Understanding Central Sensitization Chronic Pain Syndromes

Transcription

1 Understanding Central Sensitization Chronic Pain Syndromes Disclosures No relationships with industry Ruth Dubin PhD, MD, CCFP FCFP Co-Chair ECHO Ontario Learning Objectives: At the end of this session participants will be able to: Recognize central sensitization syndromes Educate patients about their condition and reduce their disease-related anxiety Support patient-centered multi-modal management strategies Understanding Central Sensitization The Journal of Pain, Vol 10, No 9 (September), 2009: pp When neurons in the dorsal horn spinal cord are subject to central sensitization, they exhibit some or all the following: development of or increases in spontaneous activity, a reduction in the threshold for activation by peripheral stimuli, increased responses to suprathreshold stimulation, and an enlargement of their receptive fields Maladaptive neuroplasticity Post shingles pain spread: 1: Pigmentary changes 2: Hyposensitivity (sensory loss) 3: Allodynia (sensory gain) Bilateral dorsolateral prefrontal cortex and right thalamus shrink in chronic lower back pain patients (Apkarian et al. J neurosci. 2004) Altered activity in many parts of the somatosensory pathway or other supraspinal areas (Mailis-Gagnon et al, Neurol.2003) Cross talk between neurons/ sprouting to cord levels above/below lesions and to contra-lateral side of cord (Warfield and Baja 2004) Glia, microglia and astrocytes, may participate in creating and maintaining pathological pain (Watkins et al 2001) Arendt-Neilsen et at J of Manual and Manipulative Therapy 19:187 Used with permission of the author Myofascial pain is a strong generator of central sensitization 1

2 Central Sensitization Syndromes Fibromyalgia Temporomandibular Joint Syndrome Interstitial Cystitis Irritable Bowel Syndrome Chronic Headache Chronic Low Back pain Chronic Widespread Pain Nondermatomal sensory deficit syndrome*: *see Mailis-Gagnon PAIN 145 (2009) and Egloff et al PAIN 145 (2009) C.S. is common in chronic pain (Kindler et al 2011 Pain Manage. Nurs. 12:15) In Temporomandibular Joint Disorder: Alteration in nociceptive processing in both the TMJ and sites distant from the head and neck region Irritable Bowel syndrome: enlarged referral patterns with cutaneous sensitivity in both lumbar and cervical regions, most apparent at lumbosacral regions (rectal and foot) Interstitial cystitis: lower pain thresholds at masseter, trapezius and ulnar muscles Headache, chronic low back pain etc. etc. CHILDHOOD ADVERSITY Risk of developing chronic pain + depression: physical abuse (OR 3.82) sex. abuse (OR 3.81) parental mental health disorder (OR 3.27) n>18,000 (Ontario Child Health Survey J Psych Res :1475) Stress and visceral pain: IBS patients have higher rates of abuse than patients with organic GI complaints (Pain :S63) Baby rats separated from their mother develop visceral hypersensitivity (Ibid) Childhood adversities* and early onset mental health disorders associated with adult heart disease, asthma, diabetes, arthritis, chronic spinal pain and headaches in 10 countries: Scott et al Arch Gen Psych 68(8):838 Diagnostic Uncertainty and CLBP (Serbic and Pincus, Pain :1540) The absence of a clear diagnosis and explanation are associated with negative cognitive, social and emotional functioning Uncertainly about diagnosis leads to a continued search for a diagnosis This may increase healthcare utilization and prevent patients from directing their attention to other aspects of life Acceptance of their chronic pain leads to improved QOL. (Lachapelle et al, Pain Res. Manage : Development of Chronic Widespread Pain over a 12 year period Stefan Bergman 1 1 R&D-centre, Spenshult hospital, Oskarström, Sweden Conclusions Results Subjects move to and from chronic widespread pain 1582 subjects (65%) responded at the 12 year (CWP) over time. follow up. Out of 959 subjects that had reported NCP at baseline, 66 (7%) reported CWP at follow Predictive factors differ between subjects with no up. Out of 192 subjects that had reported CWP chronic pain (NCP) at baseline that develop CWP, at baseline, 35 (18%) reported NCP at follow up. and subjects that improves from CWP to NCP over a twelve year period. The development of CWP from NCP over The results suggest different pathogenesis in the 12 years was predicted by: two ends of the pain spectrum. -being aged OR 2.5; 95% CI low educational level OR 3.0; 95% CI being an immigrant OR 2.4; 95% CI Background - problems falling asleep OR 8.2; 95% CI Chronic widespread pain (CWP) is often regarded as one end in a spectrum of more or less extensive pain The improvement to NCP from CWP over distribution in the body. We have previously reported 12 years was predicted by: that subjects move to and from CWP over a three year - never being a smoker OR 3.8; 95% CI period. - drinking alcohol weekly OR 3.5; 95% CI no nightly awakenings OR 4.5; 95% CI The aim of the study was to describe the multifactorial process of pain development over a 12 year period. Chronic Widespread Pain* after 11 years: 12% of those without it developed it. (Longitudinal Norwegian Population Cohort Study. Pain :1555) *Pain in the left and right sides of the body, above and below the waist, plus pain in the axial skeleton. Risk factors: Anxiety and Depression Former and current smoking Underweight (BMI <18.5) and overweight (BMI >25) Sleeping problems Method A baseline postal survey to 2425 subjects from the general population aged Localisation of pain was reported by a drawing of the body. Subjects were classified as having no chronic pain (NCP; n=1466), chronic regional pain (CRP; n=588), or CWP (n=303). 68 subjects could not be classified. Pain development was followed over 12 years. The predictive values of baseline background factors (age, sex, education, smoking, alcohol consumption, immigrant, sleep structure) were analysed by multivariate logistic regression. NCP CRP CWP ALCOHOL USE (HIGH > DRINKING > 8 OR MORE X /MON), and MODERATE = DRINKING 1 to 7 X/ MON) was PROTECTIVE stefan.bergman@spenshult.se 2

3 Figure 2 Interstitial Cystitis/Painful Bladder Syndrome and Associated Medical Conditions With an Emphasis on Irritable Bowel Syndrome, Fibromyalgia and Chronic Fatigue Syndrome Nickel et al J. Urol : Some Cases The Journal of Urology , DOI: ( /j.juro ) Copyright 2010 American Urological Association Education and Research, Inc. Terms and Conditions Central Sensitization - Christine s compression # On the Nature of Nondermatomal Somatosensory Deficits Angela Mailis-Gagnon, et al Clin J Pain Volume 27, Number 1, January 2011 Patient c/o severe pain Physical exam often displays sensory loss rather than sensory gain Vibration fork in middle of forehead midline split ie lateralizes to one side. Very often a history of mental or emotional trauma Sensory exam changes over time How a patient of mine cured herself Using traditional medicines and exercise Pain Diagram Jan year old woman, seen for post breast Bx pain Bx - July 2009, thought to be cancer: eventually determined to be benign Jan 2010: severe stabbing, burning pain L anterior hemi-thorax centered around 2 inch biopsy scar let go by MD who replaced her very trusted but now retired Family MD Prior difficulties on medications: Prozac severe suicidal ideation. (PTSD and Depression, early trauma) Prior Rx no benefit: tylenol, advil, amitriptyline, pregabalin, trazodone, a topical cream with echinacea: 3

4 Diagnosis: post surgical neuropathic pain with central sensitization I suggested: duloxetine, nabilone, 5%lidocaine cream mixture, topical capsaicin, neural-feedback with psychiatrist: not used Myofascial trigger point injections X 1: worse She chose acupuncture with a traditional Chinese acupuncturist, topical herbal and chinese medicine preparations Continued to exercise, and volunteer, involved with prayer group, support from church Finished 40 acupuncture treatments Pain still severe, still depressed, but area of allodynia/hyperalgesia had shrunk and was less sensitive Pain Diagram Oct 2010 Pain Diagram Fall 2011 Fall 2011: Enjoyed summer: gardening, exercising Socializing Pain scores still high Able to recognize many goals achieved Exercise therapy normalizes BDNF upregulation and glial hyperactivity in a mouse model of neuropathic pain Almeida et al Pain 156: Partial sciatic nerve injury in mice induces mechanical allodynia and thermal hyperalgesia 7 to 70 days post surgery Mice trained to swim (Photographs thanks to Dr. Almeida used with permission) Results Swimming increased the oxidative capacity of soleus muscle- effect disappeared after 2 weeks of sedentary behaviour Sedentary mice had persistent mechanical allodynia Mice that swam recovered from mechanical allodynia at 6 weeks. Thermal hyperalgesia lasted longer in sedentary mice than in swimming mice Thermal hyperalgesia disappeared faster in swimming mice 4

5 Biochemical changes in trophic factors after sciatic nerve ligation NGF (Nerve growth factor) induces hypernociception BDNF (Brain derived neurotrophic factor) induces hypernociception increases dorsal horn hyperexcitability Swimming reduced NGF and returned BDNF to normal The ideal treatment of CNCP* Complementary and Alternative treatments SELF MANAGEMENT MOVEMENT Physical / Rehabilitative GDNF (Glial derived neurotrophic factor) in DRG induces anti-nociception MIND Psychological MEDICINE Medications & Interventions *(R Jovey, Canadian Pain Society,2009-with input from R.Dubin) Also see: Action Plan for the organization and delivery of chronic pain services in Nova Scotia, 2006 ECHO ONTARIO: VISION Questions That all primary care providers in Ontario have the knowledge and support to manage chronic pain safely and effectively. 5