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Central Sensitization: Common Etiology In Somatoform Disorders

Central sensitization occurs when pain pathways in the spinal cord become hyperexcitable and are augmented, rather than blocked, in the thalamus and other brain centers. This leads to a cascade of neuroinflammatory, neuroendocrine, and autonomic dysregulation.
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Editor's Note: The understanding of centralization of pain from a peripheral pain site is a major scientific discovery of recent times that enhances clinical understanding and therapeutics. Once peripheral pain has centralized, aggressive therapy is required because two anatomical systems, rather than one, must be treated. One of the mysteries of pain patients is what appears to be the "de novo" occurrence in the central nervous system (CNS) of some painful conditions, such as fibromyalgia (FM), interstitial cystitis, temporomandibular joint (TMJ) disorder, and irritable bowel syndrome (IBS). While neuroinflammation resulting from glial cell activation clearly is an underlying mechanism for centralization of peripheral pain, the underlying cause of these disorders is unclear. In a scholarly presentation, the authors attempt to categorize these disorders into one group called "somatoform," purporting that "central sensitization" is a common thread among these disorders. This paper is published here to explore their theory and terminology. The authors do not discuss what produces central sensitization, such as neuroinflammation, autoimmunity, or possible infection. They focus on a hyperirritable nervous system of unknown etiology. There is no endorsement by Practical Pain Management regarding the authors' theories, conclusions, terminology, or treatment. We do endorse the fact that the authors are attempting to better understand these disorders, and, hopefully, this paper will initiate some needed interest and debate.

"Physical symptoms that are unexplained by organic cause are a relatively common phenomenon. It is estimated that modern diagnostic testing can find no organic explanation for 10% of reported and persisting physical symptoms. Furthermore, the occurrence of multiple somatic symptoms is associated with higher rates of psychopathology and predicts poorer treatment outcomes and higher healthcare utilization. Such nonorganic symptom complaints have traditionally been grouped into separate syndromes, such as FM, chronic fatigue, IBS, and TMJ disorders. Historically, different terms have been used to group these types of somatization disorders, including "functional syndromes," "medically unexplained symptoms," and "bodily distress syndrome." These syndromes also share many common features, including pain, fatigue, poor sleep, cognitive deficits, headaches, anxiety, and depression, suggesting that they may share a common etiology."
—Mayer et al.1

Most clinicians have encountered the chronic pain patient who has no specific organic basis for their pain. Among these are patients with chronic fatigue, FM, TMJ disorder, chronic headache, IBS, irritable bladder, and regional pain syndromes (such as non-cardiac chest pain). Typically, such patients have endured frustrating rounds of visits to specialists (cardiologists, rheumatologists, gastroenterologists, and others) and many diagnostic tests, procedures, and treatments—all to no avail. Such encounters are not without their own hazards and may aggravate the patient's fear of undiagnosed illness, a phenomenon called "iatrogenic reinforcement." Over the past decade or so, research has begun to elucidate basic physiological mechanisms for these disorders—namely, central sensitization (CS).2-4

CS involves an abnormal and significant amplification of pain sensations by CNS mechanisms. There is impairment of the nervous system's natural pain suppressive mechanisms (eg, endogenous opioids). Sensations not normally painful become so and minor discomforts become severe (allodynia). Rich interconnections between pain and autonomic pathways lead to visceral organ dysfunction, such as what occurs in IBS.

Yunus has proposed that the term central sensitivity syndrome (CSS) be used for nonorganic somatoform disorders that share this CS etiology.3-5 As will be discussed in this review, the CSS model provides a very appealing theoretical construct that can be used to categorize a wide array of related syndromes. Unlike in the past, when various symptom presentations were viewed as individual somatoform disorders, the CSS model is a unifying one, in which these various symptom presentations are conceptualized as simply many forms of a common CSS construct, with CS as the fundamental root cause.5-8

How Does CS Occur?

How CS comes about is not yet entirely clear. Many patients who develop CS have a history of early childhood—even prenatal—trauma; an abusive, alcoholic, or absent parent; and/or a conflicted, unhappy home life. A family history of CS is common, implying genetic influences (epigenetic regulators, which "turn genes on or off" and respond to environmental influences, may be equally important). Such environmental impacts may induce vulnerability to later stressful life influences. Many patients do well in school and into adult life. However, often one or more setbacks occur at home or at work, or an accident, injury, or even a minor illness can precipitate the disorder, and the frustrating search for cause and cure begins.

CSS: An Overview

Many technological advances have been made for investigating pain disorders,9 and concomitant studies have been conducted that have increased our ability to identify biomarkers of CS.10-14 These contributions have enhanced our understanding of the pathogenesis of pain disorders. For example, we have learned that disorders such as TMJ, FM, and IBS stem from dysregulation of interdependent bodily systems, any one of which can be disturbed from its normal function by multiple causes, and subsequently can impair the function of the next system in a cascade of maladaptive biopsychosocial sequelae.15-18 As such, the biopsychosocial model (first introduced by Engel19) has been demonstrated to be compatible with the nature and complexities of pain pathology. Furthermore, it removes the illusion of simplicity that is assumed by purely physiological models, which are only appropriate for studying etiologies of the "early" phases of pain processing.20 "Early" processing is used to describe the reactivity that occurs prior to the higher-order neurocognitive interpretations of pain that modify the pain signal during the "late" phase of pain processing, producing the perception of pain, and the subjective experience of pain.

Pain Pathways

A primary mechanism of CSS is hypersensitivity.8,18,21,22 One of the complexities of studying and treating chronic pain has been identifying where in the pain pathway the processing is augmented. The difficulty of such a task relates to the fact that responses to pain are variable during the "early" processing of pain in the periphery, and are substantially more variable in the later phases of pain processing, when many factors converge to promote CS and modulate pain processing.

Last updated on: December 15, 2014