Francois Alexandre

Similar scaling of contralateral and ipsilateral cortical responses during graded unimanual force generation

Hemibody movements are strongly considered as being under the control of the contralateral hemisphere of the cerebral cortex. However, some neuroimaging studies have found a bilateral activation of either the primary sensori-motor (SM1) areas or the rostral prefrontal cortex (PFC), during unimanual tasks. More than just bilateral, the activation of these areas was found to be symmetrical in some studies. However, the symmetrical response remains strongly controversial notably for handgrip force generations. We therefore aimed to examine the bilateral SM1 and rostral PFC area activations in response to graded submaximal force generation during a unilateral handgrip task. Fifteen healthy subjects performed 6 levels of force (ranging from 5 to 50% of MVC) during a handgrip task. We concomitantly measured the activation of bilateral SM1 and rostral PFC areas through near-infrared spectroscopy (NIRS) and the electromyographic (EMG) activity of the bilateral flexor digitorum superficialis (FDS) muscles. Symmetrical activation was found over the SM1 areas for all the investigated levels of force. At the highest level of force (i.e., 50% of MVC), the EMG of the passive FDS increased significantly and the ipsilateral rostral PFC activation was found more intense than the corresponding contralateral rostral PFC activation. We suggest that the visuo-guided control of force levels during a handgrip task requires the cross-talk from ipsi- to contralateral SM1 to cope for the relative complexity of the task, similar to that which occurs during complex sequential finger movement. We also propose alternative explanations for the observed symmetrical SM1 activation including (i) the ipsilateral corticospinal tract and (ii) interhemispheric inhibition (IHI) mechanism. The increase in EMG activity over the passive FDS could be associated with a release of IHI at 50% of MVC. Finally, our results suggest that the greater ipsilateral (right) rostral PFC activation may reflect the greater demand of attention required to control the motor output at high levels of force.

Cortical Implication in Lower Voluntary Muscle Force Production in Non-Hypoxemic COPD Patients

Recent studies have shown that muscle alterations cannot totally explain peripheral muscle weakness in COPD. Cerebral abnormalities in COPD are well documented but have never been implicated in muscle torque production. The purpose of this study was to assess the neural correlates of quadriceps torque control in COPD patients. Fifteen patients (FEV1 54.1±3.6% predicted) and 15 age- and sex-matched healthy controls performed maximal (MVCs) and submaximal (SVCs) voluntary contractions at 10, 30 and 50% of the maximal voluntary torque of the knee extensors. Neural activity was quantified with changes in functional near-infrared spectroscopy oxyhemoglobin (fNIRS-HbO) over the contralateral primary motor (M1), primary somatosensory (S1), premotor (PMC) and prefrontal (PFC) cortical areas. In parallel to the lower muscle torque, the COPD patients showed lower increase in HbO than healthy controls over the M1 (p<0.05), PMC (p<0.05) and PFC areas (p<0.01) during MVCs. In addition, they exhibited lower HbO changes over the M1 (p<0.01), S1 (p<0.05) and PMC (p<0.01) areas during SVCs at 50% of maximal torque and altered motor control characterized by higher torque fluctuations around the target. The results show that low muscle force production is found in a context of reduced motor cortex activity, which is consistent with central nervous system involvement in COPD muscle weakness.

Is nocturnal desaturation a trigger for neuronal damage in chronic obstructive pulmonary disease

Patients with chronic obstructive pulmonary disease (COPD) present many neurological disorders of unknown origin. Although hypoxemia has long been thought to be responsible, several studies have shown evidence of neuronal damage and dysfunction even in non-hypoxemic patients with COPD. Adaptive mechanisms protect the brain from hypoxia: when arterial oxygen tension (PaO2) decreases, the cerebral blood flow (CBF) increases, ensuring continuously adequate oxygen delivery to the brain. However, this mechanism is abolished during non-rapid eye movement (NREM) sleep. Any drop in PaO2 during NREM sleep is therefore not compensated by increased CBF, causing decreased cerebral oxygen delivery with subsequent brain hypoxia. Patients with may therefore be exposed to neuronal damage during this critical time. This mechanism is of vital importance for patients with COPD because of the potentially deleterious cortical effects. Nocturnal desaturation is quite frequent in COPD and affects approximately one out of two patients who are not hypoxemic during wakefulness. Although the prevalence of NREM sleep desaturation has never been specifically assessed in COPD, current data suggest that at least half of the nocturnal desaturation in desaturating patients occurs during NREM sleep. This review presents the rationale for the hypothesis that nocturnal desaturation during NREM sleep promotes neuronal damage and dysfunction in COPD.

Brain Damage and Motor Cortex Impairment in Chronic Obstructive Pulmonary Disease: Implication of Nonrapid Eye Movement Sleep Desaturation.

STUDY OBJECTIVES Nonrapid eye movement (NREM) sleep desaturation may cause neuronal damage due to the withdrawal of cerebrovascular reactivity. The current study (1) assessed the prevalence of NREM sleep desaturation in nonhypoxemic patients with chronic obstructive pulmonary disease (COPD) and (2) compared a biological marker of cerebral lesion and neuromuscular function in patients with and without NREM sleep desaturation. METHODS One hundred fifteen patients with COPD (Global Initiative for Chronic Obstructive Lung Disease [GOLD] grades 2 and 3), resting PaO2 of 60-80 mmHg, aged between 40 and 80 y, and without sleep apnea (apnea-hypopnea index < 15) had polysomnographic sleep recordings. In addition, twenty-nine patients (substudy) were assessed i) for brain impairment by serum S100B (biological marker of cerebral lesion), and ii) for neuromuscular function via motor cortex activation and excitability and maximal voluntary quadriceps strength measurement. RESULTS A total of 51.3% patients (n = 59) had NREM sleep desaturation (NREMDes). Serum S100B was higher in the NREMDes patients of the substudy (n = 14): 45.1 [Q1: 37.7, Q3: 62.8] versus 32.9 [Q1: 25.7, Q3: 39.5] pg.ml(-1) (P = 0.028). Motor cortex activation and excitability were lower in NREMDes patients (both P = 0.03), but muscle strength was comparable between groups (P = 0.58). CONCLUSIONS Over half the nonhypoxemic COPD patients exhibited NREM sleep desaturation associated with higher values of the cerebral lesion biomarker and lower neural drive reaching the quadriceps during maximal voluntary contraction. The lack of muscle strength differences between groups suggests a compensatory mechanism(s). Altogether, the results are consistent with an involvement of NREM sleep desaturation in COPD brain impairment. CLINICAL TRIAL REGISTRATION The study was registered at www.clinicaltrials.gov as NCT01679782.

Cortical motor output decreases after neuromuscular fatigue induced by electrical stimulation of the plantar flexor muscles.

Neuromuscular electrical stimulation (NMES) causes early onset of neuromuscular fatigue. Peripheral electrophysiological explorations suggest that supra‐spinal alterations are involved through sensitive afferent pathways. As sensory input is projected over the primary somatosensory cortex (S1), S1 area involvement in inhibiting the central motor drive can be hypothesized. This study assessed cortical activity under a fatiguing NMES protocol at low frequency.

Impact of Chronic Obstructive Pulmonary Disease on Cognitive and Motor Performances in Dual-Task Walking

ABSTRACT When two tasks are performed simultaneously, they compete for attentional resources, resulting in a performance decrement in one or both tasks. Patients with attention disorders have a reduced ability to perform several tasks simultaneously (e.g., talking while walking), which increases the fall risk and frailty. This study assessed the cognitive and motor performances of patients with COPD and healthy controls within a dual-task walking paradigm. A subobjective was to assess the impact of a pulmonary rehabilitation program on the dual-task performances in COPD. Twenty-five patients with COPD and 20 controls performed a cognitive task (subtraction) and a 15-m walking test separately (single-task; ST) and jointly (dual-task; DT). In addition, a subsample of 10 patients performed the same evaluations 5 weeks later after a pulmonary rehabilitation program following current recommendations. Cognitive and gait performances in ST showed no differences between patients with COPD and controls (all p > 0.05). However, COPD patients exhibited a greater increase in gait variability than controls in DT (4.07 ± 1.46% vs. 2.17 ± 0.7%, p < 0.001). The pulmonary rehabilitation program had no effect on the dual-task impairment for the subsample of patients (p = 0.87). This study provides evidence of insufficient attentional resources to successfully deal with DT in patients with COPD, and this was expressed through an exaggerated increase in gait variability in DT walking. Given the high risk of falls and disability associated with altered gait variability, dual-task training interventions should be considered in pulmonary rehabilitation programs.