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Neuroscience

Neuroscience. Pain. Pain. Pain is the sensory experience that is associated with possible tissue damage. The detection of pain suggests that a pathological condition may be occurring. Nociception is the detection of pain. Nociceptors are the receptors that detect harmful stimuli. Pain.

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Neuroscience

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  1. Neuroscience Dr. Michael P. Gillespie Pain

  2. Pain • Pain is the sensory experience that is associated with possible tissue damage. • The detection of pain suggests that a pathological condition may be occurring. • Nociception is the detection of pain. • Nociceptors are the receptors that detect harmful stimuli. Dr. Michael P. Gillespie

  3. Pain • Pain is an unpleasant feeling caused by intense or damaging stimuli. • “Pain is 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 Dr. Michael P. Gillespie

  4. Etymology • First attested in English in 1297. • The word pain comes from the Old French peine, which in turn comes from the Latin poena meaning “punishment”, “penalty”, “torment”, “hardship”, “suffering”. It also comes from the Greek poine meaning “price paid”, “penalty”, or “punishment”. Dr. Michael P. Gillespie

  5. Functions of Pain • Pain motivates the individual to • withdraw from damaging situations and stimuli. • protect a damaged body part while it heals. • avoid similar experiences in the future. Dr. Michael P. Gillespie

  6. Duration of Pain • Most pain resolves promptly once the painful stimulus is removed and the body has healed. • Some pain persists despite removal of the stimulus and apparent healing of the body. • Sometimes pain arises in the absence of any detectable stimulus, damage, or disease. Dr. Michael P. Gillespie

  7. Duration of Pain • Chronic – Pain that lasts a long time is called chronic. Pain that extends beyond the expected period of healing. • Acute – pain that resolves quickly is called acute. • An arbitrary time interval from time of onset has traditionally been used. Commonly 3 months and 6 months. Some researchers use 12 months as the transition from acute to chronic pain. Others have describes acute pain as that lasting less than 30 days and chronic pain as pain of more than 6 months in duration. Dr. Michael P. Gillespie

  8. Pain • Pain is the most common reason a patient consults a physician in the United States. • Pain can significantly interfere with a person’s quality of life and general functioning. Dr. Michael P. Gillespie

  9. Modulation of Pain • A variety of psychological factors can significantly modulate the intensity or unpleasantness of pain. • Social support • Hypnotic suggestion • Excitement • Distraction Dr. Michael P. Gillespie

  10. Classification of Pain • The International Association for the Study of Pain (IASP) classifies pain according to the following characteristics: • 1. Region of the body involved. • 2. System whose dysfunction might be causing the pain. • 3. Duration and pattern of occurrence. • 4. Intensity and time since onset. • 5. Etiology. Dr. Michael P. Gillespie

  11. Classes of Pain • Nociceptive pain • Inflammatory pain • Tissue damage and infiltration of immune cells • Pathological pain • Disease state caused by damage to the nervous system (neuropathic pain) or by its abnormal function (fibromyalgia, tension type headache, etc.) Dr. Michael P. Gillespie

  12. Nociceptive Pain • Nociceptive pain is produced by stimulation to peripheral nerve fibers that are responding to stimuli approaching or exceeding harmful intensity. • Nociceptive pain can be classified according to the mode of noxious stimulation. • Nociceptive pain can also be divided into visceral, deep somatic, and superficial somatic pain. Dr. Michael P. Gillespie

  13. Classification of Nociceptive Pain • Nociceptive pain can be classified according to the mode of noxious stimulation. • “Thermal” (heat or cold) • “Mechanical” (crushing, tearing, etc.) • “Chemical” (iodine in a cut, chili powder in the eyes) Dr. Michael P. Gillespie

  14. Visceral Pain • Visceral structures are highly sensitive to stretch, ischemia, and inflammation, but relatively insensitive to other stimuli that normally evoke pain in other structures such as burning and cutting. • Diffuse pain • Difficult to localize • Often referred to distant, usually superficial structures. • May be accompanied by nausea and vomiting along with other autonomic nervous system responses (changes in heart rate, respiration, dilated pupils, perspiration, pallor, etc.). • Often described as sickening, deep, squeezing, and dull. Dr. Michael P. Gillespie

  15. Deep Somatic Pain • Deep somatic pain is initiated by stimulation of nociceptors in ligaments, tendons, bones, blood vessels, fascia, and muscles. • It is dull, aching, poorly localized pain. • Sprains and broken bones cause this kind of pain. • Muscular ache. Dr. Michael P. Gillespie

  16. Superficial Somatic Pain • Superficial somatic pain is initiated by activation of nociceptors in the skin and other superficial tissues. • It is sharp, well defined, and clearly localized pain. • Minor wounds and minor burns (first degree) produce this kind of pain. • Pin prick. Dr. Michael P. Gillespie

  17. Neuropathic Pain • Neuropathic pain is caused by damage or disease to any part of the nervous system affecting bodily feelings (somatosensory system). • It is often described as “burning”, “tingling”, “electrical”, “stabbing”, or “pins and needles”. • Sciatica and bumping your “funny bone” are examples of this kind of pain. Dr. Michael P. Gillespie

  18. Phantom Pain • Phantom pain is pain felt in a part of the body that has been lost or from which the brain no longer receives signals. • It is a type of neuropathic pain. • Amputees often experience phantom limb pain. • Phantom pain is present in 82% of upper limb amputees and 54% of lower limb amputees. • Treatments have included the following: local anesthetic into the stump, injection of hypertonic saline into the soft tissue between the vertebrae, vibration or electrical stimulation of the stump, current from electrodes surgically implanted into the cord, and mirror box therapy. Dr. Michael P. Gillespie

  19. Psychogenic Pain • Psychogenic pain is also called psychalgia or somatoform pain. • It is pain caused, increased, or prolonged by mental, emotional, or behavioral factors. • Headaches, back pain, and stomach pain are sometimes psychogenic in origin. • People with long term pain frequently display psychological disturbances. • Some researchers suggest that neuroticism causes acute pain to turn chronic; however, clinical evidence shows that it is in fact chronic pain that causes the neuroticism. • Organic causes of pain should be ruled out before psychogenic causes are attributed to the pain. • Psychogenic pain is no less “real”, actual, or hurtful than any other source of pain. Dr. Michael P. Gillespie

  20. Dr. John E. Sarno • Dr. Sarno is the originator of the diagnosis of psychosomatic condition tension myositis. • Tension myositis syndrome (TMS) is a psychosomatic illness causing chronic back, neck, and limb pain which is not relieved by standard medical treatments. • Other ailments such as GI distress, dermatological disorders, and repetitive strain injuries can also be TMS related. • He treats patients by educating them on the psychological and emotional basis of their pain and symptoms. Dr. Michael P. Gillespie

  21. Dr. John E. Sarno Dr. Michael P. Gillespie

  22. Dr. John Sarno – Interview / Back Pain • http://www.youtube.com/watch?v=bwxPy4HVvLI • http://www.youtube.com/watch?v=yUAh6peaLtI Dr. Michael P. Gillespie

  23. Breakthrough Pain • Breakthrough pain is pain that comes on suddenly for short periods of time. • This type of pain is not alleviated by the patients normal pain management methods. • Cancer patients who have a background level of pain that is controlled by medication will often experience this type of pain. The pain will periodically “break through” the medication. Dr. Michael P. Gillespie

  24. Incident Pain • Incident pain is pain that arises as a result of activity. • Movement of a joint with arthritis, stretching a wound, etc. Dr. Michael P. Gillespie

  25. Four Stages of Nociception • Transduction • Transmission • Perception • Modulation Dr. Michael P. Gillespie

  26. Transduction • Transduction occurs when nociceptors are stimulated. • Nociceptors are located in the skin, muscles, connective tissue, circulatory system, and viscera. • Nociceptors are stimulated by the following: • Damage to the nerve endings. • Release of chemicals at the injury site. Dr. Michael P. Gillespie

  27. Transmission • Transmission involves the conduction of pain signals along afferent pathways in the periphery to the spinal cord and brain. • The primary fibers involved in transmission are A delta and C fibers. • A delta fibers • Large, thinly myelinated fibers • Transmit pain signals quickly • Sharp, stinging, highly localized, and short-lasting pain • C fibers • Thin, unmyelinated fibers • Transmit pain signals slowly • Dull, aching, poorly localized, and long-lasting pain Dr. Michael P. Gillespie

  28. Perception • Perception is conscious awareness of the pain. The cerebral cortex interprets pain signals and attaches meaning to them. • Perception involves the pain threshold and pain tolerance. • Pain threshold refers to the amount of pain stimulation required before pain is perceived. Pain thresholds are generally similar for all people. • Pain tolerance refers to the amount of pain someone is able to tolerate before seeking medical intervention. This varies widely from person to person. • The primary somatosensory area (SS1), secondary somatosensory area (SS2), posterior multimodal association area, and limbic system all play a role in the perception of pain. Dr. Michael P. Gillespie

  29. Modulation • Modulation is the modification of pain signals by centers along the pain pathway in both the central nervous system and peripheral nervous system. • Pain can be modified at the level of the peripheral nociceptor, the spinal cord, the brainstem, and the cerebral cortex. Dr. Michael P. Gillespie

  30. Qualities of Pain • Dull aching pain • Tends to be diffuse • Tends to last a long time • Carried by slow conducting, small, unmyelinated C fibers • Sharp pain • Tends to be well localized • Tends to last a short time • Carried by fast conducting, large, thinly myelinated A delta fibers Dr. Michael P. Gillespie

  31. Pain Receptors • Pain receptors are free nerve endings. • Other types of receptors, when stimulated intensely enough, may act as pain receptors as well. Dr. Michael P. Gillespie

  32. Pain Pathways • Spinothalamic Tracts • Recticulospinal Tracts • Trigeminothalamic Tracts Dr. Michael P. Gillespie

  33. Spinothalamic Tracts • The spinothalamic tracts are ascending somatic sensory pathways that convey pain signals from the skin and skeletal muscles. • Afferent signals travel from nociceptors in the skin, subcutaneous tissues, and muscles to the dorsal horn of the spinal cord where they release substance P. • The spinothalamic tract travels from the spinal cord to the thalamus, which relays signals to the primary somatosensory area of the cerebral cortex. Dr. Michael P. Gillespie

  34. Trigeminothalamic Tracts • The trigeminothalamic tracts are sensory pathways that convey pain sensation from the face. • Afferent signals travel from nociceptors in the face via the trigeminal nerve (CN V) to the thalamus from where they are relayed to the primary somatosensory area of the cerebral cortex. Dr. Michael P. Gillespie

  35. Reticulospinal Tracts • The reticulospinal tracts are descending sensory tracts that receive pain information from the periphery through afferent spinal nerves that synapse in the reticular formation of the brainstem. • The signals travel to the raphe nuclei of the brainstem. • When the raphe nuclei are excited, they release endorphins through a descending pathway to the place of pain origin to decrease the sensation of pain. Dr. Michael P. Gillespie

  36. Pathways to the Cortex • Nociceptive signals from the spinothalamic and trigeminothalamic tract are projected to the thalamus. • They signals decussate at the medulla oblongata. • The signals are then transmitted from the thalamus to the primary somatosensory area (SS1) which is located in the post central gyrus of the cerebral cortex. • Pain messages are then projected to the secondary somatosensory area (SS2) for interpretation. SS2 is located just posterior to SS1. • Pain messages are then projected to the posterior multimodal association area for integration of pain information with other sensory data. Dr. Michael P. Gillespie

  37. Analgesic Inhibition of Pain • Analgesia is an absence of pain in response to stimulation that would otherwise cause pain. • Analgesic mechanisms can be activated by the following: • Endorphins – naturally occurring substances that diminish the sensation of pain. • Enkephalin, dynorphin, and beta-endorphin • Pharmaceuticals • Opiates are analgesic drugs that block nociceptor signals without affecting other sensations. • Both endorphins and analgesic drugs bind to the same receptor site. Dr. Michael P. Gillespie

  38. Brain Stem Inhibition of Pain • There are brain stem centers that provide natural analgesia. • They are referred to as pain inhibiting centers. • Raphe nuclei in the medulla • Releases serotonin to inhibit transmission of pain signals in the spinal cord • Periaqueductal gray matter in the midbrain • When this region is stimulated, it in turn stimulates the raphe nuclei. • Locus ceruleus in the pons • The ceruleospinal tract originates here • Stimulation causes norepinephrine to be released, which binds to the spinothalamic tract and inhibits the release of Substance P Dr. Michael P. Gillespie

  39. Narcotic Drugs • Narcotic agents (opium or opium like compounds) bind to receptor sites in the periaqueductal gray, raphe nuclei, and the dorsal horn. • They induce both analgesia and stupor (a reduced state of consciousness). Dr. Michael P. Gillespie

  40. Stress Induced Analgesia • The pain inhibiting centers can be activated naturally by injury and athletic over-exertion. • Often, people severely injured or in an athletic competition may not feel pain until the event has passed. • Stress occurring during the event can trigger pain inhibition centers. • Stress induced analgesia activates the following: • Raphe nuclei descending tracts • Release of hormonal endorphins from the pituitary gland (beta-endorphins) • Release of hormonal endorphins from the adrenal medulla (enkaphalins) • Hormonal endorphins bind to opiate receptors in the brain and spinal cord. • Beta-endorphins can trigger analgesic effects that can last for hours. Dr. Michael P. Gillespie

  41. Diminishing Pain Transmission • Pain transmission can be diminished at several levels: • The periphery • Dorsal horn • Supraspinal descending systems • Hormonal systems • Cortical level Dr. Michael P. Gillespie

  42. Diminishing Pain in the Periphery • Non-narcotic analgesics (aspirin) decrease the synthesis of prostaglandins, which in turn sensitize peripheral pain receptors. • Nonsteroidal anti-inflammatory drugs (NSAIDs) (ibuprofen, naproxen) inhibit prostaglandin production, thereby reducing the number of pain chemicals available to stimulate nociceptors. • Local anesthetics can be administered to the nerve endings at the site of injury to stop propagation of the impulse. • Application of heat and cold alter the blood flow to the area and reduce swelling. Dr. Michael P. Gillespie

  43. Diminishing Pain in the Cerebral Cortex • The detection, interpretation and perception of pain can be altered at the cortical level by altering an individual’s expectations, distraction level, anxiety, and belief. • Placebo effects operate on this level. • Meditation operates at this level. Dr. Michael P. Gillespie

  44. Jon Kabat-Zinn • http://www.youtube.com/watch?v=rSU8ftmmhmw • http://www.youtube.com/watch?v=qvXFxi2ZXT0 • http://www.youtube.com/watch?v=_If4a-gHg_I Dr. Michael P. Gillespie

  45. Intensifying Pain Transmission • Edema and endogenous chemicals can sensitize free nerve endings in the periphery. • Following a burn injury, sensory stimuli that would normally be innocuous can cause heightened pain. • Fear and anxiety can also increase the sensation of pain. Dr. Michael P. Gillespie

  46. Chronic Pain / Pain Tolerance • Prostaglandins can form as a result of damaged cells. • Arachidonic acid is formed which is further broken down into prostaglandins. • Prostaglandins sensitize the nerve endings and lower the pain threshold. • Allodynia – a condition in which non-painful stimuli now produce pain. • Synaptic memory of pain in the nociceptive pathway can be formed when glutamate binds to certain pain receptors on the post synaptic neuron. Dr. Michael P. Gillespie

  47. Referred Pain • Referred pain is pain that is perceived to originate from one body region when it actually originates from a different body organ. • Usually referred pain occurs when visceral pain is perceived as originating in a somatic area. Dr. Michael P. Gillespie

  48. Referred Pain Dr. Michael P. Gillespie

  49. Noninvasive Pain Management • Massage • Electrical Stimulation • Thermotherapy • Cryotherapy • Hydrotherapy • Fluidotherapy • Kinesiotape • Acupuncture • Stress Management / Meditation • Biofeedback Dr. Michael P. Gillespie

  50. Massage (Mechanoreceptor Stimulation) • Massage stimulates mechanoreceptors in the painful area. • This activates interneurons in the dorsal horn and stimulates the release of enkephalin which binds to excited nociceptors. • This diminishes the release of Substance P. Dr. Michael P. Gillespie

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