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Are FMS and Other Chronic Conditions Associated? Are FMS and Other Chronic Conditions Associated?

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Unread 03-08-2003, 12:07 PM
Are FMS and Other Chronic Conditions Associated?

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Tamara Schuit, ImmuneSupport Staff

An article by Muhammad Yunus, MD, Professor of Medicine at the College of Medicine at Peoria, looks at how fibromyalgia (FM) and several other chronic conditions, such as chronic fatigue syndrome (CFS), myofascial pain syndrome, headaches, irritable bowel syndrome (IBS), Gulf War syndrome, etc., may possibly be similar conditions.

Dr. Yunus cites various studies that have shown how these syndromes are associated and how not just one, but several of these syndromes, can be present in the same patient. In addition, studies have proposed that these syndromes have overlapping features and are linked by common characteristics.

Researchers have come up with a common name for this occurrence – Central Sensitivity Syndromes (or CSS). CSS is related to the central nervous system’s ability to vary in developmental pattern or behavior according to varying environmental conditions on cellular, molecular, membrane, and neurochemical levels in response to outside stimulus.

These CSS syndromes share several characteristics – pain, hyperalgesia, poor sleep, and fatigue. In fact, as a group these CSS syndromes are likely to be the most common conditions that a patient consults a physician about.


Abstract

By Muhammad B. Yunus, MD

It has become increasingly clear that fibromyalgia (FMS) and several other chronic conditions, such as chronic fatigue syndrome, myofascial pain syndrome, headaches, irritable bowel syndrome, restless legs syndrome, primary dysmenorrhea, temporomandibular pain and dysfunction syndrome and female urethral syndrome are similar conditions. Gulf war syndrome is quite similar to FMS, and chemical sensitivity has not been well defined. A number of controlled studies show that these syndromes are associated with each other, and many of them are present in the same patient. In 1984, we had proposed that these syndromes have overlapping features and are unified by a common pathophysiologic mechanism which was not well understood at that time (Yunus MB, Comprehensive Therapy 1984; 10:21-28). Subsequently it became evident that the binding glue for these common conditions is a neuroendocrine aberration that is generally different from those found in psychiatric conditions (Yunus MB, Bailtieres Clin Rheum 1994; 8: 811-37). Recent research suggest, as well reviewed by Bennett (Bennett RM, Mayo Clin Proc 1999; 74:385-98), that more specified neuroendocrine abnorn1ality may well be central sensitization which is likely to be the common biopathophysiological binder of these overlapping illnesses.

Although some members of the above mentioned overlapping group of syndromes may indeed show central sensitization in response to a peripheral afferent input, it is equally possible that the central nervous system is intrinsically sensitive, even in the absence of a noxious stimulus in the peripheral tissues, in these conditions. An appropriate nomenclature for this group of syndromes has therefore been suggested to be "Central sensitivity syndromes" or CSS (Yunus MB, Journal of Indian Rheum Association, in press). The concept of central sensitization/central sensitivity and the available evidence for central sensitivity for several members of CSS will be discussed.

Central sensitization is related to central nervous system (CNS) neuroplasticity, which involves transsynaptic, cellular, molecular, membrane, and neurochemical changes in the central neurons of the spinal dorsal horn and supraspinal structures, in response to a peripheral stimulus. Such changes lead to central sensitivity with an exaggerated and prolonged response to a painful stimulus, increased receptive field, wind-up or summation effect and painful response to an otherwise non-noxious stimulus (such as touch). Central sensitization/ sensitivity is determined by other CNS factors, e.g., neurohormonal interactions and cerebral cognition.

Central sensitivity and related neurohorn1onal aberrations in FMS are suggested by persistence and spread of dysesthesia following a non-noxious electric stimulation, hyperexcitability with temporal summation to repeated electric stimulation, increased amplitude of cerebral event- related potential evoked by CO21aser stimulation, a decreased regional blood flow to thalamus and caudate nucleus, and an aberrant HPA axis. In chronic fatigue syndrome, there is widespread lower pain threshold in muscles by electric stimulation, as compared with normal controls. HPA axis abnormalities as well as brain neuroimaging studies also support that CFS is a disease of CNS.

Patients with irritable bowel syndrome (IBS) have multiple tender points as well as heightened visceral sensitivity with amplification and spread of pain in response to noxious stimuli. Cerebral neuroimaging in IBS also suggest a central dysfunction of nociception. Central sensitivity in tension-type headaches is evidenced by a widespread distribution of pain as well as a qualitative difference in pain following a peripheral noxious stimulus. The role of central mechanisms in migraine is suggested by an involvement of hypothalamus, serotonin, excitatory amino acids, central trigeminal pathways and cerebral events. Nicolodi et al examined existing data and concluded that hyperalgesia related to CNS neuroplastic changes are crucial for both migraine and FMS (Niclodi et al, Cephalgia 1998; 18 (suppI21): 41-4). With regards to myofascial pain syndrome, Bendtsen et al have demonstrated qualitatively altered nociception in this condition, suggesting aberrant central pain mechanism (Bendtsen et al, Pain 1996; 65 :259-64 ).

Several characteristics are shared by the CSS members, e.g., pain, hyperalgesia, poor sleep, fatigue, a response to a centrally acting drug, and an absence structural pathology in the tissues. The usual laboratory tests or X-rays which are useful for detecting classic pathology are normal in CSS. However, neurohormonal and newer brain imaging studies are abnormal in CSS diseases, but these abnormalities are generally different from those seen in psychiatric conditions. Thus CSS does not fit the traditional dichotomy of structural pathology or psychiatry, but a third" paradigm of central sensitivity/ neurohormonal dysfunction. It is, however, important to recognize that the boundaries between these three paradigms are not rigid and that there are some overlaps between them. For example, subgroups of rheumatoid arthritis as well as FMS have a psychological/psychiatric component, and FMS may be associated with, or triggered by, diseases of structural pathology, such as RA and systemic lupus erythematosus, as well as trauma. The diseases of these three chronic disease paradigms can be satisfactorily explained only by a biopsychosocial model. The boundaries between the so-called organic and functional disorders are more artificial than real. For this reason, I often use the tenus 'disease' and 'illness' synonymously.

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