Contemporary understanding of chronic pain with understanding of chronic pain with specific reference to co morbid psychiatric illness. Central sensitization of chronic pain ... Sullivan

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  • Contemporary understanding of chronic pain with specific reference to co morbid psychiatric illness. Central sensitization of chronic pain and diagnosing the syndrome.

    Dr Tipu Aamir MBBs, MRCPsych, FFPMANZCA The Auckland Regional Pain Service

  • Outline } Introduction and History

    } Recent Advances in Conceptualisation of Pain

    } Interface of Mental Illness and Pain

  • } Our actions and thoughts are all steered by the models we embrace. Author unknown

  • History } Evidence of Use of Opium by Sumerians, Egyptians,

    Assyrians, Greeks, Romans and other Civilizations

    } Earrings from collection of 7 fruits of a plant proved to be poppy capsules. Tomb of King Siphtah and Queen Tausrit, D. XVIII.

  • } Aristotle (384 BC 322 BC) } Pain and pleasure not as sensations but as emotions

    ("passions of the soul") } Pain was due to evil spirits and the gods which entered

    the body via an injury

  • } Hippocrates (460 BC 370 BC) } Imbalance in the vital fluids of a human } Pain is just a symptom

  • } The brain was not believed to have any direct influence; for years the heart was considered to be the centre for pain sensation.

  • } Galen (AD 129 c. 200/ c. 216) } injuries (breach of continuity) were the only cause of pain

    } Ibn Sina (Latin name Avicenna) (AD 980 1037) } true cause of pain was a change of the physical condition

    (temperament change) of the organ whether there was an injury present or not

  • } Both Galen and Ibn Sina believed that the brain was the principal organ for perception of pain

    } Galen identified three conditions for pain perception:

    the organ to receive impression, a connecting passageway and an organisational centre

  • (Gerard de Harderwyck 1496)

  • } Ren Descartes (15961650) } humans are a mechanical body governed by a rational

    soul

  • (Descartes R. Treatise of Man 1662)

  • } Implications of Cartesian Model } Direct link between the amount of tissue damage and the

    level of pain experienced, in other words, the more damage incurred, the greater the pain. (unidimensional)

    } Pain is consequently considered to be either strictly

    physical or strictly psychological.

  • } Doctors attempted to distinguish between true physical and psychologically derived pain.

    } When pain symptoms were difficult to treat or even

    understand, the question arose as to whether the pain actually was caused by a psychological condition.

  • } Bad personality } 1944 study of British soldiers with chronic pain: shy,

    mother-fixated, emotionally adolescent male virgins. } Bad behaviour rest, avoiding duties, excessive

    pain behaviour } Bad motivations attention-seeking, opioid-seeking,

    slacking } Bad coping - passive, helpless, maladaptive } Bad thoughts & feelings fear, phobia, depression

    } (Amanda C de C Williams 2013)

  • Theories of Pain } Specificity Theory Specific pain receptors in body, which projects pain to a pain centre in brain. (von Frey 1895)

    } Pattern Theory Pain is produced by intense stimulation of non- specific receptors (Sinclair 1955)

    Melzack R, Wall PD. On the nature of cutaneous sensory

    mechanisms. Brain. 1962;85:331356

  • Gate Theory of Pain

    Multiple filters in pain pathways

    } Spinal Filter - gate

    } Central Filter in Brain attention, emotions, memories

    Melzack R, Wall PD. Pain mechanisms: a new theory. Science. 1965;150:971979

  • Gate Theory of Pain

    Melzack R, Wall PD. Pain mechanisms: a new theory. Science. 1965;150:971979

  • IASP Definition of Pain An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.

  • Central Sensitization

    Central Sensitization is hyperexcitability of the central nervous system following a peripheral stimulus. (Woolf 1983)

  • Central Sensitization

    } Central sensitization represented a condition where input in one set of nociceptor sensory fibers (the conditioning input) amplified subsequent responses to other non-stimulated non-nociceptor or nociceptor fibers

    } Woolf CJ. Central sensitization: implications for the diagnosis and treatment

    of pain. Pain 2011 Mar;152(3 Suppl):S2-15.

  • Central Sensitization

    } In consequence pain could in these circumstances become the equivalent of an illusory perception, a sensation that has the exact quality of that evoked by a real noxious stimulus but which occurs in the absence of such an injurious stimulus. This does not mean that the pain is not real, just that it is not activated by noxious stimuli.

    } Woolf CJ. Central sensitization: implications for the diagnosis and treatment of pain. Pain 2011 Mar;152(3 Suppl):S2-15.

  • Central Sensitization: Uncovering the Relation between Pain and Plasticity. Woolf, C J. Anesthesiology: April 2007 106 (4) 864-867

  • Latremoliere A, Woolf CJ. Central sensitization: a generator of pain hypersensitivity by central neural plasticity. J Pain. 2009;10(9):895.

  • Latremoliere A, Woolf CJ. Central sensitization: a generator of pain hypersensitivity by central neural plasticity. J Pain. 2009;10(9):895.

  • .

    Central Sensitization This change is protective, because it helps healing by limiting use of an injured body part until the injury is fully repaired. Central sensitization becomes pathological, however, if inflammation persists, as with rheumatoid arthritis, in which no healing occurs, and in situations in which central sensitization becomes autonomous and is maintained in the absence of active peripheral pathology. Latremoliere A,WoolfCJ. Central sensitization: a generator of pain hypersensitivity by central neural plasticity.J Pain.2009;10(9):895.

  • } Woolf CJ. Central sensitization: implications for the diagnosis and treatment of pain. Pain 2011 Mar;152(3 Suppl):S2-15.

  • } Woolf CJ. Central sensitization: implications for the diagnosis and treatment of pain. Pain 2011 Mar;152(3 Suppl):S2-15.

  • Tracey I, Mantyh PW. The cerebral signature for pain perception and its modulation. Neuron.2007;55:377391

  • Central changes }Long term potentiation of hippocampal

    cells

    } RR Ji, T Kohno, KA Moore, CJ Woolf, Central sensitization and LTP: do pain and memory share similar mechanisms.Trends Neurosci, 26 (2003), pp. 696705

  • Role of glia in pathological pain processing } Collectively, glia greatly outnumber neurons in the

    CNS. } There are various cellular subtypes, such as

    astrocytes, resident microglia, perivascular microglia and oligodendrocytes.

    } Oligodendrocytes are best known for their role in myelinating axons in the CNS, are now emerging as modulators of neuronal function.

    } Modulating functions of astrocytes, resident microglia and perivascular microglia.

  • Milligan, E.D., and Watkins, L.R., Pathological and protective roles of glia in chronic pain, Nature Neuroscience Reviews, 10 (2009) 23-36.

  • Structural Brain Anomalies

    Apkarian AV, Sosa Y, Sonty S, et al. Chronic back pain is associated with decreased prefrontal and thalamic gray matter density. J Neurosci 2004; 24: 1041015.

  • Structural Brain Anomalies } A coordinate-based meta-analyses using voxel-

    based morphometry imaging showed gray matter volume (GMV) differences between chronic pain patients and healthy controls. There were 12 clusters where GMV was decreased in patients compared with controls.

    } The right hippocampus and parahippocampal gyrus were the only regions noted to have increased GMV in patients

  • Smallwood RF, Laird AR, Ramage AE, Parkinson AL, Lewis J, Clauw DJ, et al. Structural brain anomalies and chronic pain: A quantitative meta-analysis of gray matter volume. J Pain. 2013;14(7):663

    Smallwood RF, Laird AR, Ramage AE, Parkinson AL, Lewis J, Clauw DJ, et al. Structural

    brain anomalies and chronic pain: A quantitative meta

    -

    analysis of gray matter volume. J

    Pain. 2013;14(7):663

    -

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  • Diffuse noxious inhibitory controls (DNIC) } DNIC comprises a spinal-medullary-spinal pathway

    that is activated when 2 concomitant painful stimuli are applied at the same time

  • Emergence or Incidence of Pain

    Franziska Denk, Stephen B McMahon & Irene Tracey. Pain vulnerability: a neurobiological perspectivePain vulnerability: a neurobiological perspective. Nature Neuroscience. 2014 ; 17 (2) 192-200

  • Franziska Denk, Stephen B McMahon & Irene Tracey. Pain vulnerability: a neurobiological perspectivePain vulnerability: a neurobiological perspective. Nature Neuroscience. 2014 ; 17 (2) 192-200

  • Franziska Denk, Stephen B McMahon & Irene Tracey. Pain vulnerability: a neurobiological perspectivePain vulnerability: a neurobiological perspective. Nature Neuroscience. 2014 ; 17 (2) 192-200

  • Franziska Denk, Stephen B McMahon & Irene Tracey. Pain vulnerability: a neurobiological perspectivePain vulnerability: a neurobiological perspective. Nature Neuroscience. 2014 ; 17 (2) 192-200

  • Central Sensitization

    } Clinical Manifestations } Amplified Pain } Hperalgesia } Spread of Pain } Unpleasant sensations after a physical stimulus } Chronicity