Her husband said her explanation in this presentation makes sense, pain is in the brain and real.

1. Her story
   • 2008 med grad, learned: pain markers; opiate dosage; her goal was for patients to have no pain
   • 2012 started residency, knew everything, thought she could solve anything
   • 2014 felt like she was failing, pain must mean be tissue damage, but her patients got sicker
2. 2021 went to Oregon Pain Summit 2019, 2 day intensive learning about the science of pain, began listening to patients, I’m still learning, but am now closer to where I want to be.
3. My Presentation goals’
   • How to explain pain so it makes sense, i.e. what happens when I stub my toe?
   • How does pain become chronic?
   • How does knowing about pain science help?
   • In the 1600s doctors thought pain was a single, off or on signal, sent from the injured tissue location to the brain. (Jrk, That explanation probably represents the belief of most people based on their pain experiences.)
4. ‘How can we know if that pain model is true?’
   • Consider the insight from these 4 neuroscience experiments, which reveal that the danger signal sent by nociceptive sensors in the skin, is not an off/on signal. In the first three experiments a heated probe contacts the skin of a volunteer and the signal from nociceptor sensors is recorded, along with the subjective response of the volunteer.
   • The sensors begin to send ‘Danger’ signals at 105.8F, but the pain threshold (when the volunteer says ‘ouch’) occurs at 111F: so the nociceptor signal is not an off/on pain signal, but functions as a danger signal.
   • Sharp pins were applied onto but not into the volunteer’s skin, at room temperature the pin produced a sensor signal pulse rate 2/sec, hot pins caused a sensor signal rate of 10/sec, the nociceptor signal rate increased between start and ouch temps: so again, the sensor signal is not an off/on signal, and the volunteers were not able to differentiate signal rate change as the pin temperature increased.
   • Skin Probe diameters of 1, 4, and 20 mm were applied to volunteer’s skin, all at 113F, which was above the ouch threshold, the volunteers described the probe feeling as: pricking pain for a 1mm size probe , stinging pain for a 4mm probe, and a pleasant strong warmth for a 20mm probe: so the perceived sensation varied with the contact area of the probe, but the temperature was the same for all sizes of probe.
   • A fourth experiment applied a painful hot or pinching stimulus to a volunteer’s skin for 15 seconds: the recorded nociceptor danger signal was initially very active, then decayed to nothing, but the pain feeling continued to increase as the signal level decayed: so the perceived pain level did not correspond to the presence of a nociceptor signal.
5. ‘What is really happening?’
   • The nociceptor sensor was not actually in contact with the test probes, but only nearby. Other experiments revealed the activation of a nociceptor sensor initiated the release of chemicals in the sensor area that are necessary for the tissue to heal itself, (serotonin, etc.), whether the pain is perceived as acute or chronic.
   • And the response was influenced by endorphins.
   • The nociceptor signal was transmitted to the spinal cord, where the signal changed the chord sensors and they become more sensitive, based on past injuries to the same nociceptor sensor site.
   • Signals were then sent on to the thalamus in the brain, which influences other parts of the limbic system, but all parts of the brains seem to be involved, including memories and cognitive aspects: the more frequently an experience occurred, the easier it was to prompt a painful response.
6. How does pain stick?’
   • Salience is an important neuroscience concept – if a pain experience is salient to well-being, it will stick, otherwise recovery is rapid.
   • An injury will prompt either a catastrophizing loop or a recovery loop in a person’s brain.
   • The tendency for an injury to activate either loop varies for individuals.
   • This tendency is ‘hardwired’ and not the fault of the individual.
7. Institute of Medicine report in 2011 by Turk and Theodore, (pain scientists at the University of Washington) – contains a quote she loves:
   • ‘In fact, beliefs, anticipation, and expectation are better predictors of pain and disability than any physical pathology’.
   • That ties it all together for me!
   • Beliefs seem to be ‘hardwired’, rather than simply individual choices.
8. As an example, Adverse Childhood Experiences, (ACES) have been shown to be directly related to general health and longevity.
   • A 1995 study revealed that youth chronic pain was significantly associated with toxic (destructive) stress, for example fibromyalgia in youths:
   • was greater for children with a history of physical abuse, neglect, household dysfunction, and
   • The life cycle of chronic pain risk factors depended on belief about pain (see slide)
9. ‘Maslow’s hierarchy of needs’ (a theory from the 1940s)
   • (slide shows 5 levels of need: Physiological, safety, love. belonging, esteem, self-actualization.)
10. Considering pain an absence of safety, i.e. perhaps it reflects a threat to the first physiological level elements of breathing, food, water, sec, sleep, homeostasis, excretion.
11.  ‘Why does this matter?’
    • a person can change the way they think about pain. (Jrk – that’s the reason pain science understanding is important for mastering pain.)
    • (Slide contrasting two differing perspectives that consider pain either as tissue injury or protection, for these four responses to a pain experience: the person’s goal (expected outcome) of the experience, their reaction to worsening pain, their willingness to move, and their thoughts about the future.)
    • ‘Because of neural plasticity, the brain can restore connections and the experience of pain can be changed.’
12. ‘Summary – what I have learned’
    • All pain is pain
    • All pain is real
    • All pain can change