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PAIN For medical students


  1. 1. Prof. Ashraf Abdou Neuropsychiatry department Alexandria university
  2. 2. Pain Definition An unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage International Association for the Study of Pain
  3. 3. Function of Pain Pain protects humans by warning of occurrence of biologically harmful processes  reflexes, regulated at the level of spinal cord, protect by removing a body part away from danger  associated emotional arousal, experienced as distress or fear, may also motivate a person to move away from a painful stimulus  Fear of pain can also prevent a person from moving, which in turn promotes healing of the injury resulting in that pain  pain may elicit an empathic, comforting, and health promoting behavior in people observing a person in pain.
  4. 4. Age and perception of pain Children and the elderly may experience or express pain differently than adults Infants in the first 1 to 2 days of life are less sensitive to pain (or they simply lack the ability to verbalise the pain experience). A full behavioural response to pain is apparent at 3 to 12 month of life Older children, between the ages of 15 and 18 years, tend to have a lower pain threshold than do adults
  5. 5. Major Categories of Pain Classified by inferred pathophysiology: 1. Nociceptive pain (stimuli from somatic and visceral structures) 2. Neuropathic pain (stimuli abnormally processed by the nervous system)
  6. 6. Pain Language Acute pain: lasts less than 6 months, subsides once the healing process is accomplished. Chronic pain: involves complex processes and pathology. Usually involves altered anatomy and neural pathways. It is constant and prolonged, lasting longer than 6 months, and sometimes, for life.
  7. 7. Types of Somatic Sensations Musculoskeletal System Skin Pain Temperature Proprioception Touch Position Sense Pressure Vibration Kinesthesia Pain
  8. 8. Transmission/Perception of Pain  Four specific parts of the nervous system transmit pain signals from the periphery to the higher centers of the CNS:  the nociceptors,  the dorsal horn neurons,  the ascending tracts, and  the supraspinal projections. Robinson(1997), Journal of Hand Therapy
  9. 9.  Nociceptors, one type of somatosensory receptors, are the first order neurons of pain pathways.  Free nerve endings  These receptors generate pain signals in response to harmful stimuli. Nociceptors
  10. 10. Nociceptors Robinson(1997), Journal of Hand Therapy  Cell bodies of the nociceptors reside in the dorsal root ganglia (DRG).  Nerve fibers leaving the DRG bifurcate and send one branch to the periphery and the other branch to the dorsal horn (DH).  The peripheral fibers conduct pain signals from the skin, muscles, fascia, vessels, and joint capsules to the DRG
  11. 11.  The sensory peripheral fibers, have been classified into three types based on their diameter, myelination and conduction velocity: A (with four subtypes – α, β, γ and δ) B and Cfibers.  A-δ fibers (Myelinated) conduct fast pain (a sensation experienced immediately after an injury that indicates location of injury).  C-fibers (Un-myelinated) conduct slow pain (follows sharp pain and can be characterized as a dull, throbbing ache with poor localization).
  12. 12. The brain first perceives the sensation of pain The thalamus, sensitive cortex : perceiving describing of pain localising • Parts of thalamus, brainstem and reticular formation: - identify dull longer-lasting, and diffuse pain The reticular formation and limbic system: - control the emotional and affective response to pain Because the cortex, thalamus and brainstem are interconnected with the hypothalamus and autonomic nervous system, the perception of pain is associated with an autonomic response
  13. 13. Interneurons e01/03patho/index.htm
  14. 14. Thalamus contains nerve centers responsible for vision, hearing reflexes, equilibrium and posture. It also relays pain signals to the cerebrum. Crude sensation reaches consciousness in the thalamus, the cerebral cortex is responsible for the higher thought processes such as emotion and interpretation.
  15. 15. Regulation of Pain: Accentuation  Passive transmission of noxious stimuli cannot explain how people experience pain. Pain experience can be explained by an active process.  This active process includes several regulatory mechanisms that participate in attenuating or accentuating the perception of a noxious stimulus.  An accentuated pain experience can be associated with factors such as edema, fear, anxiety, and release of endogenous chemicals that sensitize nerve endings.  Spinal cord level mechanisms explain an accentuated pain experience:  1) allodynia,  2) wind-up, and  3) central sensitization.
  16. 16. Allodynia  It occurs when normally innocuous stimuli begin to produce pain.  Following intense, repeated, or prolonged stimulation, or if inflammation is present,  the threshold for primary afferent nociceptors is lowered and  the frequency of firing is higher for all stimuli.  Example: cloths become painful in case of neuropathy
  17. 17. Wind-Up  Low frequency repetitive stimulation of C-fibers produces a gradual increase in the discharge  Example: frequently touching the hot plate becomes painful  In this state there are  augmented responses to input and  enlarged receptive fields.  Input from areas that previously did not activate the WDR neuron now evoke a prominent response, and  Low threshold stimulation is able to drive the neurons.  Wind-up is elicited by any prolonged or intense C-fiber input.
  18. 18. Central Sensitization  It results in an increased responsiveness of the nociceptive dorsal horn neurons resulting in enhanced conduction of pain signals to the brain.  Example: following injury, an area of undamaged skin adjacent to the damaged tissue can evoke pain  .
  19. 19. Regulation of Pain: Attenuation  2 classic examples of pain attenuation.  First, after injuring a hand, a person may shake it vigorously to reduce pain sensation.  Second, an athlete, although injured during a game, may not feel injury related pain until end of game.  Regulatory mechanisms that attenuate pain act at four levels of the CNS: 1) the dorsal horn 2) the descending fibers (from periaqueductal gray, raphe nuclei, and locus ceruleus), 3) hormonal system ( Cerebral Cortex Descending Fibers Hormonal System Dorsal Horn
  20. 20. Theory of pain production and modulation ON GATE CONTROL THEORY (created by Melzack and Wall) • According to this theory, nociceptive impulses are transmitted to the spinal cord through large A-δ and small C- fibers. These fibers create synapses in the SG • The cells in this structure function as a gate, regulating transmission of impulses to CNS Stimulation of larger nerve fibers (A- α, A- β} causes the cells in SG to •A "close the gate". closed gate decreases stimulation of T-cells (the 2nd afferent neuron), which decreases transmission of impulses, and diminishes pain perception
  21. 21. Gate theory
  22. 22. Pain Factors that lower pain threshold Factors that raise pain threshold Discomfort Insomnia Fatigue Anxiety Fear Sadness Depression Boredom Introversion Mental isolation Social abandonment Relief of symptoms Sleep Rest Empathy Companionship Diversional activity Reduction in anxiety Elevation of mood Analgesics Anxiolytics Antidepressants
  23. 23. Neuropathic Pain
  24. 24. Neuropathic Pain Abnormal processing of the impulses either by the peripheral or central nervous system May be caused by injury (amputation and subsequent phantom limb pain), scar tissue from surgery (back surgery high risk), nerve entrapment (carpal tunnel), or damaged nerves (diabetic neuropathy)
  25. 25. Painful Mononeuropathies and Polyneuropathies  Diabetic neuropathies  Entrapment neuropathies  Postherpetic neuralgia  Trigeminal and other CNS neuralgias
  26. 26. Nociceptive Pain Neuropathic Pain PNS peripheral nervous system Peripheral PNS “Healthy” sensitization Abnormal nociceptors nociceptor s Central CNS Normal central transmissio sensitizatio nervous system n n Central Physiologi c state Pappagallo M. 2001. reorganizatio n Pathologic state CNS
  27. 27. The Concept of Total Pain Physical Psychological Total Pain Spiritual Social
  28. 28. World Health Organization (WHO) Step Ladder Approach Severe Pain 7-10/10 Moderate Pain 4-6/10 Mild Pain 1-3/10 ASA, Tylenol, NSAIDS Potent opioids (e.g. morphine) +/non-opioids Weak opioids +/- nonopioids (e.g. Tylenol #3®)
  29. 29. Targets of pain treatment
  30. 30. Drugs for Neuropathic Pain  NSAIDs  Opiates  antidepressants  anticonvulsants  local anesthetics  steroids  other
  31. 31. NSAIDs  Non-steroidal anti-inflammatory drugs  Reduce synthesis of PGs  Cox inhibitors (cyclooxygenase)  Diminish nociceptor activation  Block peripheral sensitization  Antipyretic  Anti-hyperalgesic  No sedation 39
  32. 32. Opioids  Spinal cord  Decreasing neurotransmitter release  Blocking postsynaptic receptors  Activating inhibitory pathways  Supraspinal analgesia  Peripheral analgesia (prevent nociceptor sensitization) 40
  33. 33. Antidepressants  Tricyclic antidepressants  Analgesic effects separate from anti-depressant effects.  Amitriptyline: most studied, but most side effects  Nortriptyline & desipramine: better tolerated, less well studied  SSRIs: little evidence of analgesic effect.  SNRI’s  inhibit both norepinephrine and serotonin reuptake  efficacy in neuropathic pain syndromes or pain associated with depression (duloxetine [Cymbalta®], venlafaxine [Effexor®])
  34. 34. Anticonvulsants  Agents for neuropathic pain  Carbamazepine  Gabapentin (Neurontin®)  Pregabalin (Lyrica®)  Start low, go slow  Watch for side effects