Reversal of long term potentiation-like plasticity in primary motor cortex in patients with progressive supranuclear palsy

Matteo Bologna, Kelly Bertram, Giulia Paparella, Claudia Papi, Daniele Belvisi, Antonella Conte, Antonio Suppa, David R. Williams, Alfredo Berardelli

Research output: Contribution to journalArticleResearchpeer-review

Abstract

Objective Abnormal primary motor cortex plasticity might be involved in the pathophysiology of progressive supranuclear palsy. In the present study we aimed to investigate possible abnormalities of depotentiation, a mechanism involved in plasticity regulation, in this condition. Methods Primary motor cortex excitability, investigated with single and paired-pulse transcranial magnetic stimulation, as well as long-term potentiation-like plasticity and its reversibility, were studied using theta burst stimulation in 15 patients with progressive supranuclear palsy and 11 healthy controls. Participants underwent two sessions using (1) the intermittent theta-burst stimulation (potentiation protocol) and (2) intermittent theta-burst stimulation combined with a depotentiation protocol (a short continuous theta-burst stimulation). Results Patients with PSP had higher corticospinal excitability and lower intracortical inhibition than healthy controls. Intermittent theta-burst stimulation elicited an abnormally increased long term potentiation-like effect in patients in comparison to healthy subjects. However, the depotentiation protocol was able to reverse the effects intermittent theta-burst stimulation on motor cortex excitability both in patients and in healthy controls. Conclusions Altered primary motor cortex plasticity in patients with PSP does not reflect an abnormality of depotentiation. Significance This study provides information for a deeper understanding of the possible pathophysiological mechanisms underlying the altered M1 plasticity in PSP.

Original languageEnglish
Pages (from-to)1547-1552
Number of pages6
JournalClinical Neurophysiology
Volume128
Issue number9
DOIs
Publication statusPublished - 1 Sep 2017

Keywords

  • Plasticity
  • Primary motor cortex
  • Progressive supranuclear palsy
  • Transcranial magnetic stimulation

Cite this

Bologna, Matteo ; Bertram, Kelly ; Paparella, Giulia ; Papi, Claudia ; Belvisi, Daniele ; Conte, Antonella ; Suppa, Antonio ; Williams, David R. ; Berardelli, Alfredo. / Reversal of long term potentiation-like plasticity in primary motor cortex in patients with progressive supranuclear palsy. In: Clinical Neurophysiology. 2017 ; Vol. 128, No. 9. pp. 1547-1552.
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Reversal of long term potentiation-like plasticity in primary motor cortex in patients with progressive supranuclear palsy. / Bologna, Matteo; Bertram, Kelly; Paparella, Giulia; Papi, Claudia; Belvisi, Daniele; Conte, Antonella; Suppa, Antonio; Williams, David R.; Berardelli, Alfredo.

In: Clinical Neurophysiology, Vol. 128, No. 9, 01.09.2017, p. 1547-1552.

Research output: Contribution to journalArticleResearchpeer-review

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AU - Bologna, Matteo

AU - Bertram, Kelly

AU - Paparella, Giulia

AU - Papi, Claudia

AU - Belvisi, Daniele

AU - Conte, Antonella

AU - Suppa, Antonio

AU - Williams, David R.

AU - Berardelli, Alfredo

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N2 - Objective Abnormal primary motor cortex plasticity might be involved in the pathophysiology of progressive supranuclear palsy. In the present study we aimed to investigate possible abnormalities of depotentiation, a mechanism involved in plasticity regulation, in this condition. Methods Primary motor cortex excitability, investigated with single and paired-pulse transcranial magnetic stimulation, as well as long-term potentiation-like plasticity and its reversibility, were studied using theta burst stimulation in 15 patients with progressive supranuclear palsy and 11 healthy controls. Participants underwent two sessions using (1) the intermittent theta-burst stimulation (potentiation protocol) and (2) intermittent theta-burst stimulation combined with a depotentiation protocol (a short continuous theta-burst stimulation). Results Patients with PSP had higher corticospinal excitability and lower intracortical inhibition than healthy controls. Intermittent theta-burst stimulation elicited an abnormally increased long term potentiation-like effect in patients in comparison to healthy subjects. However, the depotentiation protocol was able to reverse the effects intermittent theta-burst stimulation on motor cortex excitability both in patients and in healthy controls. Conclusions Altered primary motor cortex plasticity in patients with PSP does not reflect an abnormality of depotentiation. Significance This study provides information for a deeper understanding of the possible pathophysiological mechanisms underlying the altered M1 plasticity in PSP.

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