Document 23985

2012 Addiction Studies Institute Sponsored by The Ohio State University, Talbot Hall August 22-­‐24, 2012 The Greater Columbus Convention Center, Columbus, Ohio Concurrent Session D (D4): Friday, August 24 2012 10:15 AM – 12:30 PM Still Hurting? What’s Behind Your Symptoms and Pain William B. Salt II, MD Deborah Hoy, RN, MSN, CNS “What is behind the symptom?” The Vital Balance (1963) KARL MENNINGER, MD “The whole is more than the sum of its parts.” Aristotle’s Metaphysics ARISTOTLE “Disease is dysfunction involving mind, brain, and body. Symptoms are the expression. Everyone hurts. Life is hard, complicated, lived too fast, very stressful, and quite emotional. We weren’t biologically designed to live like this. From time to time, everybody loses balance and suffers with dysfunction and disease expressed as chronic pain, fatigue, symptoms, and syndromes. Most people suffer chronically with some dysfunction that cannot be detected with conventional medical tests.” By looking behind the pain and symptoms, we can regain our balance and recover. This session will cover a complexity science-­‐based biopsychosocial model of chronic disease and explain central sensitivity syndromes (CSS), which are collections of medically unexplained chronic pain and symptoms. The presenters will integrate the neurobiology of addiction with the latest management concepts for high-­‐risk individuals and those with opiate dependence. William Salt II, MD, Gastroenterologist, Ohio Gastroenterology Group, Columbus, OH Deborah Hoy, RN, MSN, CNS, Clinical Nurse Specialist, Talbot Hall/OSU Hospital East, Columbus, OH LEARNING OBJECTIVES 1. Replace the traditional terms for functional somatic syndromes, such as irritable bowel syndrome and fibromyalgia with "central sensitivity syndromes," or "CSS." 2. List the most common CSS. 3. Recognize central (nervous system) sensitization (the pathophysiology that underlies CSS) in the clinical setting. 4. Describe central sensitization: amplification of interoceptive bodily information by the central nervous system, which results in a diffuse hyperalgesic state. 5. Recognize that peripheral input (e.g. from the gastrointestinal tract) can initiate and potentiate central sensitization. 6. Review an original illustrated CSS model based upon a metaphor intended to facilitate patient/caregiver education, understanding, and shared decision-­‐making. 7. Apply the concept of CSS and model to the development of plans for patient care in high-­‐risk populations and those with the disease of addiction. 2 8. Learn strategies for collaborative treatment that could result in improved clinical outcomes and diminished potential for relapse. INTRODUCTION Functional symptoms syndromes, such as irritable bowel syndrome (IBS) and fibromyalgia (FM) are collections of medically unexplained chronic pain and symptoms that are among the most common, confusing, and frustrating clinical problems encountered by caregivers from diverse disciplines. Medical tests do not show cause(s). Opioids are prescribed by some caregivers, despite the potential these drugs have for exacerbation of the syndrome (e.g. narcotic bowel syndrome complicating IBS), lack of efficacy (e.g., fibromyalgia), and risks of misuse and addiction. An original integrative biopsychosocial model of functional symptom syndromes, which are now called “Central Sensitivity Syndromes” or “CSS”, will be described here. “Central” refers to central nervous system (CNS). The model is based upon the emerging concept that CNS dysfunction (central sensitization or amplification) underlies all CSS, which results in a diffuse hyperalgesic state characterized by multifocal pain, symptoms, and fatigue commonly involving multiple systems. Peripheral bodily dysfunction can initiate and potentiate CNS sensitization and amplification and contribute directly to symptom generation (e.g., gastrointestinal dietary and bacterial contents triggering abdominal pain and diarrhea in IBS and osteoarthritis augmenting the central pain of FM). Sensitization of pain modulating systems cannot be detected with conventional medical testing. This confounds caregiver/patient communication, understanding, and shared decision-­‐making. 3 SYMPTOM SYNDROMES Nearly every specialty describes at least one symptom syndrome. These syndromes are collections of medically unexplained symptoms. Some of the most common include: • Irritable bowel syndrome (IBS). Over 30 functional gastrointestinal disorders (FGIDs) are now defined. Other common FGIDS include non-­‐cardiac chest pain, functional heartburn that fails to respond to proton pump inhibition therapy, functional dyspepsia, and functional abdominal pain ( • Fibromyalgia • Headache (tension > migraine, mixed) • Chronic fatigue syndrome • Temporomandibular dysfunction (TMD) • Idiopathic chronic low back pain • Multiple chemical sensitivity • Chronic pelvic pain • Primary dysmenorrhea • Interstitial cystitis/painful bladder syndrome • Chronic prostatitis/painful prostate syndrome CENTRAL SENSITIVITY SYNDROMES (CSS) Several terms have collectively been applied to these symptom syndromes: • Functional somatic (and visceral) syndromes • Medically unexplained syndromes • Chronic pain syndromes • Chronic multisymptom illnesses • Somatoform disorders • Central sensitivity syndromes (CSS) 4 CSS is the emerging term that reflects the shared pathophysiology of central sensitization common to these symptom syndromes. CO-­‐OCCURRENCE, SYMPTOM OVERLAP, AND CORE SYMPTOMS CSS often co-­‐occur. One of the most common syndrome combinations is irritable bowel syndrome with fibromyalgia. Symptoms commonly overlap syndromes. For example, pain and fatigue are clinical features of both fibromyalgia and chronic fatigue syndrome. Several “core” symptoms are usually found in CSS. When present, central sensitization can be suspected. • Multifocal pain • Fatigue • Insomnia • Cognitive or memory problems While some individuals only have one of these symptoms, more often they have many. Furthermore, the precise location of pain and predominant symptom can change over time. DEPRESSION AND ANXIETY ARE COMMON COMORBIDITIES CSS are associated with a higher rate of co-­‐morbid mood disorders and psychological distress, including depression and anxiety. Psychosocial factors can contribute to the illness experience and maintenance of chronic pain and symptoms. Functional brain systems of emotion and pain/symptom processing are separate, but they are integrated and share similar neurotransmitters. Once patients understand this, they may be more accepting of the therapeutic importance of addressing psychosocial factors. Furthermore, the analgesic benefit of antidepressant drugs is largely independent of their effects on mood and affect and can be achieved with doses lower than would be necessary to treat depression. 5 CENTRAL SENSITIZATION IS THE SHARED PATHOGENESIS OF CSS Emerging science from diverse disciplines confirms the convergent concept that CSS, their interrelationships, and their common association with “stress” can be collectively understood by viewing them as expressions of dysfunction of CNS pain modulating systems. CSS share common pathophysiology and predisposing influences. Yet clinical application of this holistic “big picture” biopsychosocial “lumping” perspective lags far behind in the practice of medicine, where divisive biomedical specialty-­‐driven “splitting” predominates. CSS are manifestations of CNS dysfunction driven pain conditions, which results in a diffuse hyperalgesic state identifiable using experimental sensory testing and functional neuroimaging. Central sensitization is also called, central “amplification.” Peripheral bodily dysfunction also contributes. CSSs have several common clinical characteristics, share predisposing factors, and are related to stress. Slides from Medscape Education Fibromyalgia and the Brain: New Insights and Rationale for Treatment Moderator: Michael Clark, MD; Panelists: Daniel J Clauw, MD and Donald L Goldenberg, MD January 31, 2012 6 7 8 9 10 The volume control setting is increased in those suffering with CSS, resulting in central sensitization and the diffuse hyperalgesic state. Elevated levels of neurotransmitters that tend to be pronociceptive (i.e. on the left side of the figure), or reduced levels of neurotransmitters that inhibit pain transmission (i.e. on the right side of the figure) increase the volume control. Drugs that block neurotransmitters on the left or augment activity of those on the right may be helpful. Non-­‐pharmacologic approaches can be as effective as drug therapy in reducing the gain setting. The arrows in the figure indicate the direction of the abnormalities in these neurotransmitter levels (either in the CSF or brain) that have been identified to date in fibromyalgia. 11 OPIOIDS The only neurotransmitter system that has been studied to date and not found to be out of line in a direction that would cause augmented pain transmission is the endogenous opioid system. Both CSF levels and brain activity by functional neuroimaging appears to be augmented, not reduced (as would cause augmented pain processing) in FM, which may be why opioidergic drugs do not work well to treat FM and related pain syndromes. 12 13 PAIN AND SYMPTOMS: MORE THAN A FEELING Pain is ultimately experienced in the brain rather than in the peripheral tissues and organs of the body, regardless of central or peripheral origin. This is a difficult concept for patients (and some caregivers) to understand, as are the absence of evident cause on medical tests and significance of any psychosocial factors that may be present. The frustration for both patients and caregivers who have limited time available in relationship contributes to unnecessary medical testing, further referral, and unsatisfactory outcomes from the perspective of both parties. Patients continue to suffer with real pain and symptoms and with their pain cognitions, which are commonly maladaptive. From the neurobiological perspective, it is of primal evolutionary importance that all tissues and organs respond to stressors and triggers in the external environment and within the body with “interoceptive” information that reflects their physiologic condition. These “homeostatic feelings” include pain, visceral sensations, and muscle ache that are transmitted to the CNS in real time, where they are processed and responsively expressed in multiple dimensions, including: • Location • Severity • Autonomic nervous system output • Affective • Motivational These responses are “homeostatic emotions” and are to be distinguished from primary and complex emotions. Central sensitization is CNS dysfunction that results in negative expression, amplification, and even distortion of homeostatic emotions. The “how” and “why” of central sensitization and CSS can 14 be understood through holistic simplification of a complex systems view that integrates modern theories and concepts of complexity science, functional connectivity of mind/brain, body and their information transfer systems, interoception, chronic pain, stress, affect/emotion, cognition, and chronic inflammation. A METAPHOR FOR UNDERSTANDING CENTRAL SENSITIZATION AND CSS An educational model based upon a language/communication metaphor integrated and expressed with building illustrations facilitates explanation and understanding of these complex concepts. The simplified goal is that both caregivers and patients understand the quotes that open this presentation. The analogy offered in this model pictures the body and brain verbally speaking with one another about pain and symptoms. All parts of the body are telling the brain 24/7 how they feel as they respond to the complicated and stressful world without and within. (Nature and nurture factors are both equally important “response influences.”) When some part of the body reports a responsive feeling (read: symptom), such as pain, a gut cramp, or muscle aching, this “body word” (homeostatic feeling) is “heard” by the brain. 15 There are four integrated intercommunicating centers in the brain: 16 All four brain centers confer 24/7 about body words and render interpretations. (Most of this happens behind closed doors, so we are not aware of what is going on.) The Symptom Generator is charged with the responsibility of expressing the interpretation through a speaker that has a volume control dial: 17 When dysfunction (central sensitization is present), the Symptom Generator system of the mind/brain transmits “body talk” (homeostatic emotions) to the body, projecting a negative tone of voice and turning the volume up so that it is loud and distorted. Body talk is multidimensional, unlike body words: 18 The figure below represents the complete illustration of the model following the “builds” as components are introduced and explained: Caption (Written for the health care professional) An individual’s body (represented by the figure) interacts (bidirectional gray arrow) with the environment (globe), which is physical, social, and man-­‐made. Tigers represent trigger/stressors in the environment, gut (intestinal contents), and mind/brain (conscious and subconscious). Lifelong patterns of response to tigers, including vulnerability to and variations of symptom expression are shaped by response factors (orange call-­‐out), which include genetics, development, experience, culture, and gender. These response factors constitute “nature and nurture,” whose contributions are roughly equal. 19 The mind/brain, spinal cord, and vagus nerves comprise the central nervous system (represented in black). Connections (two vertical gray arrows) are the information transfer systems between the body proper and the mind/brain. The five senses, gut, and tiny homeostatic afferent nerves innervating all tissues and organs relay information in response to triggers/stressors to the mind/brain. These interoceptive responses are “homeostatic feelings,” including visceral sensations, muscle ache, and pain, which are transmitted to the mind/brain. Four ovals within the mind/brain represent functional connectivity networks: • STRESS RESPONSE (green) • EMOTION (orange) • CONSCIOUSNESS, COGNITION, AND MEMORY (yellow) • SYMPTOM GENERATOR (red) The ovals overlap to emphasize integration and intercommunication of the four systems. The Symptom Generator (which includes the insular cortex) is activated by visceral and somatic stimuli (homeostatic feelings) and also by stimuli originating centrally from the other networks. It expresses “homeostatic emotions” (read: pain) in multiple dimensions: location, intensity, affective and motivational output, and autonomic responses. The “volume control” represents facilitative or inhibitory central modulation of input, which influences expression and perception of pain and symptoms through ascending and descending pathways respectively. Adverse neuroplastic changes and dysfunction result in “central sensitization” or amplification, which is conceptualized as an increase in the volume control setting. Symptoms influence behaviors (gray arrow), which can augment or diminish them. 20 MANAGEMENT OF CSS Conceptually, treatment of CSSs can be directed centrally and/or peripherally and is both pharmacological and non-­‐pharmacological, aiming to reduce the volume setting. It includes management of any associated psychosocial issues, which optimally can be addressed once patients understand central sensitization. Central Therapy In contrast to acute and purely “peripheral” pain states that are responsive to NSAIDs and opioids, central pain conditions respond best to CNS neuromodulating agents, such as tricyclic antidepressants (TCAs), serotonin-­‐norepinephrine re-­‐uptake inhibitors (SNRIs) and anticonvulsants. Peripheral Therapy Treatment directed to peripheral pain contribution can also be important, particularly because noxious peripheral nociceptive input can initiate and contribute to central dysfunction. As exemplified by the CSS, irritable bowel syndrome, peripheral gut luminal stressors (including dietary intestinal content and bacterial flora) can trigger and perpetuate symptoms. Treatment can be directed to these peripheral symptom generators, which can also reduce central sensitization. Recent findings show that subsets of individuals with heretofore-­‐
considered “peripheral” or nociceptive pain states, such as knee osteoarthritis (KOA) and chronic low back pain (CLBP), may have prominent CNS contributions to their pain and respond to the combination of peripheral and centrally directed therapy. In gastroenterology, many patients with inflammatory bowel disease (ulcerative colitis and Crohn’s disease) also have IBS and central sensitization. Opioid Therapy Nevertheless, opioids may be prescribed for CSS, despite their relative lack of efficacy (e.g. fibromyalgia), requirement for indefinite 21 treatment without endpoint, potential for exacerbation of the syndrome (e.g., narcotic bowel syndrome complicating IBS), and risks of misuse and addiction. Treatment with opioids is best avoided for most patients with CSS. Non-­‐Pharmacologic Therapy Non-­‐pharmacologic approaches can be as effective as drug therapy, including an effective patient/health care professional relationship, education, cognitive reframing, and good self care, including eating an anti-­‐inflammatory diet, exercise, achieving and maintaining a healthy weight, restorative sleep, and stress management. CONCLUSION There are several reasons that caregivers do not usually apply a broad clinical biopsychosocial perspective of CSS. First, multiple medically unexplained symptoms and symptom syndromes are commonly attributed to depression. Second, the concept of central sensitization is emerging and not yet appreciated by most health care professionals outside of the specialty of rheumatology, where it is integral to the understanding, diagnosis, and management of fibromyalgia. Other specialists usually focus upon the symptoms and syndromes within their own expertise, disregarding the “big picture” diagnostic and therapeutic implications of presence of multifocal pain, fatigue, a “positive review of systems,” and diagnosis of one or more other CSS. It will take some time before the concept of central sensitization is widely accepted and applied by most specialties. Third, time constraints significantly interfere with the patient/caregiver relationship. Fourth, effective CSS educational materials and methods to facilitate patient/caregiver shared management and decision making are lacking. We propose that the concept of central sensitization as described in this illustrated metaphor-­‐based model can facilitate patient/caregiver-­‐
shared understanding and decision-­‐making across disciplines. Furthermore, patients may then be more willing to discuss and accept 22 the importance of addressing psychosocial factors that contribute to the illness experience. It is usually in the best interest of patients suffering with CSS to avoid treatment with opioids, but these drugs will likely continue to be prescribed for several years. We suggest that this CSS model can be applied to the development of plans for patient care in high-­‐risk populations and in those with the disease of addiction. Strategies for collaborative treatment, which can result in improved clinical outcomes and diminished potential for relapse will also be offered in session. SELECTED REFERENCES Craig AD. How do you feel-­‐-­‐now? The anterior insula and human awareness. Nat Rev Neurosci. 2009 Jan;10(1):59-­‐70. Damasio A. The Feeling of What Happens: Body and Emotion in the Making of Consciousness. New York, Mariner Books, 2000. Davidson RJ, McEwen BS. Social influences on neuroplasticity: stress and interventions to promote well-­‐being. Nat Neurosci. 2012 Apr 15;15(5):689-­‐95. Drossman DA, Morris CB, Edwards H, Wrennall CE, Weinland SR, Aderoju AO, Kulkarni-­‐Kelapure RR, Hu YJ, Dalton C, Bouma MH, Zimmerman J, Rooker C, Leserman J, Bangdiwala SI. Diagnosis, Characterization, and 3-­‐Month Outcome After Detoxification of 39 Patients With Narcotic Bowel Syndrome. Am J Gastroenterol. 2012 Jun 19. doi: 10.1038/ajg.2012.142. [Epub ahead of print]. Human Connectome Project. (Accessed 18 August, 2012). 23 Jayasinghe C. Complexity science to conceptualize health and disease: Is it relevant to clinical medicine? Mayo Clin Proc. April2012;87(4):314-­‐
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