The multiple dimensions of dyspnea: review and hypotheses

Abstract

Although dyspnea is a common and troubling symptom, our understanding of the neurophysiology of dyspnea is woefully incomplete. Most measurements of dyspnea treat it as a single entity. Although the multidimensional dyspnea concept has been mentioned for many decades, only recently has the concept been the subject of experimental tests. Emerging evidence has begun to favor the hypothesis that dyspnea comprises multiple dimensions or components that can be measured as different entities. Most recently, studies have begun to show that there is a separable 'affective dimension' (i.e. unpleasantness and emotional impact). Understanding of the multidimensional measurement of pain is far in advance of dyspnea, and has enabled progress in the neurophysiology of pain, including identification of separate neural structures subserving various elements of pain perception. We propose here a multidimensional model of dyspnea based on a state-of-the-art pain model, and review existing evidence in the light of this model.

Figures

Fig. 1

Pain and Dyspnea in the Anterior Insula. One of the key brain regions activated in both dyspnea and pain is the anterior insula. The “P” symbols show the locations of pain activations of the insula in a transverse slice at Z=+8. Pain data from various studies summarized by a meta analysis (Peyron et al. 2000). The larger circle labeled “D” shows the area activated by dyspnea (Banzett et al. 2000b).

Fig. 2

Definitions of the perceptual model (enclosed within dashed line) Components of the Sensory Dimension: SI = Sensory Intensity, SQ = Sensory Quality; SL = Sensory location; ST = Time course of sensation Components of the Affective Dimension: A1 = Immediate Unpleasantness: first stage of the affective dimension; A2 = Emotion/Evaluation: second stage of affective dimension

Fig. 3

Change in the ratio of “dyspnea-related anxiety” (a component of A2) to sensory intensity of “shortness of breath” during supervised exercise training in patients with obstructive lung disease. Data re-plotted from (Carrieri-Kohlman et al. 2001). Time points are sessions at 3 day intervals. Both SI and A2 declined, but A2 declined more quickly , causing a marked fall inA2/SI ratio with the first few sessions of exercise therapy. The values shown are calculated from published values for group mean ratings, individual data for paired statistical comparisons were unavailable.