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The Overlapping Neurobiology of Depression and Pain: WHAT CAN WE DO TO CHANGE THINGS?

The Overlapping Neurobiology of Depression and Pain: WHAT CAN WE DO TO CHANGE THINGS?. Rakesh Jain MD , MPH. Introduction: Four Things to Keep in Mind. ‘Abnormal’ psychological problems – such as anxiety and depression, are very common in pain conditions

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The Overlapping Neurobiology of Depression and Pain: WHAT CAN WE DO TO CHANGE THINGS?

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  1. The Overlapping Neurobiology of Depression and Pain: WHAT CAN WE DO TO CHANGE THINGS? Rakesh Jain MD, MPH

  2. Introduction: Four Things to Keep in Mind • ‘Abnormal’ psychological problems – such as anxiety and depression, are very common in pain conditions • This creates a bi-directional, ‘spiral down’ negative impact on the pain patient • Multiple links exist between pain and psychological issues – neuro-endocrine, neuro-inflammation, autonomic disruptions, etc • Treatment – pain outcomes are negatively impacted if psychological issues are not well identified (thankfully, the reverse is equally true!)

  3. Is Pain Impacted by the Co-occurrence of Anxiety and/or Depression ? *p<0.001 * 8 Pain only (n=271) * * 7 * * * 6 Pain + Anxiety (n=15) 5 Brief Pain Inventory Pain Score (mean) range : 0-10 Pain + Depression (n=98) 4 3 Pain + Anxiety + Depression (n=116) 2 1 Pain Severity Pain Interference Bair MJ et.al. Psychosom Med 2008;70:890-7

  4. Chronic Pain after Accidental Injury & its Relationship to Anxiety / Depression (HADS-Depression and anxiety score) *p<0.05 * • 3 years later – 45% had chronic pain • 3 years after accident – 4.4% developed PTSD • 10%+ developed subsyndromal PTSD • all but one patient with PTSD (full or sub-syndromic) had chronic pain 5.4 * 4.6 3.1 2.0 Jenewein J et al. J Psychosom Res 2009;66:119-26

  5. Neck Pain and Anxiety – Increasing Pain Predicts Increasing Anxiety n=448*p<0.001 HADS Anxiety Sub-scale Mean Scores (s score range 0-21) HADS – Hospital Anxiety and Depression ScaleNPAD-d – Neck Pain and Disability Scale German Version Blozik E et al. BMC Musculoskel Dis 2009;10(13):1-8

  6. DPNP Patients – Relationship Between Pain and Mental Disorders n=255 *p<0.01 * * * Mean Score BPI – DPN Average Pain Severity HADS = Hospital Anxiety and Depression ScaleBPI = Brief Pain Inventory Gore M et al. J Pain Symptom Manage 2005;30(4):374-85

  7. Do Anxiety, Depression, or Sleep Problems Predict the Development of Pain? Odds ratio Odds ratio Depression(HAD Depression sub-score) Anxiety(HAD Anxiety sub-score) 15-month prospective study, 3171 followed, 324 developed chronic widespread pain Odds ratio Sleep(Sleep Problem Scale) Gupta A et.al. Rheumatology 2007;46:666-71

  8. The Pain Circuit Involves Sensory, Emotional, and Cognitive Regions of the Brain Somatosensory cortex Limbic system Cerebrum Thalamus Brainstem Slow, unmyelinated C-fibers Spinal cord Spinothalamic tract Dorsal ganglion Fast, myelinated A-fibers Afferent nerve fiber Adapted from Giordano J. Pain Physician 2005;8:277-90

  9. A Closer Look at Shared Anatomy: Complex Circuits Involve Sensory, Cognitive and Emotional Regions Apkarian AV et al. Eur J Pain 2005;9:463-84

  10. Primary nociceptive afferents (-) BRAINSTREAM MIDBRAIN (-) PSTT (-) (+) (+) (+) CORTICO- LIMBIC INPUT GABA INTER-NEURON SPINAL INTER-NEURON NRM 5-HT PAG OPIOIDS RMC NE (+) (-) (+) DLF Many Neurotransmitters are Shared by Pain and Anxiety (+) 5-HT=5-hydroxytryptamine; DLF=dorolateral funiculus; NRM=nucleus raphe mangus; RMC=reticular magnocellular nuclei; PAG=periaqueductal grey substance; PSTT=paleospinothalic tract. Giordano J. Pain Physician 2005;8:277-90

  11. Neuroendocrine and Neuroimmune Dysregulation in Pain Syndromes Red = inhibitory pathway Green = stimulatory pathway 1) Raison CL et al. Trends Immunol 2006;27:24-31. 2) Nestler EJ et al. Neuron 2002;34:13-25 3) Blackburn-Munro G et al. J Neuroendocrinol 2001;13:1009-23

  12. A Comprehensive, Neurobiological View of Pain and Psychology Jain R et al. Curr Diab Rep 2011;11:275–84

  13. Immunologic Impact of Pain With Increasing Duration of Pain Catecholamines, Neurokinin K Increased sympathetic activity Substance P IL-6 Sympathetic mediated pain IL-8 IL-IRa Hyperalgesia, fatigue, depression Serum IL-8 Serum IL-Ra Serum IL-6 * 764.9 *p<0.05 556.25 pg/mL * 37.08 18.45 7.1 • IL-8 is a proinflammatory cytokine, and mediates sympathetic pain • IL-Ra is involved with stress • IL-6 is involved with stress, fatigue, hyperalgesia, depression, and it activates sympathetic pain 7.3 <2-yr symptoms n=23 >2-yr symptoms n=23 Patients met ACR criteria for FM. Wallace DJ et al. Rheumatology 2001:40:743-9 Schwartz YA et al. Am J Resp Cell Mol Biol 1999;21:388-94

  14. Autonomic Dysregulationmay Augment Pain Norepinephrine-evoked pain 100 10 94.3 P<.05 9 80.0 P<.05 8 80 7 6 P =NS 60 5 54.3 54.3 56.3% P≤0.05 Patients (%) Visual analog scale (norepinephrine-placebo) 4 3 40 P =NS 30.0 30.0 2 1 20 0 11.9% -1 11.9% 16/20 6/20 6/20 0 -2 FM RA HC FM RA HC n=20 n=20 n=20 n=20 n=20 n=20 Martinez-Lavin M et al. BMC MusculoskeletDisord 2002;3:2

  15. Back Pain: Gray Matter Atrophy in Areas involved with Cognition and Emotional Regulation Patients with chronic back pain (CBP) had 5-11% less whole brain gray matter, equivalent to 10-20 years of normal aging ApkarianAV et.al. J Neurosci2004;24(46):10410-5

  16. In Pain Patients - Brain Perfusion Studies Implicate Anxiety Regulatory Centers Bilateral parietal perfusion (BA7) Bilateral post-central perfusion (BA4) Left anterior temporal perfusion Negative correlation Positive correlation GuedjE et al. J Nucl Med 2008;49;11:1798-803

  17. Grey Matter Loss in Pain – in Regions also Involved With Anxiety Regulation *p<0.001 * Volume (mm3) * Patients with FM (n=10) had significantly less GM volume in posterior cingulate, insular cortex, MFC, and parahippocampalgyrus. Rate of age-related decline was significantly greater in patients with FM than in controls (n=10; p<0.001) Patients with FM were losing 10.5 cm3 of gray matter/year since their diagnosis MFC=medical frontal cortex. Kuchinad A et al. J Neurosci 2007;27:4004-7

  18. A Suggested Clinical Pathway to Managing Anxiety/Depression in a Patient with Pain Routinely screen for anxiety D/Os Optimize treatment of pain Use scales / screeners Non-pharmacological treatment/s Pharmacological treatment/s If anxiety still persists

  19. Scales for Diagnosing Anxiety Disorders Hamilton Anxiety Scale (HAM-A) Beck Anxiety Inventory (BAI) Hospital Anxiety and Depression Scale (HADS)

  20. A Clinically Useful Anxiety Screener – GAD-7 KroenkeK et al. Ann Intern Med 2007;146:317-25

  21. GAD-7 – Useful for Detecting Multiple Anxiety Disorders GAD-7 Score of ≥8 Generalizedanxiety D/O Panic D/O Socialanxiety D/O PTSD KroenkeK et al. Ann Intern Med 2007;146:317-25

  22. Pharmacological Treatment Options for Anxiety Disorders

  23. Mind-Body Intervention for Older Adults with Chronic Pain Change from Baseline Scores CES-D STAI BPI - Interference Berman RLH et al. J Pain 2009;10(1):68-79

  24. Cognitive Behavioral Management of Chronic Pain * • Six weekly 90 minute group sessions • Based on CBT attention management manual * *p<0.05 * * * * Average pain (0-10 scale) n=18 Pain-related anxiety(Pass-20) n=20 (n=41; data for individuals completing 6-month follow-up) Elomaa MM et al. Eur J Pain. 2009; 13(10):1062-7

  25. Multidisciplinary Treatment: Impact on Improvement and HPA Changes 3 weeks of multidisciplinary treatment consisting of education, stretching, CBT, relaxation training, and aerobic exercise Before admission and treatment Before treatment After treatment 69 64.1 63.1 * 57.3 48.9 * p <.05 * 38 24.9 * 22.4 13.5 13.3 13.3 * 5.5 Positive VAS % of Pain CES-D Tender Score Area Score Points N=12. CBT=cognitive behavioral therapy; CES-D=Center for Epidemologic Studies Depression Rating Scale. Bonifazi M et al. Psychoneuroendocrinology2006;31:1076-86

  26. Anxiety, Stress, Neuroendocrine, and Immune Dysfunction as Potential Pain Mediators Genetic predisposition Poor sleep ANS dysfunction Psychological factors, stress Trauma Neuroendocrine- immune dysfunction Infections, Inflammation Neonatal, Childhood trauma Hyperexcitement of central neurons Environmental, Chemical Other factors Central sensitization Other mechanisms Central sensitization Central sensitivity syndromes Yunus MB. Semin Arthritis Rheum 2007;36:339-56

  27. In Conclusion – Emerging Data Reveal Pain has sensory, emotional, and cognitive components Although not all patients with pain disorders have comorbid mood disorders, they are present in a substantial number of patients Emerging data reveal a strong Bio – Psycho – Social interactional model between pain and anxiety / depression Clinical decisions in patients with overlapping pain and anxiety / depression should focus on amelioration of both conditions

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