Fibromyalgia: The Latest in Diagnosis and Care

Daniel J. Clauw, MD; Philip J. Mease, MD; Bret S. Stetka, MD


September 17, 2014

In This Article

Editor's Note: In response to a number of recent advances in the understanding, diagnosis, and management of fibromyalgia (FM), Medscape recently spoke with Daniel J. Clauw, MD, Professor of Anesthesiology, Medicine (Rheumatology), and Psychiatry at the University of Michigan; and Philip J. Mease, MD, Clinical Professor in the Departments of Rheumatology and Internal Medicine at the University of Washington School of Medicine, about the latest evidence and care standards in this puzzling, painful condition.

What Is Fibromyalgia?

Medscape: Can you briefly summarize how the understanding of FM has evolved over the years?

Dr Clauw: In the old days (prior to 1980 or so), FM was called fibrositis—implying that there was some type of inflammation in the connective tissues causing widespread pain. The name was changed to "fibromyalgia" when it became clear that there was no such inflammation. That led to lots of research looking at the role that the central nervous system (CNS) plays in contributing to the pain, fatigue, sleep, and memory problems that these individuals experience. That research—and a parallel movement to study the CNS in other chronic pain states—has led FM to the present point, where it is thought to be the poster child for a "centralized" pain state. This can occur in isolation or as a comorbidity with other primarily "peripheral" pain states (eg, osteoarthritis, rheumatoid arthritis, lupus).

Dr Mease: I agree with Dan's synopsis of where we currently are in our understanding about FM as a condition characterized by "central sensitization," or a state in which one can see an increase in "bad" neurochemicals in the CNS that are associated with the experience of pain, fatigue, sleep disturbances, and the so-called "fibrofog"; along with a decrease in compensatory neurochemicals that normally work to offset the effects of these "bad" neurochemicals.

Some of this is triggered by chronic pain stimuli, such as conditions like osteoarthritis or irritable bowel syndrome; but it is also probably influenced by genetic factors, such as the genes that control the synthesis of catechol-O-methyltransferase. Constitutional influences such as early life stressors, which may influence genetic or epigenetic elements in a person, may also contribute to the condition.

If we go back in history to the late 1800s, we find descriptions of "neurasthenia" and other terminology that suggested that patients with chronic musculoskeletal pain without obvious tissue pathology had a primarily psychiatric/psychosomatic/neurotic reason for their symptoms. Because FM occurs primarily in women, they were considered to be weak, sensitive, depressed, anxious, and in need of psychotherapy.

However, in the early 1900s, pathologists incorrectly thought that they saw evidence of inflammation in muscle tissue of FM patients, as Dan has pointed out. There was even a fad for a while in the early part of the last century of removing organs such as the appendix or others that were thought to be the source of some kind of infectious stimulus to inflammation in tissues! Fortunately, these ideas were ultimately laid to rest. Whereas it is true that we may see a slightly higher frequency of depression or anxiety in FM than in the general population, we now know that there is a more biologic basis for the condition than being a pure psychiatric disease.

In the 1970s, Harvey Moldofsky did pioneering sleep studies that demonstrated that many FM patients have a fundamental abnormality in sleep physiology. But here too we now realize that this is an important associated problem but not necessarily the primary root of the condition. So now in the 21st century, with the aid of sophisticated neuroimaging techniques; neurochemical studies of the CNS; genetic analyses; as well as family, developmental, and psychological studies, we are recognizing that FM results from a complex interplay of neurochemical and genetic dysregulation, perhaps in the context of psychological factors; it can occur either on its own or in association with many chronic diseases, especially chronic pain and inflammatory diseases.


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