B58-18 Central Sensitization of the Central Nervous System: A Previously Unidentified Contributor to Dyspnea Severity

Abstract Many patients with COPD have uncontrolled symptoms despite optimal treatment. In chronic pain conditions, the presence of central sensitization (CS) amplifies sensory experiences, but little is known about how these same processes might contribute to symptom burden in COPD. The project was a prospective, cross-sectional study of ambulatory patients with COPD (n = 113). Participants were administered a fibromyalgia self-report measure that has been used as a surrogate for CS, including quantifying body regions affected by pain and a severity scale for sleep, memory, and fatigue (range 0-31). Dyspnea was assessed using the Multidimensional Dyspnea Profile (range 1-10), and quality of life used the Short Form - 36. Linear regression was used to test the association between the key exposures - pain and dyspnea - and CS, adjusting for age, gender, smoking status, forced expiratory volume in 1 second (FEV1), and comorbidities. Study population characteristics include: mean age 68, 53% male, 84% White, FEV1 51+/-22 % predicted and a mean Charlson Comorbidity Index of 3. Distribution of CS scores were higher than healthier patients, as 20% of this COPD sample would meet criteria for fibromyalgia (compared to 2 - 6% of the general population). This cohort also had higher rates of chronic pain than the general population, with 55% of patients reported moderate daily pain and 24% of patients reporting pain interference at least somewhat in day-to-day activities. CS was associated with more severe dyspnea across all dimensions - immediate discomfort, number of sensations, intensity of sensation, and affective dimensions. The strongest associations were noted for immediate discomfort, air hunger, and anxiety. A one unit increase in CS was associated with 0.20 (0.11-0.29) unit increase in immediate discomfort, 0.28 (0.16-0.41) unit increase in air hunger, and 0.37 (0.26-0.48) unit increase in anxiety. CS, previously described as a mechanism prevalent in chronic pain, is identified here as potentially prominent feature in COPD. This study suggests higher rates of pain than in the general population and a strong relationship between measures of CS and worse dyspnea. Since it is known that CS leads to hyper-responsiveness to both external and internal sensory stimuli (i.e. exteroception and interoception), it is conceivable that in COPD this sensory amplification is playing a similar role in symptom expression. CS is proposed as the mechanistic link between objective dyspnea receptor inputs and the subjective experience of breathlessness. CS may be an important contributor to symptom burden in COPD. This abstract is funded by: Kreml Foundation