reconceptualizing pain maximizing patient outcomes

Reconceptualizing Pain: Maximizing Patient Outcomes Through Pain - PowerPoint PPT Presentation

Reconceptualizing Pain: Maximizing Patient Outcomes Through Pain Neuroscience Education AN D Y R OOF, M P T, OCS OCTOB ER 14 , 2 0 16 N u r s e P r a c t i t i o n e r s o f O r e g o n E d u c a t i o n Co n f e r e n c e Learning

  1. Reconceptualizing Pain: Maximizing Patient Outcomes Through Pain Neuroscience Education AN D Y R OOF, M P T, OCS OCTOB ER 14 , 2 0 16 N u r s e P r a c t i t i o n e r s o f O r e g o n E d u c a t i o n Co n f e r e n c e

  2. Learning Objectives  1. To gain an understanding of the current model of chronic pain and how this differs from the standard "tissue lesion-based" model.  2. To have an evidence-based understanding of the need for pain neuroscience education in the treatment of chronic pain.  3.To learn "talking points" regarding pain education such that all practitioners are consistent with their message to patients.

  3. What is Pain?  International Association of the Study of Pain (IASP) definition: “An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage”

  4. What Is Pain?  Alternative definition: An unpleasant, but protective, sensory experience in response to what your brain judges to be a threatening situation.

  5. Acute vs. Chronic Pain Acute Pain Chronic Pain  Pain that persists beyond  Experienced in response the normal basic tissue to disease, inflammation healing times of 6-8 or tissue injury weeks  Experienced in response  Pain is related to to tissue fatigue/ hypoxia hypersensitivity in the  Involves nociception nervous system rather than tissue damage or  Pain is a symptom nociception  Resolves with time and  Pain is the primary healing disorder

  6. Chronic Pain may have co-existing pain conditions:  Chronic Fatigue Syndrome  Endometriosis  Fibromyalgia  Inflammatory bowel disease  Insterstitial cystitis  Temporomandibular joint disease  Vulvodynia

  7. Chronic Pain Neurophysiology  Central sensitization is characterized by widespread hypersensitivity of the central nervous system  This involves impaired functioning of brain-induced descending anti-nociceptive mechanisms and overactivation of descending and ascending pain facilitatory pathways… this leads to an augmentation of nociceptive transmission 1

  8. Changes in the Neuromatrix in Chronic Pain  Increased activity in brain areas known to be involved in acute pain sensation e.g. insula, anterior cingulate cortex and prefrontal cortex  Brain activity in regions usually not involved in acute pain sensations e.g. various brain stem nuclei, dorsolateral frontal cortex and parietal associated cortex  “Cognitive emotional sensitization:” the capacity of the forebrain centers to exert powerful influences on various brainstem nuclei involved in descending facilitatory pathways 2

  9. Peripheral influences  Chronic pain can originate from a period of massive peripheral (nociceptive) input in the acute and subacute stage (e.g. whiplash, multiple surgical procedures)  In response, the central nervous system modulates the sensitivity of the somatosensory system  Any further peripheral injury or stress can further sustain or aggravate the process of central sensitization

  10. All Pain is Real Pain  Each person’s pain is unique and needs to be acknowledged  All pain experiences are a normal response to what your brain thinks is a threat  Real pain can exist without any damage to the tissues  The construction of a pain experience in the brain relies on many sensory cues  The pain experience relies on a very complex electrical and chemical response in the body

  11. However…  The degree of injury does not always correlate with degree of pain  Diagnostic imaging may not accurately indicate a tissue “responsible” for the pain  Psychological factors such as depression and anxiety can make pain worse  Social environment may influence perception of pain  Improving an individual’s understanding of pain through education may reduce the need for care

  12. Pain Neuroscience Education  Defined as an educational session outlining the neurobiology and neurophysiology of pain  Does NOT focus on tissue injury and/ or nociception  Describes how the nervous system, via up/ downregulation, has the capacity to modulate the pain experience.  Explains peripheral nerve sensitization, central sensitization, synaptic activity and brain processing in laymen’s terms.

  13. This form of education is indicated when:  The clinical picture is dominated by central sensitization  Maladaptive pain cognitions, illness perceptions and/ or coping strategies are present  Patient is ruminating about pain and is hypervigilant to somatic signs

  14. Underlying Theme of this Education:  The nervous system processes MANY inputs including psychological and cognitive information in its construction of the pain experience.  It is not all about nociception!

  15. Benefits of Pain Neuroscience Education  Studies have shown that neuroscience education can:  1. Decrease fear and positively affect patient’s perceptions of their pain 3  2. Make improvements in pain, cognition and physical performance 4  3. Increase pain thresholds during physical tasks 5  4. Improve outcomes of therapeutic exercises 6

  16. Goal of Pain Neuroscience Education  To change the patient’s concept of pain so that they are more inclined to exercise, move, and physically function while accepting some level of discomfort as “normal” rather than indicative of ongoing tissue injury.

  17. The BRAIN controls pain: You can have no pain with extreme tissue damage  Even if problems exist in your bones, joints, muscles, ligaments, nerves or anywhere else, it won’t hurt unless your brain thinks you are in danger.  Examples:  Professional athletes and injury  Military personnel and GSW’s

  18. The BRAIN creates pain based on its interpretation of what is happening to the body  Pain is an output of the brain, not an input.  The information given to the brain by the nervous system is: where the pain is, the amount of danger and the nature of the danger. The “stretching,” “ripping,” “burning” sensations are produced by the brain’s construction of events.

  19. Phantom Limb Pain  70% of people who lose a limb experience a “phantom limb” that can itch, tingle and hurt  This relates to the “virtual limb” in our brain. There is still a brain-constructed representation of that limb in our heads even though the actual limb is missing.  This “virtual limb” representation is changed in chronic pain states.

  20. Degenerative Changes  It is a normal process of aging for our tissues to degenerate, or at least look a little different than they did at age 16.  Disc degeneration, degenerative joint disease and arthritic changes are all normal age-related processes.  Since these processes occur slowly and over time, our brains usually do not perceive them as threatening, therefore there is no pain.

  21. Pain Relies on Context  We will experience more or less pain based on sensory cues that we are receiving in conjunction with the pain  “Stubbing your toe hurts more on a stressful day than at your birthday party.”

  22. Neuroanatomy/ Neurophysiology Overview  Group education format  Whiteboard cartoon

  23. Sensors  Millions of little sensors all throughout your body that survey their area and convey information to the spinal cord  When sensors respond to a stimulus (can be mechanical pressure, changes in temperature, or chemical changes) they open so that positively charged particles from outside the neuron rush into the neuron; this sets up an electrical impulse in the neuron.

  24. Action Potential  When enough sensors open, and enough + charged particles rush in, a rapid wave of electrical current travels up the neuron..this is called an Action Potential  Action Potentials are the way that nerves carry a single message. This message from the nerve to the spinal cord only says “danger,” not “pain.” The spinal cord and brain receive and process these inputs to create a pain sensation.

  25. Synapse  When AP reaches the other end of the neuron at the spinal cord, it causes chemicals to be poured into the gap or “synapse” between the sensory neuron, its neighboring neurons, and the second order neuron that then goes up to the brain. If enough of the correct chemicals are released into the synapse and open enough sensors on the second order neuron, an AP is produced that carries a “danger” message to the brain.

  26. Brain Processing  Danger message is ultimately delivered to the brain, which processes that message, along with all other information that is arriving at the brain.  Brain uses memory, reasoning and emotional processes and includes consideration of the potential consequences of a response.

  27. Pain Ignition Nodes  Rather than just one “pain center” in the brain, there are multiple “ignition nodes.”  These nodes include parts of the brain used for sensation, movement, emotions and memory.  These nodes are “ignited” during a pain experience and link up to each other electrically and chemically.  In chronic pain, these nodes become overactive and nearly dedicated to creating the pain experience. a skipping record… (“nerves that fire together, wire together”)


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