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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)
} René Descartes (1596–1650) } 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;85:331–356
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;150:971–979
Gate Theory of Pain
Melzack R, Wall PD. Pain mechanisms: a new theory. Science. 1965;150:971–979
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, Woolf CJ. 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;55:377–391
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. 696–705
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: 10410–15.
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
-
75
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
Physical History } pain(s), tingling, numbness, cramp(s), swelling } migraine } tinnitus } asthma } IBS/IBlS } menstrual dysfunction } flushes/night sweats } cold(hot) hands/feet } itch +/- nonspecific rash Past History Psychosocial History
Physical Examination } nonspecific tenderness – diffuse/focal tender points
(deep somatic allodynia) } skin colour/temperature/texture } paravertebral skin roll test (prone) - bunching, tethering, oedema } muscle tone/tension } Sensory changes in non-dermatomal distribution
(NDSD) } bilateral symptoms determine laterality
} Quantitative Sensory Testing (QST)
Laboratory investigations
} FBC } Renal Functions } Liver Functions } CRP } ESR } Rh Factor } Mg, Ca, P } ANA } ENA } CCP IgG } Chest Xray, bone scan, MRI, USG
Epidemiology of Pain
Models of Development of Psychopathology
Biological Predisposing Pain
Life Events Pre morbid Personality Traits
Substance abuse
Depression
Anxiety Disorder
Somatoform
Personality Disorder
Aamir, T. Large, R. G. , (2007). Pain as a cause of psychiatric illness. Encyclopedia of Pain (Schmidt, R. F. , Willis, W. D. Ed.). Springer Berlin Heidelberg
Models of Development of Psychopathology
} Stage 1 - initial psychological distress } Stage 2 - depression, distress, anger, somatization and learned helplessness } Stage 3 - acceptance of the “sick role” and
consolidation of “abnormal illness behaviour” Gatchel RJ, Dersh J (2002) Psychological Disorders and Chronic Pain: Are There Cause and Effect Relationships. Psychological Approaches to Pain Management :30–51
Relationship between Pain and Mood Disorder
Pain and Depression } antecedent, } consequence } scar hypotheses } Common pathogenetic mechanisms
Fishbain DA, Cutler R, Rosomoff HL, Rosomoff RS (1997) Chronic Pain-Associated Depression: Antecedent or Conse- quence of Chronic Pain? A review. Clin J Pain 13:116–137
} In non depressed participants(n=1769), a higher level of pain was predictive of incident depression after correction for sociodemographic characteristics, life-style characteristics, functional limitations, and chronic diseases
} In the pain-free participants (n = 1420), depression measure did not independently predicted the onset of pain in the fully adjusted models.
Hilderink P, Burger H, Deeg D, Beekman A & Oude Voshaar R (2012) The temporal relation between pain and depression: results from the longitudinal aging study Amsterdam. Psychosomatic Medicine 74, 945–951.
Pain and Depression
} Learned Helplessness (Seligman – 1967)
Relationship between Pain and Anxiety Disorder
Fear Avoidance Model
Misdirected problem-solving model
Prevalence of Alcohol use and Pain Disorder
} Prevalence of opiod addiction in chronic pain patients is between 1-50%
} Most of the cases fall into Aberrant Drug Related Behaviour
Ballantyne JC, Sullivan MD, Kolodny A. Opioid dependence vs addiction: a distinction without a difference? Arch Intern Med 2012;172:1342–3.
} “A ‘modality’ class such as ‘pain’, which is a linguistic label for a rich variety of experiences, represents just such an abstraction from the information that is sequentially re examined over long time by the entire somesthetic symptom”
} Melzack R, Wall PD. Pain mechanisms: a new theory. Science. 1965;150:971–979
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