ID 278 – Motor cortical disinhibition is more pronounced in Progressive Supranuclear Palsy than in Parkinson's disease: Evidence from TMS. Issue 3 (March 2016)

• Record Type: Journal Article
• Authors: Fichera, M.; Houdayer, E.; Avantaggiato, F.; Chieffo, R.; Comi, G.; Volonté, M.A.; Leocani, L.
• Is Part Of: Clinical neurophysiology. Volume 127:Issue 3(2016:Mar.)
• Page Start: e121
• Publication Date: 2016-03
• Subjects: Neurophysiology -- Periodicals; Electroencephalography -- Periodicals; Electromyography -- Periodicals; Neurology -- Periodicals; 612.8
• DOI: 10.1016/j.clinph.2015.11.412
• Languages: English
• ISSNs: 1388-2457

Abstract

Abstract : Objective: Progressive Supranuclear Palsy-PSP is the second most common parkinsonian syndrome after Parkinson's disease-PD. Non-invasive neurophysiological techniques, such as transcranial magnetic stimulation-TMS, could prove useful to gain insight into these pathologies and for differential diagnosis. Methods: Seventeen PD, 13 PSP and 11 healthy controls-CT were included in this study. TMS evaluation included resting motor threshold-RMT, motor evoked potentials-MEP amplitude, response to inhibitory-SICI and facilitating-ICF conditioning stimuli, cortical-CSP and ipsilateral silent period-iSP. Statistical analysis was performed using either parametric or non-parametric ANOVA and post-hoc tests according to data distribution. Results: PSP and PD groups did not significantly differ in UPDRS. RMT distributed differently across groups (p.008), with PSP patients showing highest values and PD lowest (PSPvs.PD p.002). Group also affected iSP duration (p.016), being longest in PSP and lowest in HC (PSPvs.CT p.005). On paired-pulse inhibition and facilitation, a significant effect for inter-stimulus interval-ISI ( p < .001) and group (p.035) but not interaction was found, with lower SICI and higher ICF in PSP vs. PD (p.017) and CT (p.032). Conclusions: This study suggests that TMS can help differentiate PD and PSP. PSP patients displayed different response to the perturbation induced by conditioning stimuli and iSP elongation, probably due to impairment of GABA-mediated neurotransmission.