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Advanced Neurology Neurophysiology in hypokinetic disorders

3.2.2. Transcranial magnetic stimulation (TMS) the muscle condition by restoring the recruitment of the

TMS is a useful tool for characterizing extrapyramidal motor units. 21
disorders, such as PD. A recent study reported that 3.2.3 Cortical potentials and electroencephalography
12
tremor-dominant PD patients exhibited reduced resting
motor threshold (RMT) and active motor threshold as The clinical use of cortical potentials in PD has progressively
7,22
13
compared to akinetic-rigid PD patients. In another study, decreased in recent years. It was recently reported that
tremor was assessed by spectral analysis, corticomuscular the amplitude of the late contingent negative variation
coherence (CMC), and tremor resetting produced by (CNV) over the central vertex was significantly reduced
TMS over M1. Re-emergent tremors displayed similar in advanced PD patients, and this decrease correlated with
14
22
CMC and tremor resetting at a slightly higher frequency the severity of the motor symptoms of PD. Moreover, the
as compared with rest tremors, indicating the direct use of cortical potentials (e.g., P300 and BP) was recently
7
involvement of M1 in generating tremors. Likewise, proposed as a therapeutic strategy for PD management.
14
M1 is also a crucial factor for tremor suppression in Nonetheless, EEG remains the widely used method for
PD. Patients with tremor suppression exhibited a higher PD management. 23-27 The cortical networks, involved in the
CMC at tremor frequency during both rest and postural restoration of normal movements after the occurrence of
tremors and a higher postural tremor resetting index upper limb freezing in PD, were studied with 62-channel
15
as compared to those without tremor suppression. surface EEG during a repetitive finger-tapping task.
23
It was also observed that the rest tremor frequency Before the task (at voluntary stops), it was observed that
was similar between the two groups (with vs. without alpha power decreased over the primary sensorimotor
tremor suppression), but the postural tremor frequency cortex (C3), whereas beta power increased over C3. The
23
was lower in patients with tremor suppression. A restoration of a regular tapping motion led to a decrease in
15
reduction in short-interval intracortical inhibition (SICI) beta power over C3 (i.e., reduction in the beta activity of
was observed on the less affected side (LAS) in non- parieto-occipital areas), involving the frontocentral regions
dyskinetic and dyskinetic PD patients, as well as in drug- and subsequently, the ipsilateral right frontotemporal
naïve patients, where LAS was minimally symptomatic. areas. This finding suggested that different cortical
16
23
These results suggested a very early cortical disinhibition, pathways are involved in movement reinitiation after
16
possibly a prodromal feature of PD. Moreover, an freezing or voluntary movement stops during PD freezes.
23
increase in short-interval intracortical facilitation (SICF) Furthermore, EEGs over the supplementary motor area
was observed in drug-naïve PD patients, and SICF was (SMA) and M1 were analyzed during ankle dorsiflexion
17
reportedly further enhanced in dyskinetic patients. A movement to evaluate possible pathophysiology
18
triple-pulse protocol revealed that in the presence of SICI, mechanisms of the freezing of gait (FOG). The normal
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SICF was further enhanced in healthy controls but not in beta desynchronization over the Cz channel, recorded
PD patients with more severe motor impairment and in before movement initiation, was partially replaced
the OFF-medication state. The SICF of these PD patients by the theta band synchronization (over contralateral
normalized after levodopa administration. This finding SMA) in PD patients with freezing, thereby suggesting
19
indicated that PD could alter functional networks at the the involvement of cognitive processing over the motor
cortical level, which subsequently aggravates PD severity cortex in regulating cue-based voluntary movements as
19
and reduces the efficacy of dopaminergic therapy. a compensatory mechanism associated with FOG. A
24
Another study reported that quadripulse magnetic combination of resting-state EEG with spectral power
stimulation (QPS) induced long-term potentiation analysis within seven frequency bands and subsequent
(LTP)-like effects that were reduced in PD, suggesting data elaboration was used to develop characterization
that cortical impairment is related to bradykinesia and models for PD cognitive profiles, essentially to identify
rigidity of the hand muscles. In addition, dopaminergic markers of cognitive worsening. The EEG features were
20
25
treatment with levodopa restored the QPS-induced then mined with two machine-learning algorithms, that
LTP-like effects. Input-output (I-O) curves were is, support vector machines and k-nearest algorithms,
20
utilized to evaluate the recruitment properties of the with accuracies of 84% and 88%, respectively. These
25
corticospinal pathway to upper limbs in PD after 8 weeks results suggest the use of EEG in daily clinical practice as
21
of focused training. The I-O threshold and slope after a screening tool to predict the progression of cognitive
training remained unchanged, but the plateau value was impairment in PD. A multimodal study was performed
25
significantly higher, suggesting that large type II motor to evaluate the use of EEG as a quantitative biomarker for
units (responsible for fast and durable movements) were PD by combining resting-state EEG data and dopamine
impaired in PD patients and that exercise could improve transporter positron emission tomography (PET) imaging
Volume 3 Issue 1 (2024) 5 https://doi.org/10.36922/an.1961