Chris Kelly1, Sanjay Johann Mathew1, Xiangling Mao2, Gizely Andrade1, Rebecca B. Price1, Paul S. Nestadt1, Susan M. Levine3, Dikoma C. Shungu2
1Psychiatry, Mount Sinai School of Medicine, New York, NY, USA; 2Radiology, Weill Medical College of Cornell University, New York, NY, USA; 3Private Practice, Infectious Diseases/Internal Medicine, New York, NY, USA
Chronic fatigue syndrome (CFS) is a controversial diagnosis due to the lack of biomarkers for the illness, and its symptom overlap with neuropsychiatric, infectious, and rheumatologic disorders. The CDC case definition requires at least 6 months of new-onset fatigue with four or more symptoms, including impaired memory or concentration, muscle pain, new headaches, unrefreshing sleep, and post-exertional malaise. Many of these symptoms are also found in patients with major depressive disorder (MDD), a much more prevalent illness, resulting in frequent misdiagnosis of CFS. Significant alterations in g-aminobutyric acid (GABA) and glutamate levels have been previously reported in symptomatic and remitted major depressive disorder (MDD) using proton magnetic resonance spectroscopy (1H MRS) in occipital cortex (OCC) and prefrontal cortical regions [1-4]. To our knowledge, no previous studies have investigated in vivo amino acid neurotransmitter function in CFS patients. OCC and anterior cingulate cortex (ACC) were selected as ROIs based on previous studies in depression and feasibility of obtaining high-quality spectroscopic data in these regions. In this pilot study, we compared cortical levels of GABA and glutamate + glutamine (Glx) levels in CFS patients and a cohort of unmedicated patients with MDD and healthy volunteers.