Current Rheumatology Reviews - Volume 12, Issue 1, 2016

Cognitive-Behavioral Therapy (CBT) is a formal therapeutic approach that encourages selfmanagement of illnesses in accordance with the BioPsychoSocial model. CBT is composed of numerous skills grounded in known principles of behavioral and cognitive change. Each skill is designed to influence one of the facets associated with the perception of pain (i.e., sensory factors, emotional factors, or cognitive factors). Across the various Central Sensitivity Syndromes (CSS), CBT is thought to be beneficial to at least a portion of individuals afflicted. This paper provides a description of CBT, some recommendations for integrating CBT into clinical practice, and a brief review of the evidence supporting the use of CBT with various forms of CSS.

Symptoms of irritable bowel syndrome (IBS) are common in population studies including chronic abdominal pain associated with altered bowel habits. Patients often have associated gastrointestinal and somatic symptoms suggesting a possible common contributing mechanism, but the heterogeneous symptom patterns of individual patients make generalizations difficult. The pathophysiology of IBS is incompletely understood but includes disturbances of the brain-gut axis. Central mechanisms are: the psychosocial history and environment, dysfunctional brain processing of peripheral signals attributed to the intestine including the enteric nervous system, the microbiome and the innate and adaptive immune system. As a result there is visceral hypersensitivity and disturbed intestinal secretory and motor activity. Some mechanisms of visceral pain hypersensitivity may overlap with other pain syndromes including fibromyalgia (FMS). Central Sensitization (CS) would offer a way to conceptualize an integration of life experience and psychologic response into a biopsychosocial framework of pathophysiology, diagnosis and treatment of IBS. Corticotropin-releasing factor, a principle regulator in the stress and pain response may contribute to a neuroendocrine mechanism for the brain-gut interaction. The positive diagnostic approach to IBS symptoms to avoid excess testing and enhance the patient-provider therapeutic relationship requires the recognition of the “cluster” of IBS symptoms while identifying “alarm” symptoms requiring specific attention. The severity of the symptoms and other individual psychosocial factors characterize patients who seek medical care. The presence of significant psychosocial comorbidities adds to the complexity of management which often requires a multidisciplinary approach. Several treatment options exist but no single method is effective for all the symptoms of IBS. The therapeutic benefit of the well-executed physician-patient relationship is considered essential to success in managing IBS symptoms over the long term.

Chronic pelvic pain in men has often been misdiagnosed as prostatitis. After excluding serious or acute urological, neurological or colorectal conditions, it is essential to approach these patients with a much more comprehensive criteria. Thoughtful interview and methodical physical examination can very often reveal pelvic floor muscle dysfunction, Myofascial pain syndromes, Functional Somatic Syndrome/Central Sensitization Syndromes and/or psychosocial distress. One must be aware that many of these syndromes frequently overlap. Acknowledgement of these conditions and validation of both their physical and psychological distress is paramount to creating trust and confidence in the patient. These are the cornerstones for empowerment and self-care required in the management of chronic pelvic pain.

Temporomandibular disorders (TMD) have been discussed for more than 70 years without reaching consensus on causes, etiological factors, pathophysiology, or rationale management. Indeed, TMD pain remains an enigma and a diagnostic and management challenge for many clinicians. Perhaps the many and often conflicting views on TMD pain by different health care providers are routed in professional traditions, personal beliefs, experience, and clinical training. This review aims to provide an updated and critical discussion on what is known and supported by scientific evidence about myofascial TMD pain and which gaps there still may be in our understanding of this condition. It has not been the intention to make a systematic review on all aspects of TMD but rather to point out some of the more recent (and important) pieces of information that may help us to better appreciate TMD pain as a complex and multifaceted pain disorder manifested in the craniofacial system.

Central sensitivity syndromes are characterized by distressing symptoms, such as pain and fatigue, in the absence of clinically obvious pathology. The scientific underpinnings of these disorders are not currently known. Modern neuroimaging techniques promise new insights into mechanisms mediating these postulated syndromes. We review the results of neuroimaging applied to five central sensitivity syndromes: fibromyalgia, chronic fatigue syndrome, irritable bowel syndrome, temporomandibular joint disorder, and vulvodynia syndrome. Neuroimaging studies of basal metabolism, anatomic constitution, molecular constituents, evoked neural activity, and treatment effect are compared across all of these syndromes. Evoked sensory paradigms reveal sensory augmentation to both painful and nonpainful stimulation. This is a transformative observation for these syndromes, which were historically considered to be completely of hysterical or feigned in origin. However, whether sensory augmentation represents the cause of these syndromes, a predisposing factor, an endophenotype, or an epiphenomenon cannot be discerned from the current literature. Further, the result from cross-sectional neuroimaging studies of basal activity, anatomy, and molecular constituency are extremely heterogeneous within and between the syndromes. A defining neuroimaging “signature” cannot be discerned for any of the particular syndromes or for an over-arching central sensitization mechanism common to all of the syndromes. Several issues confound initial attempts to meaningfully measure treatment effects in these syndromes. At this time, the existence of “central sensitivity syndromes” is based more soundly on clinical and epidemiological evidence. A coherent picture of a “central sensitization” mechanism that bridges across all of these syndromes does not emerge from the existing scientific evidence.