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