Brain Activation during Perception and Anticipation of Dyspnea in Chronic Obstructive Pulmonary Disease
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Brain Activation during Perception and Anticipation of Dyspnea in Chronic Obstructive Pulmonary Disease. / Esser, Roland W; Stoeckel, Maria C; Kirsten, Anne; Watz, Henrik; Taube, Karin; Lehmann, Kirsten; Magnussen, Helgo; Büchel, Christian; von Leupoldt, Andreas.
in: FRONT PHYSIOL, Jahrgang 8, 2017, S. 617.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - Brain Activation during Perception and Anticipation of Dyspnea in Chronic Obstructive Pulmonary Disease
AU - Esser, Roland W
AU - Stoeckel, Maria C
AU - Kirsten, Anne
AU - Watz, Henrik
AU - Taube, Karin
AU - Lehmann, Kirsten
AU - Magnussen, Helgo
AU - Büchel, Christian
AU - von Leupoldt, Andreas
PY - 2017
Y1 - 2017
N2 - Background: Dyspnea is the impairing cardinal symptom in COPD, but the underlying brain mechanisms and their relationships to clinical patient characteristics are widely unknown. This study compared neural responses to the perception and anticipation of dyspnea between patients with stable moderate-to-severe COPD and healthy controls. Moreover, associations between COPD-specific brain activation and clinical patient characteristics were examined. Methods: During functional magnetic resonance imaging, dyspnea was induced in patients with stable moderate-to-severe COPD (n = 17) and healthy control subjects (n = 21) by resistive-loaded breathing. Blocks of severe and mild dyspnea were alternating, with each block being preceded by visually cued anticipation phases. Results: During the perception of increased dyspnea, both patients and controls showed comparable brain activation in common dyspnea-relevant sensorimotor and cortico-limbic brain regions. During the anticipation of increased dyspnea, patients showed higher activation in hippocampus and amygdala than controls which was significantly correlated with reduced exercise capacity, reduced health-related quality of life, and higher levels of dyspnea and anxiety. Conclusions: This study suggests that patients with stable moderate-to-severe COPD show higher activation in emotion-related brain areas than healthy controls during the anticipation, but not during the actual perception of experimentally induced dyspnea. These brain activations were related to important clinical characteristics and might contribute to an unfavorable course of the disease via maladaptive psychological and behavioral mechanisms.
AB - Background: Dyspnea is the impairing cardinal symptom in COPD, but the underlying brain mechanisms and their relationships to clinical patient characteristics are widely unknown. This study compared neural responses to the perception and anticipation of dyspnea between patients with stable moderate-to-severe COPD and healthy controls. Moreover, associations between COPD-specific brain activation and clinical patient characteristics were examined. Methods: During functional magnetic resonance imaging, dyspnea was induced in patients with stable moderate-to-severe COPD (n = 17) and healthy control subjects (n = 21) by resistive-loaded breathing. Blocks of severe and mild dyspnea were alternating, with each block being preceded by visually cued anticipation phases. Results: During the perception of increased dyspnea, both patients and controls showed comparable brain activation in common dyspnea-relevant sensorimotor and cortico-limbic brain regions. During the anticipation of increased dyspnea, patients showed higher activation in hippocampus and amygdala than controls which was significantly correlated with reduced exercise capacity, reduced health-related quality of life, and higher levels of dyspnea and anxiety. Conclusions: This study suggests that patients with stable moderate-to-severe COPD show higher activation in emotion-related brain areas than healthy controls during the anticipation, but not during the actual perception of experimentally induced dyspnea. These brain activations were related to important clinical characteristics and might contribute to an unfavorable course of the disease via maladaptive psychological and behavioral mechanisms.
KW - Journal Article
U2 - 10.3389/fphys.2017.00617
DO - 10.3389/fphys.2017.00617
M3 - SCORING: Journal article
C2 - 28878693
VL - 8
SP - 617
JO - FRONT PHYSIOL
JF - FRONT PHYSIOL
SN - 1664-042X
ER -