Fatigue as a core symptom in major depressive disorder: overview and the role of bupropion

Abstract

Fatigue is one of the most common symptoms found in both community and medical care settings. Fatigue may imply a prodromal or residual symptom of major depressive disorder or an adverse reaction to antidepressant treatment. Fatigue may also compromise antidepressant treatment by delaying response to antidepressants. Despite the importance of fatigue as a core depressive symptom, data specific to the effects of fatigue on pharmacological treatment are still lacking. Bupropion is an atypical antidepressant, chemically unrelated to classical agents such as tricyclic antidepressants, selective serotonin reuptake inhibitors and other contemporary antidepressants. With a pharmacological profile that involves neurotransmitter reuptake inhibition, bupropion shares a broad range of biological properties with psychostimulants. The primary action mode of bupropion involves dopaminergic and noradrenergic neurotransmissions rather than serotonergic mechanisms, although its exact pharmacodynamic properties remain uncertain. Hence, it is possible that bupropion may play a role in the treatment of fatigue-related symptoms of major depressive disorder. This paper presents a brief overview of the clinical implications and neurobiology of major depressive disorder-related fatigue, as well as the pharmacological profile of bupropion and currently available clinical data related to its treatment of fatigue-related symptoms of major depressive disorder.

Keywords::

• bupropion
• fatigue
• major depressive disorder

Financial & competing interests disclosure

C-U Pae has received research support from GlaxoSmithKline Korea, GlaxoSmithKline, AstraZeneca Korea, Jansssen Pharmaceutcals Korea, Eli Lilly and Company Korea, Korean Research Foundation, Otsuka Korea, Wyeth Korea, and Korean Institute of Science and Technology Evaluation and Planning. He has received honoraria and is on the speaker’s bureaus of GlaxoSmithKline Korea, Lundbeck Korea, AstraZeneca Korea, Jansssen Pharmaceutcals Korea, Eli Lilly and Company Korea, McNeil Consumer and Specialty Inc., and Otsuka Korea.

C Han has received research support from Korea Research Foundation Grant (MOEHRD) (KRF-2007-013-E00033) and from Korea University Neuropsychiatric Alumni Grant.

AA Patkar is a consultant for Bristol-Myers Squibb, GlaxoSmithKline and Reckitt Benckiser; is on the speaker’s bureau of Bristol-Myers Squibb, GlaxoSmithKline and Reckitt Benckiser; has received research support from National Institutes of Health, AstraZeneca, Bristol-Myers Squibb, Forest, GlaxoSmithKline, Janssen, McNeil Consumer and Specialty Inc, Organon, Jazz Pharmaceuticals, and Pfizer.

PS Masand is a consultant for Bristol-Myers Squibb Company, Cephalon Inc., Eli Lilly and Company, Forest laboratories Inc., GlaxoSmithKline, i3CME, Janssen Pharmaceutica, Jazz Pharmaceuticals, Organon, Pfizer, Inc., Targacept Inc., and Wyeth Pharmaceuticals; is on the speaker’s bureau of AstraZeneca, Bristol Myers Squibb Company, Forest laboratories Inc., GlaxoSmithKline, Janssen Pharmaceutica, Pfizer Inc. and Wyeth Pharmaceuticals; has received research support from AstraZeneca, Bristol-Myers Squibb Company, Cephalon Inc., Eli Lilly and Company, Forest laboratories Inc., GlaxoSmithKline, Ortho McNeil Pharmaceutical, Inc., Janssen Pharmaceutica and Wyeth Pharmaceuticals.

DC Steffens is on the Speaker's bureau and has received honoraria from Wyeth Pharmaceuticals and Forest Pharmaceuticals.

The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.