
and PDD patients, as described by Braak et al. [42] hallmark in progressive disease.
The current SSEP study showed that the central sensory The changes in specific parts registered by the
conduction time latency was increased in patients with electrophysiological tests, which denote damage to
MSA-C and MSA-P, while the rest of the patients’ SSEP specific parts of the midbrain, pons, anterior visual, and
values are within normal limits (Table 2). N13 reflects thalamocortical pathways in the brain allow us to identify
postsynaptic activity in the central gray matter of the severe involvement in these areas. Although the IPD is
cervical cord. The N20 waveform is a composite made of known to primarily affect the striatum and midbrain
signals from multiple generators within or close to the dopaminergic system, the involvement of these areas
primary cortical receiving area. Pramstaller et al. and would denote a widespread nature of the disease, which
[43]
Abbruzzese et al. reported that they did not find any is accompanied by non-motor symptoms such as sleep
[44]
SSEP latency abnormalities in patients with MSA, whereas disorders and visual hallucinations and motor symptoms
Takeda et al. reported increased N13 and N20 latency such as postural instability. Even if these areas show normal
[45]
in patients with CBD. As previously discussed, patients brain magnetic resonance imaging (MRI) results, other
with degenerative changes were noted in brainstem nuclei, assessments such as VEP, BAER, and SSEP tests might
which may cause abnormal SSEP response in MSA patients, generate abnormal results, which are indicative of the
but further research is needed for underlying pathology. disease. Thus, more in-depth studies on evoked potentials
[41]
APS patients had significantly prolonged N13 and N20 are warranted to establish distinct pathological profiles for
latency and increased somatosensory CCT compared to both IPD and APS.
HCs in our study.
5. Conclusion
On the contrary, IPD patients did not manifest these
changes. The head-to-head comparison also showed Overall, the IPD and APS patients had significant VEP,
significantly prolonged somatosensory CCT and BAER, and SSEP abnormalities of demyelination and

Volume 2 Issue 4 (2023) 11 https://doi.org/10.36922/an.1907