Abstract
Chronic fatigue syndrome (CFS) and myalgic encephalomyelitis (ME) affect approximately 1 million Americans ( Jason , Richman, Rademaker, Jordan, Plioplys, Taylor, et al., 1999a ); while some individuals believe that CFS and ME refer to the same illness, others characterize ME as a more severe, neurological disorder that is discrete from CFS (Twisk, 2015 ).
This controversy will be reviewed in detail.
The widespread, debilitating symptoms of the illnesses include but are not limited to feeling sick after activity (known as post-exertional malaise), memory and concentration problems, and unrefreshing sleep ( IOM, 2015 ).
Some researchers suggest that ME and CFS were first conceptualized under the diagnostic label “neurasthenia,” defined as a neurological disease characterized by muscle weakness or fatigue. Notably, neurasthenia was one of the most frequently diagnosed illnesses in the late nineteenth century. However, use of this term had substantially decreased by the mid-twentieth century ( Wessely, 1994 ).
Throughout the twentieth century, several outbreaks of idiopathic, fatigue-related illnesses occurred, including “atypical poliomyelitis” at Los Angeles County Hospital in 1934 ( Meals, Hauser, & Bower, 1935 ), “encephalomyelitis” at the Royal Free Hospital in London in 1955 ( Crowley, Nelson, & Stovin, 1957 ), and “chronic mononucleosis–like syndrome” in Lake Tahoe, Nevada, in 1984 ( Barnes, 1986 ). After the Lake Tahoe outbreak, national attention began to focus on this illness ( Wessely, 1994 ), and in 1988, it was named chronic fatigue syndrome by the Centers for Disease Control and Prevention (CDC; Holmes, Kaplan, Gantz, Komaroff, Schonberger, Straus, et al., 1988).
For over two decades, the case definition that the CDC developed ( Fukuda, Straus, Hickie, Sharpe, Dobbins, & Komaroff, 1994) has been prominently used in research and clinical practice; however, the Institute of Medicine (IOM) recently developed an updated clinical case definition ( IOM, 2015 ).
The annual direct and indirect costs of ME and CFS in the United States are estimated to be between $19 and $24 billion ( Jason, Benton, Johnson, & Valentine, 2008 ).
Individuals with ME and CFS have an increased risk of cardiovascular-related mortality and a lower mean age of death by suicide and cancer in comparison to the general US population ( McManimen, Devendorf, Brown, Moore, Moore, & Jason, 2016).
In addition, arthritis, high blood pressure, fibromyalgia, and multiple chemical sensitivities are commonly comorbid ( Jason, Porter, Hunnell, Brown, Rademaker, & Richman, 2011).
Although no virus has been identified as the cause of ME and CFS, the immune system may be overactive ( Fischer, William, Strauss, Unger, Jason, Marshall, et al., 2014), and there is evidence that ME and CFS may be caused by, or associated with, immune and/or brain dysfunction ( Jason, Zinn, & Zinn, 2015 ).
Our chapter focuses on the best methods that have been implemented in ME and CFS research. We provide insights about why certain procedures were used in order to guide other investigators who are conceptualizing and implementing their research in similar or overlapping areas.
The next section begins with a discussion of the challenges faced by patients, particularly given the stigma associated with ME and CFS ( Jason, Holbert, Torres-Harding, & Taylor, 2004 ).
The section after that describes existing case definitions for ME and CFS, highlighting their limitations and the resulting methodological complications for researchers and clinicians.
Subsequent sections review the prevalence of ME and CFS, innovative research in immunology, and approaches to ME and CFS treatment. Finally, we conclude with a summary of the strengths and limitations of current research and suggests areas for future research.
