Skip to main content
OpenTrials
Completed

NCT Number: NCT03368703

Physiopathology of Lower Cortical Activation in COPD Patients: Contribution of Cortical Neuromodulation

Patients with COPD have lower cortical activation and higher cortical inhibitory levels. The purpose of this study is to test the reversibility the lower cortical activation by counterbalancing the increased cortical inhibitory levels with neuro-modulation.

Completed

Looking for future studies?

Notify Me

Key information

About this study

Chronic obstructive pulmonary disease (COPD) patients exhibit not only respiratory symptoms but also a peripheral muscular weakness. This weakness is characterized by a loss in strength, harmful for the patients' life quality and vital prognostic. Even if many papers have enlightened damages at a peripheral level, the muscular atrophy itself cannot totally explain the loss in force. Furthermore, the contractile properties of COPD muscles fibres are preserved. Consequently, it seems that the peripheral muscle weakness cannot only be explained by peripheral factors and central structures may be involved.

A recent work showed that during quadriceps voluntary contraction, cortical activation in COPD patients was significantly lower than in healthy subjects, contributing in the loss in strength. However, the pathophysiology underlying this loss of strength is still unclear and two hypotheses can be advanced: 1) the influence of anatomical lesions in the brain of COPD patients and 2) the particular metabolism of this population. Indeed, COPD patients show a reduced oxidative activity and an increased glycolytic contribution (decreased type I fibres and increased type II fibres, increased glycolytic enzymes activity, increased metabolites production). This specific metabolic may lead to an over-activation of type III-IV afferents, projecting onto somatosensory cortex sensitive to metabolites at a peripheral level, and produce inhibitory activity on the primary motor cortex, seat of the motor control. What is reported in the literature so far, is that COPD patients display increased cortical inhibitory values than healthy subjects.

Therefore, beyond understanding better the nervous mechanisms involved in the COPD's peripheral muscle weakness, the aim of this study is to counterbalance this increased cortical inhibitory level.

We hypothesize that modulating inhibitory processes at a cortical level would induced a reduction of inhibitions in patients with COPD and an increase in the force produced. In case this hypothesis would be verified, we will be able to confirm that this increased cortical level in COPD patients is reversible and may be a target for rehabilitation.

Who can participate

Healthy volunteers accepted: Yes

Only the study team can determine whether someone qualifies for participation.

Inclusion criteria

  • Health insurance
  • Patients : COPD Gold II-IV
  • Patients : No rehabilitation since at least 1 yrs
  • Control : sedentary (< 9 Voorips)

Exclusion criteria

  • Pregnant women
  • Seizures
  • Unable to give written consent
  • Metalic object above shoulders
  • Dermatological issue concerning surface electrodes
  • Drugs influencing central nervous system
  • Caffeine consumption > 4 coffee / day
  • Neurological disorders
  • Patients : recent exacerbation (< 4 weeks)

Treatment and study plan

Anodal transcranial direct-current-stimulation

Device

2mA / 20min Anodal and Sham tDCS over dominant M1. Anodal tDCS consists of 30s of ramp up followed by 20min of stimulation and 30s of ramp down.

Sham transcranial direct-current-stimulation

Device

Sham tDCS consists of only 30s of ramp up followed by 30s of ramp down and no further stimulation.

Participants therefore have the same feeling for both modalities : slight itching due to the induced current at the beginning of the protocol (during around 30s) allowing no differentiation by the participant between the anodal or sham sessions.

Primary outcomes

  1. Change in motor-evoked potentials

    Time frame: Baseline (pre-intervention) ; Post-Stim (immediately post-intervention) ; Post-30 (30min post-intervention)

    Cortical excitability

Secondary outcomes

  1. Change in short-interval intracortical inhibition

    Time frame: Baseline (pre-intervention) ; Post-Stim (immediately post-intervention) ; Post-30 (30min post-intervention)

    Cortical inhibition level

  2. Change in cortical silent period

    Time frame: Baseline (pre-intervention) ; Post-Stim (immediately post-intervention) ; Post-30 (30min post-intervention)

    Cortical inhibition level

  3. Change in cortical voluntary activation

    Time frame: Baseline (pre-intervention) ; Post-Stim (immediately post-intervention) ; Post-30 (30min post-intervention)

    Motor command

  4. Change in strength

    Time frame: Baseline (pre-intervention) ; Post-Stim (immediately post-intervention) ; Post-30 (30min post-intervention)

    Functional output

Sponsors and collaborators

Lead sponsor

5 Santé

Other

Registry information

Important dates

Study start
2017
Primary completion
2018
Study completion
2018
First posted
Dec 11, 2017
Registry last updated
Jan 13, 2020

OpenTrials presents study information sourced from ClinicalTrials.gov. The official registry record should be consulted for the latest information.

View the official ClinicalTrials.gov record (opens in a new tab)

This listing is for discovery and informational purposes only. It is not medical advice, does not guarantee that a study is recruiting, and does not determine eligibility. Contact the study team and a qualified healthcare professional when considering participation.

Published trials that share one or more normalized conditions with this study.