Dyspnoea: underlying mechanisms and treatment

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Dyspnoea: underlying mechanisms and treatment T. Nishino British Journal of Anaesthesia Volume 106, Issue 4, Pages 463-474 (April 2011) DOI: 10.1093/bja/aer040 Copyright © 2011 The Author(s) Terms and Conditions

Fig 1 Schematic illustration of ascending pathways, subcortical structures, and cerebral cortical structures involved in processing of dyspnoea and pain. ACC, anterior cingulate cortex; AMYG, amygdala; CB, cerebellum; MDT, medial dorsal thalamus; MO, medulla oblongata; M1, primary motor cortex; PAG, periaqueductal grey; PCC, posterior cingulate cortex; PFC, prefrontal cortex; SMA, supplementary motor cortex; S1, primary somatosensory cortex; S2, secondary somatosensory cortex; VPT, ventroposterior thalamus. British Journal of Anaesthesia 2011 106, 463-474DOI: (10.1093/bja/aer040) Copyright © 2011 The Author(s) Terms and Conditions

Fig 2 Motor command–afferent mismatch. Dyspnoea is the result of a dissociation between amplitudes of the central efferent discharge (motor output) and afferent sensory inputs (feedback) from peripheral mechanoreceptors. British Journal of Anaesthesia 2011 106, 463-474DOI: (10.1093/bja/aer040) Copyright © 2011 The Author(s) Terms and Conditions

Fig 3 Schematic of DNIC. PAG, periaqueductal grey; RM, rostral medulla; PN, projection neurone; PAF, primary afferent fibre. A thick broken line indicates the neural pathway for counterirritation. British Journal of Anaesthesia 2011 106, 463-474DOI: (10.1093/bja/aer040) Copyright © 2011 The Author(s) Terms and Conditions