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Advanced Neurology Neurophysiology in hypokinetic disorders

from PD patients in the OFF-medication state. An supplemented with LDR to levodopa. Moreover, indirect
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increase of EEG beta coherence in the cortico-cortical and surrogate markers of neuroplasticity, such as P300, MEPs,
cortico-thalamic coupling, correlating with PD severity and BP, could be used to evaluate changes in the cortical
and dopamine transporter activity, was observed, and areas influencing the basal ganglia of PD patients, further
through machine learning, an EEG discriminant classifier highlighting the prospects of neurophysiology in clinical
was identified to parallel the loss of dopamine synapses practice and PD treatment. 7
in PET imaging. Such observations could support the
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utility of EEG in monitoring disease progression, also in 3.3. Neurophysiological assessments of APSs
a clinical routine setting. The influence of dopaminergic APSs typically include alpha-synucleinopathies (e.g., MSA)
26
treatment on PD cortical activity was recently explored and tauopathies (i.e., PSP and CBS). Despite the recent
by combining EEG data and graph theory to evaluate declining interest in the neurophysiology of APS, several
changes in the connectome and processing areas of the studies have attempted to better characterize the different
resting state after levodopa treatment. Enhanced gamma conditions in APS to offer a valid differential diagnosis that
27
brain connectivity and reduced beta band connections in is comparable to the gold standard of diagnosis, that is,
the basal ganglia were observed after levodopa treatment, post-mortem investigation. 30-39 A more precise diagnosis in
demonstrating that dopaminergic treatment could affect the clinical setting could facilitate the accurate enrollment
the high-frequency brain connectome. 27 of APS patients in new and ongoing APS-related clinical
trials. The neurophysiological features of MSA, PSP, and
3.2.4. Neurophysiological examinations for the
therapeutic management of early PD CBS accordingly, based on the research findings from 2019
to August 2023, are summarized in Table 2. 30-35
Despite the complex pathophysiological of PD, several
recent studies (involving drug-naïve PD patients) have 3.3.1. Neurophysiological features of MSA
reported a practical neurophysiological approach to Recent studies have studied the neurophysiological
manage PD with the best medical treatment. 7,28 features of MSA through EMG examinations. 30,31 An
Impaired cortical excitability was recently observed EMG study assessed the adductor thyroarytenoid and
in untreated PD patients at an early stage through the the abductor posterior cricoarytenoid muscles of MSA
combined use of surrogate markers of neuroplastic patients affected by nocturnal stridor during diurnal
30
changes, for example, P300, MEPs, and BP. These time. Both MSA patients with Parkinsonian phenotype
7
abnormalities were ameliorated, and neurophysiological (MSA-P) and MSA patients with cerebellar phenotype
parameters were restored based on the patients’ long- (MSA-C) predominantly exhibited a dystonic pattern in
duration response (LDR) to chronic levodopa treatment the adductor thyroarytenoid muscle during inspiration,
(i.e., 250 mg every 24 h for 15 days). The patients but MSA-C also exhibited neurogenic findings of the vocal
7,29
also performed specific motor exercises in a double- cord muscles. The observed neurophysiological features
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task setting to evaluate the effect of motor learning on highlighted the different pathophysiology of stridor
7
neuroplasticity. Patients who did not achieve LDR after between MSA phenotypes, possibly related to dysfunctional
the 15-day treatment also did not display improvements supranuclear mechanisms in MSA-P (i.e., dystonic
in neurophysiological parameters, regardless of the motor pattern) and the additional nuclear damage in MSA-C
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exercises. In summation, motor learning alone could not (i.e., dystonic-plus pattern). Besides that, the clinical
7
improve the surrogate markers of cortical excitability, and presentation of MSA and PD could be relatively similar,
it was only with the synergistic association of both LDR for example, MSA patients may respond to levodopa in the
and motor training that the neurophysiological markers absence of cerebellar signs, while PD patients may exhibit
of neuroplasticity were restored (with adaptive changes to autonomic symptoms at the early stages of PD. A normal
the basal ganglia and cortical networks). This finding was EMG examination of the external anal sphincter (EAS)
7
also corroborated in another study that detected changes could reportedly differentiate PD from MSA patients,
in the grey matter volume of cortical areas involved in particularly within the first 5 years of the disease onset.
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motor control of early PD patients with a predisposition A recent study identified EMG neurogenic patterns in the
28
to develop LDR to levodopa. Therefore, clinicians should EAS of MSA patients, permitting prognoses according to
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only provide levodopa treatment to achieve sustained LDR neurophysiological findings. The increasing severity of
and induce positive adaptive changes to the basal ganglia EAS electrophysiological impairment paralleled diagnostic
and cortical networks. Moreover, significantly better accuracy and prognosis of the disease, suggesting that
outcomes (e.g., neuroplastic and motor improvements) can the technique could be employed in clinical practice to
be achieved when exercises and rehabilitation in PD are predict the severity and the progression of MSA. A recent
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Volume 3 Issue 1 (2024) 6 https://doi.org/10.36922/an.1961