COPD-related cerebrovascular damage has been implicated, with studies showing that impaired lung function is associated with cerebral white matter lesions ( 13, 14) and the presence of widespread white matter microstructural damage in stable COPD ( 15). Hypoxemia, systemic inflammation, oxidative stress, sympathetic nervous system activation, accelerated aging, and autoimmunity are a selection of plausible pathophysiological mechanisms for brain pathology and cognitive dysfunction in COPD ( 12). In addition, there appears to be a dose–response relationship between COPD duration of more than 5 years at baseline and risk of mild cognitive impairment ( 11). A self-reported diagnosis of COPD in mid-life has been found to be independently associated with subsequent cognitive impairment (hazard ratio, 1.85) ( 10). Mild cognitive impairment has been shown in 36% of patients with moderate to severe COPD (vs. Understanding of the mechanisms that result in cognitive problems and their clinical impact remain incomplete in COPD. Importantly, cognitive ability is critical for self-management and education, which underpin effective care ( 8). It has been suggested that impaired cognition may also be a predictor of mortality and disability in certain COPD populations ( 6, 7). Impairments are often global but most commonly involve executive functions, memory, and attention ( 4, 5). Cognitive impairment has been demonstrated in cross-sectional studies of COPD, with moderate to severe impairment in up to 57% of patients hospitalized because of an exacerbation ( 1). The potential impact of COPD on cognitive ability has an emerging clinical relevance ( 1– 3). It is plausible that cerebrovascular comorbidities explain previously described cognitive pathology in COPD.Ĭhronic obstructive pulmonary disease (COPD) is a complex, multisystem disorder. There was no association between executive function impairment and frequency of hospitalization, and there was a possible modest association with survival. Lung function, Pa O 2, smoking, survival, and hospitalizations were not significantly different in those with executive dysfunction.Ĭonclusions: In this large population of patients with severe emphysema and heavy cigarette smoking exposure, there was no significant decline over 2 years in cognitive executive function as measured by TM tests. Changes in TM scores were not associated with frequency of hospitalization. Changes in TM B times were modestly associated with survival, but changes in TM B − A times were not. There was no significant change over 2 years in TM A or B times after adjustment for covariables. George’s Respiratory Quotient, reduced well-being, and lower social function. Compared with those who did not, these patients were older, less educated, had higher oxygen use, higher Pa CO 2, worse quality of life as measured by the St. At the time of enrolment, 38% had executive dysfunction. Measurements and Main Results: The average age of the patients was 66.4 years, and the average FEV 1 was 23.9% predicted. Associations with survival and hospitalizations were examined using Cox regression and linear regression models. To assess executive function, we analyzed trail making (TM) A and B times at enrollment in the trial (2,128 patients), and at 12 (731 patients) and 24 months (593 patients) after enrollment, adjusted for surgery, marriage status, age, education, income, depression, Pa O 2, Pa CO 2, and smoking. Methods: This study was performed on patients enrolled in the National Emphysema Treatment Trial. Objectives: We examined longitudinal changes in sensitive measures of executive function in a well-characterized population of patients with severe COPD. Rationale: Cognitive dysfunction has been demonstrated in chronic obstructive pulmonary disease (COPD), but studies are limited to cross-sectional analyses or incompletely characterized populations.
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