Editors' note: Comorbid anxiety, depression, and cognition in MS and other immune-mediated disorders

Abstract

In their cross-sectional study of patients with any of 3 immune-mediated inflammatory diseases (IMIDs)—including multiple sclerosis (MS)—and patients without IMID but with anxiety and/or major depressive disorder, Whitehouse et al. sought to evaluate the impact of anxiety/depressive symptoms on cognitive performance. The investigators hypothesized that patients with IMID and anxiety/depression would demonstrate poorer cognitive function than patients with IMID but no anxiety/depression; furthermore, they posited that such cognitive impairment would be more severe than in patients with anxiety/depression who are unaffected by IMID. Although the patients in each clinical group (multiple sclerosis vs rheumatoid arthritis vs inflammatory bowel disease vs non-IMID anxiety/depression) were not matched for age, sex, years of education, or other socioeconomic factors, the rates of clinically meaningful anxiety or depressive symptoms were similar across the 3 IMID groups. As expected, compared with patients with rheumatoid arthritis and inflammatory bowel disease, patients with MS were more likely to have impaired processing speed, verbal learning, and memory recall. Furthermore, symptoms of anxiety in all patients seemed to correlate with slower mental processing, impaired working memory, and reduced verbal learning. Under this immune-mediated cognitive impairment hypothesis, Dr. Golan alleges that IMID severity should be an important contributor to cognitive dysfunction and should have been included in multivariable models. As such, Dr. Golan argues that it is very unlikely that anxiety is independently associated with cognitive performance in IMID. In response, the authors state that psychiatric comorbidities and anxiety are related to disease progression in MS and a shorter disease recurrence in IBD by citing additional evidence. They also emphasize that anxiety affects cognition in a general population, and therefore, the association is unlikely to be the result of confounding. In their cross-sectional study of patients with any of 3 immune-mediated inflammatory diseases (IMIDs)—including multiple sclerosis (MS)—and patients without IMID but with anxiety and/or major depressive disorder, Whitehouse et al. sought to evaluate the impact of anxiety/depressive symptoms on cognitive performance. The investigators hypothesized that patients with IMID and anxiety/depression would demonstrate poorer cognitive function than patients with IMID but no anxiety/depression; furthermore, they posited that such cognitive impairment would be more severe than in patients with anxiety/depression who are unaffected by IMID. Although the patients in each clinical group (multiple sclerosis vs rheumatoid arthritis vs inflammatory bowel disease vs non-IMID anxiety/depression) were not matched for age, sex, years of education, or other socioeconomic factors, the rates of clinically meaningful anxiety or depressive symptoms were similar across the 3 IMID groups. As expected, compared with patients with rheumatoid arthritis and inflammatory bowel disease, patients with MS were more likely to have impaired processing speed, verbal learning, and memory recall. Furthermore, symptoms of anxiety in all patients seemed to correlate with slower mental processing, impaired working memory, and reduced verbal learning. Under this immune-mediated cognitive impairment hypothesis, Dr. Golan alleges that IMID severity should be an important contributor to cognitive dysfunction and should have been included in multivariable models. As such, Dr. Golan argues that it is very unlikely that anxiety is independently associated with cognitive performance in IMID. In response, the authors state that psychiatric comorbidities and anxiety are related to disease progression in MS and a shorter disease recurrence in IBD by citing additional evidence. They also emphasize that anxiety affects cognition in a general population, and therefore, the association is unlikely to be the result of confounding.