Anhedonia Underlies Executive Dysfunction in Persons with Multiple Sclerosis
Emily Dvorak1, James Sumowski2
1Teachers College, Columbia University, 2Icahn School of Medicine At Mount Sinai
Objective:
To investigate differences in executive functioning, specifically working memory, in relapsing versus progressive multiple sclerosis, and to what extent depression, specifically anhedonia, drives such dysfunction.
Background:
Our previous work on executive dysfunction, such as working memory (WM) difficulty, in persons with multiple sclerosis (MS) suggests that dysfunction in progressive disease is driven by frontal cortical atrophy whereas dysfunction in relapsing disease is largely driven by depression. More research is needed to understand how specific phenotypes of depression (e.g., dysphoric vs anhedonic) may differentially impact WM in persons with MS, with important implications for treatment.
Design/Methods:
Working memory maintenance and manipulation was assessed in persons with MS (n=191; 21 progressive) with WRAML-3 Verbal Working Memory (VWM); persons hear increasing sequences of animals and non-animals, repeat back the animals reorganized in size order, and then state the non-animals. Normative data classified impairment (≤5th percentile). PHQ-2 assessed sadness and anhedonia as “not at all,” “several days,” or “more than half the days.” Chi square tests examined differences in VWM impairment (a) across symptom severity levels for sadness and anhedonia, and (b) between relapsing and progressive courses.
Results:
Rate of VWM impairment differed across levels of symptom severity for anhedonia (9.7%, 20.0%, 39.1%; p=0.002) but not for sadness (13.5%, 16.1%, 29.2%; p=0.169). This link between anhedonia and VWM impairment was consistent across relapsing (7.0%, 17.6%, 31.6%) and progressive (30.8%, 50.0%, 75.0%) courses. Note that patients with progressive disease showed VWM impairment even without anhedonia, but patients with relapsing disease were only impaired with anhedonia.
Conclusions:
Persons with progressive disease demonstrated WM deficits that worsen with anhedonia, whereas persons with relapsing disease only have WM deficits in the context of anhedonia. Results highlight anhedonia as a potential target to improve working memory/executive function in MS.
Disclaimer: Abstracts were not reviewed by Neurology® and do not reflect the views of Neurology® editors or staff.