A Pain Clinic Approach to Fibromyalgia Brigitte Gertoberens, Pain Medicine Specialist Malcolm Johnson,Clinical Psychologist Murray Hames, Senior Physiotherapist The Auckland Regional Pain Service
Prevalence in the general population is approximately 2% Female : Male ratio 7:1 Most frequently diagnosed in middle aged women, prevalence increases with age Up to 40 % of the pain clinic presentations
Wide spread musculoskeletal pains Muscle weakness and tenderness, muscle cramps Unexplained soft tissue swellings Hypersensitivity to touch and temperature Tingling, numbness,pins and needle sensations Disturbed temperature regulation Phono- and photo-hypersensitivity Itch without dermatological or metabolic pathology Symptoms are unspecific and variable in time course! Headaches Tinnitus Sleep disturbances Fatigue Poor memory and concentration Irritable bowel and bladder syndrome Dysmenorrhia Menometrorrhagias TMJ disorder Co-diagnosis of anxiety/depression/ptsd is commonly found
Diagnosis is based on: Taking a profound history including a medication/substance use history a clinical examination with specific attention to tenderness and sensory disturbances and using the ACR assessment criteria 2010 plus Fibromyalgia Survey Questionnaire Exclusion of other sinister pathology Routine blood tests: full blood counts, ESR, CRP, CK,Ca, TSH Routine testing for antibodies associated with rheumatoid diseases or lupus not recommended
Widespread Pain Index (0-19) Pain or tenderness over the past 7 days: Shoulder R / L Upper arm R / L Lower arm R / L Hip R / L Upper leg R / L Lower leg R / L Jaw R / L Chest Abdomen Upper back Lower back
Symptom Severity Scale (SS scale): 0 (no problem) 1 (mild or intermittent) 2 (moderate) 3 (severe) Over the past week: Fatigue Trouble thinking /remembering Waking up tired Over the past 6 months Pain or cramps in lower abdomen Depression Headache
The American College of Rheumatology 2010 1. Widespread Pain Index >= 7 and Symptom Severity Score >= 5 or Widespread Pain Index between 3-6 Symptom Severity Score >= 9 2. Symptoms have been present at a similar level for at least 3 months 3. Patient does not have a disorder that would otherwise explain the pain.
Specific inflammatory/autoimmune diseases (in particular polymyalgia rheumatica,esr ) Cave: misinterpretation of slightly elevated ANA or CRP Small- Fibre- Polyneuropathy Multiple Sclerosis Hypothyroidism
Concept of Central Sensitization Up-regulation of receptor activity and availability Loss of descending inhibition Dysregulation of dopaminergic neurotransmission within the limbic system? Genetic predisposition Stress seems to be a strong trigger HX of childhood maltreatment
Central sensitization: implications for the diagnosis and treatment of pain. Woolf CJ 1. Author information 1 FM Kirby Neurobiology Center, Children's Hospital Boston, Department of Neurobiology, Harvard Medical School, Boston, MA, USA. clifford.woolf@childrens.harvard.edu Abstract Nociceptor inputs can trigger a prolonged but reversible increase in the excitability and synaptic efficacy of neurons in central nociceptive pathways, the phenomenon of central sensitization. Central sensitization manifests as pain hypersensitivity, particularly dynamic tactile allodynia, secondary punctate or pressure hyperalgesia, aftersensations, and enhanced temporal summation. It can be readily and rapidly elicited in human volunteers by diverse experimental noxious conditioning stimuli to skin, muscles or viscera, and in addition to producing pain hypersensitivity, results in secondary changes in brain activity that can be detected by electrophysiological or imaging techniques. Studies in clinical cohorts reveal changes in pain sensitivity that have been interpreted as revealing an important contribution of central sensitization to the pain phenotype in patients with fibromyalgia...
No curative, specific treatment known Pharmacological approaches aim at symptom control Target is to improve patient s function and subsequently quality of life by teaching self management strategies Multidisciplinary approaches shown to be most effective
Tricyclics SSRIs / SNRIs Up to 40 % of the pain clinic presentationsanticonvulsants (Gabapentin/Pregabalin) Tramadol as rescue medication NSAIDs not recommended Opioids are not recommended as too many significant (conterproductive) side effects in CNCP
1. A. Vania Apkarian, Javeria Hashmi,Marwan Baliki : Pain and the brain: Specificity and plasticity of the brain in clinical chronic pain. Pain 2010, 11.010 2. Clifford J. Woolf: Central Sensitization: Implications for the diagnosis and treatment of pain. Pain 3/2011, 152, S2-15 3. Clifford J Woolf: Central Sensitization - Uncovering the Relation between Pain and Plasticity. Anaesthesiology 2007 Vol.No 4 4. Irene Tracey and M. Catherine Bushnell: How Neuroimaging Studies Have Challenged Us to Rethink: Is Chronic Pain a Disease? 5. M.C. Bushnell, A.V. Apkarian, S.B. McMahon, M.Koltzenburg : Representation of pain in the brain. Wall s and Melzack s Textbook of Pain,Vol 5 London,Elsevier 2006 pp107-124 6. A.Kuchinad, P.Schweinhardt,D.A. Seminovicz, P.B. Wood, B.A. Chizh and M.C.Bushnell : Accelerated Brain Grey Matter Loss in Fibromyalgia Patients: Premature Aging of the Brain? The Journal of Neuroscience 4/2007,27 (15) 4004-4007 7. Louise Oaklander : Objective evidence that small- fibre polyneuropathy underlies some illnesses currently labled fibromyalgia Pain Nov 2013 Vol 154 Issue11 pp 2310-16 8. W. Haueser, Kati Thieme, C.Turk : Guidelines on the management of fibromyalgia syndrome - a systematic review European Journal of Pain Jan 2010 Vol 14 p 5-10