Clinical and Electrophysiological Hints to TMS in De Novo Patients with Parkinson’s Disease and Progressive Supranuclear Palsy

Abstract

Background: Transcranial magnetic stimulation (TMS) can non-invasively probe cortical excitability in movement disorders, although clinical significance is still controversial, especially at early stages. We compare single-pulse TMS in two prototypic synucleinopathy and tauopathy—i.e., Parkinson’s disease (PD) and Progressive Supranuclear Palsy (PSP), respectively—to find neurophysiological differences and identify early measures associated with cognitive impairment. Methods: 28 PD and 23 PSP de novo patients were age-matched with 28 healthy controls, all right-handed and drug-free. Amplitude and latency of motor evoked potentials (MEP), central motor conduction time, resting motor threshold (rMT), and cortical silent period (CSP) were recorded through a figure-of-eight coil from the First Dorsal Interosseous muscle (FDI), bilaterally. Results: Mini Mental Examination and Frontal Assessment Battery (FAB) scored worse in PSP; PD had worse FAB than controls. Higher MEP amplitude from right FDI in PD and PSP than controls was found, without difference between them. CSP was bilaterally longer in patients than controls, but similar between patient groups. A positive correlation between FAB and rMT was observed in PSP, bilaterally. Conclusions: Despite the small sample size, PD and PSP might share, at early stage, a similar global electrocortical asset. rMT might detect and possibly predict cognitive deterioration in PSP.

A Transcriptome Analysis of mRNAs and Long Non-Coding RNAs in Patients with Parkinson’s Disease

“…The main pathogenetic feature of PD is the progressive loss of dopaminergic neurons in the substantia nigra of the midbrain, which leads to striatal dopamine deficiency and, subsequently, causes motor dysfunction [7,9]. Main clinical symptoms are resting tremor, rigidity, bradykinesia, and posture instability [10,11], although non-motor symptoms are frequent and disabling, such as cognitive impairment until dementia, autonomic dysfunction, sleep disorders, depression, hyposmia, and behavioral-emotional changes [12][13][14][15]. At present, PD diagnosis mainly relies on clinical manifestations, and no effective disease-modifying treatment strategies exist.…”

Clinical Neurophysiology, Neuroimaging, and Neuromodulation of Neuropsychiatric Disorders

“…The results showed that the amplitude of MEPs was higher in the patient groups than in healthy controls, and there was no difference between PD and PSP groups; CSPs were longer in both M1 in patient groups than in healthy controls, but were similar between patient groups. Furthermore, RMT was positively correlated with frontal lobe function in the PSP group, indicating that RMT may be an indicator reflecting cognitive decline in PSP [8].…”

Neurophysiological Aspects of REM Sleep Behavior Disorder (RBD): A Narrative Review

“…Non-invasive brain stimulation techniques, such as transcranial magnetic stimulation (TMS) and transcranial direct current stimulation, are widely used to functionally investigate the neural pathways and brain network in vivo, also providing prognostic measures and neuromodulatory activity [ 94 , 95 , 96 , 97 , 98 , 99 , 100 ]. Accordingly, the data from EEG and functional neuroimaging, during both wakefulness and sleep, have suggested the involvement of different transmission systems which seem to be impaired in synucleinopathy, including PD, multiple system atrophy, and DLB [ 101 , 102 ].…”