Activation of the Prefrontal Cortex Is Associated with Exertional Dyspnea in Chronic Obstructive Pulmonary Disease

Department of Rehabilitation Medicine, Kinki University, Faculty of Medicine, Osaka, Japan.
Respiration (Impact Factor: 2.59). 04/2011; 82(6):492-500. DOI: 10.1159/000324571
Source: PubMed


Exertional dyspnea is the primary symptom that limits exercise in patients with chronic obstructive pulmonary disease (COPD). It is unknown which activated brain area is associated with this symptom in COPD patients.
To investigate the activation of cortical areas associated with dyspnea during exercise in COPD patients.
COPD patients (n = 10) and age-matched controls (n = 10) performed mild-intensity constant work rate cycle exercise (40% of their symptom-limited peak work rates) for 10 min, while cerebral hemodynamics and oxygenation were measured by near-infrared spectroscopy (NIRS). Ventilatory responses (breathing pattern and pulmonary gas exchange) and Borg scale ratings of dyspnea and leg fatigue were measured during exercise. Three NIRS probes were placed over the prefrontal and temporoparietal cortical regions of the subjects' heads. Changes in cortical oxyhemoglobin (oxy-Hb), deoxyhemoglobin (deoxy-Hb), and total hemoglobin (total Hb) concentrations from baseline recordings were measured. Increased oxy-Hb (oxygenation) was assumed to reflect cortical activation.
Oxy-Hb concentration was significantly increased in the prefrontal region during exercise in both groups but not in the temporoparietal regions. The change in prefrontal oxy-Hb concentration of COPD patients was not different from that of controls. Dyspnea scores were positively correlated with changes in oxy-Hb concentrations of the prefrontal regions in both groups. Multivariate analysis showed that oxy-Hb concentration in the prefrontal region was the best predictor of dyspnea in both groups.
Exertional dyspnea was related to activation (oxygenation) of the prefrontal cortex in COPD patients and control subjects.

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Available from: Kanji Fukuda, Jun 16, 2015
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    • "At least in those who are not overtly hypoxemic at rest, effective cerebral vasodilation may offset mild-to-moderate decrements in PaO 2 thereby preserving cerebral oxygenation (COx) (Jensen et al., 2002; Van de Ven et al., 2001). In fact, we (Oliveira et al., 2012) and others (Higashimoto et al., 2011) have found similar increases in COx (measured by near-infrared spectroscopy) during exercise in nonto mildly-hypoxemic COPD patients and healthy controls. A different scenario, however, may emerge in the presence of a common and disabling co-morbidity of COPD: heart failure (Rutten et al., 2006; Güder and Rutten, 2014). "
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