December 10, 2012
Pain, Part 2
By Lewis Mehl-Madrona
I continue to reflect upon chronic pain, beginning with some comments from my colleague, Peter Blum, who is a hypnotherapist and all around healer-guy in Woodstock, NY, and then leading into some brain science that shows that our brains are changed by the experience of pain and begin to link all kinds of unrelated experiences to that pain so that pain becomes multiply determined by more than just the sensations.
In my last blog I blog, I began the discussion of chronic pain. My friend and colleague, Peter Blum, of Woodstock, New York (who actually does everything, including hypnosis, and is a Buddhist, Jewish, Native American priest of sorts who married Barbara and me) had important things to say.
Peter said, "This is a topic that has been particularly significant in my life, and I would like to weigh in on this discussion. As a hypnotherapist, I have addressed the issue of pain management with numerous clients over the years. As a practicing Buddhist, I have read and studied and meditated for many years on the "Four Noble Truths" - the essence of the Buddha's teaching - which deals with the nature of suffering and attachment. And perhaps most importantly, as a recovering drug addict, I have had direct experience with the cunning, baffling, and seductive nature of what is currently often viewed as the "disease" of addiction.
"In your article, I loved what you said about the "seeking system", and that "seeking has been found in studies to be more rewarding than finding". That would be validated by many addicts, who speak of the "high" of the hunt... the actual physical/emotional thrill of figuring out ways to get more of whatever it was they were addicted to. I was a bit surprised at the revelation, in your article, that in patients receiving prolonged opioid therapy, there is an increase in production of one of the body's endogenous opiates.
"Years ago an acupuncturist (who was explaining how acupuncture was beneficial to people who were in the process of detoxing from opiate addiction) used the metaphor of the body having little "factories" which produced the endorphines and enkaphalons, the feel-good neurotransmitters, which also regulate pain control. When a person starts "importing" external opiates, such as morphine, heroin, codeine, etc., on a regular basis, these little factories shut down. So a person's natural ability to manage pain, and regulate mood, is impaired and becomes dependent on continuing to receive these "imports".
"It was heartening to read of others who responded to your posting on this thread speaking of utilizing mindfulness meditation as a tool in helping clients understand the working of mind/body, and find other ways of coping with or alleviating pain as an alternative to synthetic opiates. A recent issue of "The Buddhist Review Tricycle" (Fall 2012) contained an insightful article by Andrew Olendzki, entitled "Pinch Yourself - A Physical Sensation Becomes An Experience To Be Explored". To quote briefly, in the opening paragraph, Olendzki, a Ph.D., and senior scholar at the Barre Center for Buddhist Studies, says "Pinch yourself. Go ahead and give yourself a good hard pinch on the arm or the back of the hand. Now, according to Buddhist psychology, you should be able to distinguish at least three different components to the experience: the touch, the pain of the touch, and the aversion to the pain of the touch. Our mind if very good at merging these all together, but there are actually three different processes - synthesized by three different brain systems - that are then synchronized with one another and interpreted as a unified experience."
"Our culture continually bombards us with media advertisements encouraging us to immediately turn to the pharmacy to deal with the slightest pain. So before we even sit with the touch, and the pain of the touch, we are proceeding instantly to aversion to the pain of the touch. What if, instead, we were to center ourselves and allow ourselves to sit with the pain. My experience, in hearing the stories of many who use opiates, is that the "cover story" of needing them to deal with physical pain, is frequently masking the deeper, underlying story - of inability or unwillingness to deal with metaphysical pain. Some of the therapeutic guidance we can give, is to encourage a person to actually feel their pain - emotional, psychic, etc. To be willing to take a look at the pain of their lives, and look at the situational reinforcements of isolation and obsessive/compulsive behavior that, unless addressed and ameliorated, will bring a person cycling back over and over again to the same lonely and desperate places.
"It was particularly heartening to read your last paragraph: "For all these reasons, I believe we need to work together to create communities of pain sufferers, to change their brains through social interaction (the social brain hypnothesis) and to help each other to live better lives with or without pain." This reinforces the hochoka project - of having community healing circles. Many have found the rooms of Narcotics Anonymous to also fulfill that function.
"But whatever it is, it is a pervasive and rapidly growing problem. Many are probably aware that prescription pain-killers are the drug of choice these days recreationally among many high school and college age folks and are overtaking heroin and cocaine as a cause of death by overdose; hospitalization for complications, and treatment in detox and rehab facilities. Not to be overlooked in this discussion is the mega-bucks of the pharmaceutical industry, and their continued investment in pushing more pills. Thank goodness we have some independent thinkers amongst our prescribing physicians who are willing to explore other, healthier and more wholistic ways of helping clients deal with pain."
In our pain group, we are attempting to create community with people who have been trained to avoid community. Our American culture trains people who are in pain to isolate which only serves to increase their pain. So often, I hear people in pain say, "I hate other people." We have to make them come to the group at first in order to get their narcotics. They must come twice per month. Some eventually come more often. Some eventually begin to find that they enjoy coming to group and come more often. Slowly the stories we tell in group begin to diffuse into the people. Some begin to feel that they could have an influence by what they do on how much pain they feel.
No correlation exists between the perceived severity of chronic pain and tissue pathology.1 Chronic pain is diffuse and often spreads well beyond the original area of injury. The measures that are successful in treating acute pain rarely work for chronic pain. This is because chronic pain is manufactured in our brains as a modifying response to acute pain. Chronic pain is very much a phenomenon of our brains and must be addressed as such. It's something we invent after an acute pain. This is why we need each other to manage our chronic pain.
Eighty million Americans suffer with chronic pain and nearly one-third obtains little or no relief from conventional approaches to pain.2 Therefore, new approaches are needed besides the conventional model of writing prescriptions. We need to combine medicine with physical therapy, family therapy, cognitive/behavioral therapy, biofeedback, support groups, and more. In addition to caring for the chronic pain patient, the entire family is affected and needs to be involved in the recovery process. Care needs to involve all the stakeholders in the chronic pain patient's life.
Treatment with opioids alone is not enough for chronic pain.3 For some people, opioids may reduce chronic pain to a more tolerable level. However, they should not be prescribed with the expectation that they will completely alleviate chronic pain, treat depression or a sleep disorder, or completely relieve suffering. For other people, opioids are ineffective. The deeper issue is, as Peter Blum puts it, how can we allow ourselves to feel what we don't want to feel? Our culture is formed from stories that teach us to avoid pain. We are full of magic potion stories in which a substance takes that pain away. Unfortunately, the stories don't seem to fully work. They are incomplete. The pain doesn't leave. The magic potions are not fully effective. What are we to do in those cases?
Specific regional gray matter decreases correlate with duration of chronic pain, its intensity, and the interaction between duration and intensity4-6, suggesting that being in chronic pain changes the structure of the brain. Distinct chronic pain conditions have differential impacts on brain anatomy. These brain changes are reversible with pain relief .7-9 Apparently, some of the brain changes are a direct consequence of the presence of the pain, and most likely the underlying mechanism is based on synaptic plasticity that tracks the impact of the pain on the brain. Structural brain changes can be observed at early time points from initial injury as well as after long periods from injury, best illustrated in 2 animal studies.10,11
People with chronic pain rarely just feel pain. They have a myriad of other symptoms, including fatigue, poor sleep, depression, anxiety, migraine, and so many more.1. Persistent stress alters neuroendocrine rhythms. Chronic pain quickly becomes a comprehensive mind-body-community-spirit phenomenon. It must be addressed from all those levels.
"We found that of the people who have tears in their discs [between the vertebrae in the spine], some manage well with it and some manage poorly with it," said Dr. Eugene Carragee, associate professor of functional restoration at the Stanford University Medical Center in California. Carragee and his team compared the results of magnetic resonance images and vertebral disc tear tests among 96 patients who had known risk factors for disc degeneration. Such tears have traditionally been thought to directly cause lower back pain, with ruptures in the discs that cushion contact between the vertebra bones resulting in painful pressure being placed on sensitive nerves.
The researchers were surprised to find that those patients with disc problems were only slightly more likely to have back pain then those without any disc degeneration. They also noted that 25% of those who did have disc problems had no lower back pain at all. Carragee and his colleagues concluded that torn discs are not always painful, and not all lower back pain is a result of a torn disc.
From psychological tests, the researchers found that pain is actually more accurately associated with the patient's state of mind -- with depression and poor coping skills often being a better predictor of back pain than disc damage. The researchers therefore cautioned that treating a patient for emotional and perceptual concerns may be more beneficial in reducing lower back pain than the more standard invasive, costly, and oftentimes unsuccessful back fusion surgery option.
Carragee said that pre-existing psychological problems seem to have a clear relationship with both the onset of lower back pain and the manner in which it is managed.
"Those people who suffered from depression or an over-reaction to pain or fear of being hurt reported a lot more pain," he noted. "If someone has a tendency to hyperbolize whatever problems they have -- like headaches -- when they do get a back pain episode they really cope with it very badly. There are some people who, when they hurt, will try and stay in as good shape as possible and in most of those people the pain will go away. And that's the normal course of back pain for 85% of the people. It will go away in a matter of a few weeks. But for the others, they get into a real cycle of getting more disabled, getting more pain, getting more discouraged, and 2 years go by and those people can become a real wreck."
Carragee suggested that for some people addressing the psychological dimension could help reduce the pain and quicken relief.
"The best thing for them and their physicians is to work towards taking away the stigma of their having a serious pathology in their back," he said. "It would be easier to help them and get them going. It's mentally hard to get someone to rehabilitate if they think they have a serious mechanical problem in their back. And if people are depressed, confronting whatever those issues are head-on could help as well."
Our perceived sensory experiences are heavily shaped by interactions between our expectations and incoming sensory information. As the magnitude of expected pain increases, activation increases in the thalamus, insula, prefrontal cortex, anterior cingulate cortex (ACC) and other brain regions. Pain-intensity related brain activation are identifiable in a widely distributed set of brain regions but overlap partially with expectation-related activation in regions, including the anterior insula and ACC. When expected pain is manipulated, expectations of decreased pain powerfully reduced both the perceived experience of pain and the activation of pain-related brain regions, such as the primary somatosensory cortex, insular cortex, and ACC. These results confirm that a mental representation of an impending sensory event can significantly shape neural processes that underlie the formulation of the actual sensory experience and provide insight as to how positive expectations diminish the severity of chronic disease states.12
Chronic pain can be viewed as a state of continuous learning coupled with reduced opportunity for forgetting]13=15. Many studies illustrate the potency of painful events to induce learning, the majority of which pair pain (electrical shock) with a variety of other previously unassociated events. These studies repeatedly show that single painful stimuli are learned and remembered for weeks and months. Once the associated learning occurs, the extinction of this association requires repeated exposure to the conditioned stimulus in the absence of the painful event. As chronic pain is fundamentally a state of continuous presence of pain, we can then conclude that it is also a state of continuous acquisition of associations with random events surrounding the organism, especially at time points when the pain is high. Moreover, as the pain remains unremitting, the organism does not have the opportunity of extinguishing these random associations, which requires frequent exposure to the same environment in the absence of pain. The contradiction between the subject's conscious knowledge that the pain is not associated with the environment and the brain circuitry that continuously make such associations may be the core cognitive/emotional source of the suffering that chronic pain patients experience. Information about pain accesses the cortex through multiple pathways and not just by the spinothalamic projection, which is the known pain pathway. Even within the spinothalamic system medial thalamic cortical projections access large portions of the frontal cortex targeting mainly superficial layers]16. This pathway is a reticulo-thalamocortical network that relays widespread pain information to widespread cortical regions and most likely provides modulatory influences on large prefrontal cortical processes.
Other nociceptive pathways such as the parabrachialamygdala projections, spinal basal ganglia projections, spinal hypothalamic and spinal prefrontal projections17-20 and other monosynaptic and polysynaptic spinal-reticular-cortical projections provide ample opportunities for pain processing accessing various cortical circuitry and modulating such circuitry as a function of a continuous barrage of inputs associated with chronic pain. Thus, continuous input to the brain both reorganizes memories and their associations, and reorganizes motivational and memory consolidation properties of the limbic cortex, which is the emotional center of the brain. The functional brain imaging studies for chronic pain point to the recurring theme that chronic pain conditions engage preferentially medial prefrontal cortical areas as well as subcortical limbic regions, especially portions of the dorsal and ventral basal ganglia], amygdala, and hippocampus.
What this all means is that chronic pain is multiply determined and that we need to change the brain to change pain. Pain is associated with emotion and becomes correlated with multiple events that happen in a person's life. These events become linked with pain and their memory triggers pain. It's hard to get rid of these triggers without active intervention. The longer the person has chronic pain, the more triggers develop. To remove chronic pain, we need to work with these associations and their paired emotions to reduce the triggers. This is largely psychological work.
1. Bennett, R.M. (1999). Emerging Concepts in the Neurobiology of Chronic Pain: Evidence of Abnormal Sensory Processing in Febromyalgia. Mayo Clin Proc 74: 385-398.
2. McNeely C. (2000). The role of he family in thee treatment of chronic pain. Pain Practitioner,10:5-6.
3. Gallaher, R.M. (2005). Integrating Treatment in Pain Medicine: Challenges and Opportunities. In Bennett, G.J., Byas-Smith, M., Fishman, S.M., Fishbain, D.A., & Gallagher, R.M. Treatment Advances in Chronic Neuropathic Pain. Advancing Mental Health Expert Opinion Series 1(4) 92-114.
4. Apkarian AV, Sosa Y, Sonty S, Levy RE, Harden RN, Parrish TB, Gitelman DR. Chronic back pain is associated with decreased prefrontal and thalamic gray
matter density. J Neurosci 2004;24:10410--5.
5. Geha PY, Baliki MN, Harden RN, Bauer WR, Parrish TB, Apkarian AV. The brain in chronic CRPS pain: abnormal gray--white matter interactions in emotional and autonomic regions. Neuron 2008;60:570--81.
6. Kuchinad A, Schweinhardt P, Seminowicz DA, Wood PB, Chizh BA, Bushnell MC. Accelerated brain gray matter loss in fibromyalgia patients: premature aging of the brain? J Neurosci 2007;27:4004--7.
7. Gwilym SE, Fillipini N, Douaud G, Carr AJ, Tracey I. Thalamic atrophy associated with painful osteoarthritis of the hip is reversible after arthroplasty; a longitudinal voxel-based-morphometric study. Arthritis Rheum 2010;62:2930--40.
8. Obermann M, Nebel K, Schumann C, Holle D, Gizewski ER, Maschke M, Goadsby PJ, Diener HC, Katsarava Z. Gray matter changes related to chronic posttraumatic headache. Neurology 2009;73:978--83.
9. Rodriguez-Raecke R, Niemeier A, Ihle K, Ruether W, May A. Brain gray matter decrease in chronic pain is the consequence and not the cause of pain. J Neurosci 2009;29:13746--50.
10. Metz AE, Yau HJ, Centeno MV, Apkarian AV, Martina M. Morphological and functional reorganization of rat medial prefrontal cortex in neuropathic pain. Proc Natl Acad Sci USA 2009;106:2423--8.
11. Seminowicz DA, Laferriere AL, Millecamps M, Yu JS, Coderre TJ, Bushnell MC. MRI structural brain changes associated with sensory and emotional function in a rat model of long-term neuropathic pain. Neuroimage 2009;47:1007--14.
12. Koyama, T., McHaffle, J.G., Laurientl, P.J.. & Coghil, R.C. (2005). The Subjective Experience of Pain: Where Expectations Become Reality. PNAS 102(36), 12950-12955.
13. Apkarian AV. Pain perception in relation to emotional learning. Curr Opin Neurobiol 2008;18:464--8.
14. Apkarian AV, Baliki MN, Geha PY. Towards a theory of chronic pain. Prog Neurobiol 2009;87:81--97.
15. Millecamps M, Centeno MV, Berra HH, Rudick CN, Lavarello S, Tkatch T, Apkarian AV. D-Cycloserine reduces neuropathic pain behavior through limbic NMDA-mediated circuitry. Pain 2007;132:108--23.
16. Monconduit L, Villanueva L. The lateral ventromedial thalamic nucleus spreads nociceptive signals from the whole body surface to layer I of the frontal cortex. Eur J Neurosci 2005;21:3395--402.
17.. Braz JM, Nassar MA, Wood JN, Basbaum AI. Parallel ""pain'' pathways arise from subpopulations of primary afferent nociceptor. Neuron 2005;47:787--93.
18. Gauriau C, Bernard JF. Pain pathways and parabrachial circuits in the rat. Exp Physiol 2002;87:251--8.
19. Kostarczyk E, Zhang X, Giesler Jr GJ. Spinohypothalamic tract neurons in the cervical enlargement of rats: locations of antidromically identified ascending axons and their collateral branches in the contralateral brain. J Neurophysiol 1997;77:435--51.
20. Newman HM, Stevens RT, Apkarian AV. Direct spinal projections to limbic
and striatal areas: anterograde transport studies from the upper cervical
spinal cord and the cervical enlargement in squirrel monkey and rat. J Comp
Authors Website: www.mehl-madrona.com
Lewis Mehl-Madrona graduated from Stanford University School of Medicine and completed residencies in family medicine and in psychiatry at the University of Vermont. He is the author of Coyote Medicine, Coyote Healing, Coyote Wisdom, and Narrative Medicine.