Today, the Senate Committee on Health, Education, Labor & Pensions is holding a hearing on chronic pain. This hearing came about through the work of the Chronic Pain Research Alliance. I was invited to provide written testimony to the hearing on behalf of The CFIDS Association, and the full text of my testimony follows below. I am honored that my testimony was submitted in memory of Christy Gaffey, who lost her battle with CFS and interstitial cystitis last Thursday. I hope the Senators HEAR our pleas for action to help all of us suffering with chronic pain because Christy, myself, and millions of others do not have time to waste!
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U.S. Senate Committee on Health, Education, Labor & Pensions
Full Committee Hearing on
Pain in America: Exploring Challenges to Relief
February 14, 2012
TESTIMONY OF JENNIFER SPOTILA
This testimony is submitted on behalf of the CFIDS Association of America, in loving memory of Christy Gaffey of Williamsburg, Iowa. Christy lost her battle with chronic fatigue syndrome (CFS) and interstitial cystitis on February 9, 2012 at the age of 52. She was an advocate for these medical conditions and, in days of better health, participated in lobby days organized by the CFIDS Association. With this testimony at today’s hearing chaired by Sen. Tom Harkin — her senator — we recognize Christy’s life and the voice she once gave to all who have been jailed by chronic pain conditions. We implore, in Christy’s memory and for all those who have been lost too early to these conditions, that today’s hearing mark the beginning of serious action to address and curb the personal, family, community, state and national toll exacted by conditions marked by chronic pain.
Chronic fatigue syndrome is the name of my illness. I cannot count the number of people who have said to me, “I had no idea that CFS had pain as a symptom.” But it does. Think about the last time you had the flu. Did you lie in bed, shaking and aching all over, too weak to sit up? Yes. That is what my pain is like, but it is like that every day. Pain is always with me. It follows me around like my shadow. Just as a shadow changes shape with the light, my pain expands, contracts, and tries to swallow me whole. There is nowhere I go, nothing I do that is unaffected by pain.
Aching, throbbing, heavy, sharp, tingling, stabbing, crushing – all these words cannot fully describe my pain. Sometimes I lie in bed, weighed down by it. Or I might be sitting up and feel pain like a lance through trigger points in my back. My wrists ache, my toe joints hurt. One day, it’s my calves that tighten and cramp. Another day, my neck pinches and headaches loom. There are times when my whole spine is on fire and nothing I do alleviates the pain. There are times when the gentlest touch is more than I can bear, even my husband’s hand on my arm or my hair brushing against my neck.
I’ve worked with physical therapists. One said there was no hope when my body did not respond to the prescribed program. My current physical therapist has made great progress in loosening the trigger points in my back, but there has been no change in my overall pain level or experience. And the catch-22 is that the exertion of going to physical therapy twice a week and the daily stretching regimen does, in itself, increase my pain. I tried acupuncture, too. The needles are supposed to be painless, but I felt ropes of fire shooting out from every needle site.
I’ve consulted with pain management experts. Over the years I’ve tried aspirin, bextra, celebrex, cymbalta, flexeril, gabapentin, ibuprofen, imitrex, lidocaine injections, lidoderm patches, lyrica, pamelor, percocet, soma, topomax, tylenol, tylenol 3, tramadol, venlafaxine, vicodin, and wellbutrin. Most of these medications either did not help, or helped but came with intolerable side effects. Pamelor caused dreadful acid reflux. Topomax caused flashing lights in my peripheral vision. When my doctor decided to discontinue venlafaxine, it took me more than two months to wean off the dose and even then I endured withdrawal symptoms. I developed a frightening hypersensitivity reaction to tramadol, forcing me to discontinue the one drug that worked very well for me. Opiates like percocet and vicodin were a dream come true. The few weeks I was on percocet after the tramadol hypersensitivity were the only pain-free weeks I have had in more than fifteen years. But no doctor is willing to prescribe them for me long term. Instead, my pain management doctor believes the goal is to keep my pain manageable, not to make me pain-free.
Pain is intertwined with fatigue like a snarl of barbed wire. Being in pain makes me more tired. Activity makes me more tired and increases the pain. I always have to be careful about my physical position – legs and back fully supported, neck not too bent. Some days, I cannot get out of bed at all. Even when I am able to function, pain limits what I can do. I am fortunate not to have intense, localized pain that might prevent me from reaching for an object or moving in a specific direction. Instead, the pain hovers in the background, creeping ever higher. The generalized ache grows stronger and louder until it overwhelms every thought or intention. I might take a few steps out of my cell but Pain, my jailer, will always shove me back in and slam that cell door shut.
On good days, I get through the day with a few hours of activity such as cooking or paying bills. But by the time dinner is over and the dishes are done, I am on the verge of collapse. A hot pack and bed by 7pm – I feel like a 90 year-old invalid. On bad days, I max out on all my pain medications. If I am very lucky, the medications will keep the pain to a tolerable level. But there have been many nights when all I could do was whimper. More than once, I have contemplated going to the emergency room for pain relief on nights like that. But what would they do for me? How would they view me, a 40-something with normal blood work who insists she needs medication for intractable pain? I have never bothered to find out.
Living with this pain is like juggling while riding a unicycle. One lapse of focus, one dropped ball and everything comes crashing down. The delicate balance of rest, medication, and physical therapy will keep the pain at bay, but inevitably, something destroys that balance and the pain comes roaring back. No one can pedal a unicycle indefinitely. I try my best, but sometimes, living with this pain doesn’t feel much like living at all.
My testimony is also posted on Research 1st.
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Thank you for this wonderfully written testimony. It describes my reality too (but much better than I could ever word it).
Hello Jennie,
I noted your mention that the only medication you have had success with for pain was the opiate meds. I wanted to inform you that this has been my experience and opiate pain medications have been the only thing that have basically kept me from committing suicide due to the pain and lack of sleep. I think I can explain not only why they are so helpful, but also how this fits into the general physiology of the disease.
The more I study this disease, the more I have realized that the research demonstrating deficiencies in beta endorphin are not a coincidence and the facts that NMDA/glutamate antagonists are the most successful class of medications (dextromethophan, MK801, cannabinoids, opiates, GABA agonists, etc.) for palliative treatment are also not a coincidence since the main antagonists for glutamate (which acts at the NMDA receptor) are GABA and endorphins. In essence, when we take opiate medications, they are functioning as a form of “endorphin replacement therapy” and what opiate addicts experience in withdrawal is akin to a temporary form of hyperalgesia (I have noticed a similarity between descriptions of withdrawal and the hyperalgesic component of the pain in ME/CFS and FM. Also, descriptions of normal, healthy patients given endorphin blockers are also similar.) The fact that I have never experienced an iota of psychoactive effect from pain medications (unlike before I got sick and small amounts of pain medications caused a noticeable “high) is just one sign that opiate pain medications are functioning in a fundamentally different manner than in non-hyperalgesic pain conditions.
In addition, I have noticed that pain medications do not just help with pain (although they seem to primarily help with the hyperalgesic component and not the physical pain actually coming from the muscles due to micro-circulatory impairment; to which I’ll return in a moment) they seem to help with cognitive symptoms, sleep, and the startle reflex. I would posit that as one of the primary NMDA/glutamate antagonists in the brain, opiates are actually blocking the micro-seizure (discovered by EEG expert Frank Duffy) that are causing the Alpha/Delta wave sleep anomaly, the cognitive symptoms found in neuropsych studies (micro-seizure interrupting long term potentiation in memory formation, and causing problems with focus and attention, impulsivity etc.) along with the hyperalgesic component of the pain. Glutamate has been implicated in the neurophysiology of seizure disorder and it’s no coincidence that other NMDA/glutamate antagonists are also helpful with ME/CFS and FM and that GABA agonists (Neurontin and Lyrica) in particular are known to be anti-seizure medications. Interestingly, I also hypothesized that ADD would have a similar mechanism of micro-seizure (since the sensation I experienced before being prescribed pain medications could only be described as an intense version of ADD) and I hypothesized it would have a glutamatergic mechanism. I recently read an article in which the author stated that glutamatergic mechanisms are being looked at in ADD; viola! More recently, I found a paper (co-authored by Ian Lipkin) that demonstrated initial evidence that opiates blocked post encephalitic seizures in rats and I think this may be preliminary evidence for the effect I have noted. Yet more evidence in this direction.
Most telling, my startle reflex has normalized which I believe is due to the antagonism of the micro-seizure as well. In a normal physiology, a person who has a “warning” that they are about to be startled can maintain vigilance for at least 5 seconds and not startle, whereas we do not have this normal ability (according to studies.) This lack of “pre-pulse inhibition” can also be accounted for by the micro-seizure interrupting the maintenance of vigilance and in essence, we are “forgetting” to maintain vigilance in between the “warning” event and the actual startling phenomenon; and thus we startle abnormally (I hope this makes sense.)
Additionally, I do not think it’s a coincidence that the hyperalgesic component of the pain is helped before any of the physically caused pain is helped in any way. I have noted that when I have pain from sources not related to the disease, it does not feel at all like the pain medications are having any effect at all on these “normal” types of pain and I believe this can be explained. In a normal sensory gating/pain control physiology, a person who takes opiate pain medications for an intense, acute pain will have concurrent control of lesser pain; whereas this does not seem to be the case with what I have experienced in treating the ME/CFS/FM pain. This makes sense in the context that the majority of what opiate pain medications are doing for us it to replace the deficient endorphins and bring our sensory gating physiology back to normal (i.e., normalizing the hyperalgesia which is a sensory gating phenomenon. In essence the sensory gating and pain control systems are contiguous and interrelated systems that use the same neurochemistry.) This also fits nicely with the recommendations I have seen for post surgical pain care that recommend “twice as much for twice as long.” The first half of the “twice as much” is in essence bringing us to a normal sensory physiology and to give us a “normal” amount of pain medications post surgery would be akin to giving a normal person (without hyperalgesia) no medications at all.
While I do not think that this “endorphin replacement therapy” is suitable for all patients and not all subsets or individuals in the “ME/CFS and FM continuum” will have endorphin deficiency as their primary mechanism for the hyperalgesia and cognitive symptoms (some patients certainly appear to be very sensitive to opiates, just like most of us experience with most medications) it does appear to be very normalizing for at least a subset of us. Patients who are not endorphin deficient will probably find more relief with other NMDA/glutamate antagonists.
As an aside, the fact that pain medications help with virtually all of the central nervous system related symptoms, but NOT the symptoms occurring peripherally and systemically in the body (i.e., the physical pain caused by micro-circulatory dysfunction and the deficient muscle recovery/post exertional malaise) has helped convince me that CNS symptoms are not the primary driver of dysfunction and symptomology but rather are secondary in nature. When one puts the diastolic dysfunction together with nitric oxide related micro-circulatory dysfunction, a perfect recipe for metabolic dysfunction in the muscles is created and it is no coincidence that research is finding that we are having problems with aerobic metabolism and we are over-relying on anaerobic resources (i.e., glycogen stored in the muscles.) In essence, as we increase activity, the blood flow to the muscles actually decreases which results in these problems with muscle metabolism. I have also noticed that the “raggedy ann/andy” fatigue is cyclical and reactive to activity and as a former athlete who has experienced what it is like to “bonk” or “hit the wall,” it makes a great deal of sense that this cyclical nature of the “raggedy fatigue” can be explained by our running out of glycogen (again, since it is being over-relied upon.) What researchers have described a “neurally mediated hypo-tension” is more likely “metabolically mediated hypo-tension” that is occurring because of the problems with blood flow to the muscles and the raggedy ann/andy fatigue (with the drop out in blood pressure) is probably a pathological form of a “bonk” that occurs when we run out of the aforementioned glycogen. This also explains why we have such an abnormal stiffening of the muscles during even light activity; the lack of blood flow that is not bringing aerobic energy and additional anaerobic energy to the muscles is also not removing the metabolic by-products from the muscles, hence the muscles turning into “steel cables.”
Further putting the pieces of this puzzle together, the drop outs in blood pressure that occur as a result of this pathological version of a “bonk” nicely explain why Goldstein found that patients are more likely to have a positive SPECT and/or PET later in the day. What these scans are documenting is this metabolically driven drop out in blood pressure. Although an initial encephalitis may be important for starting the disease (as in Post polio for example) it would appear that the heart dysfunction may be what continues the illness and allows not only the systemic symptoms to occur, but as I mention below, it may actually drive the continuation of the neurological dysfunction.
Given that one of the three main causes of excitotoxic brain damage is transient ischemia (lack of blood flow) in the CNS (along with direct infection and direct chemical affect which are both probably related to other subsets in the ME/CFS and FM continuum) it actually makes sense the diastolic dysfunction and micro-circulatory dysfunction could actually be the main cause of excitotoxic brain damage and all of the related CNS symptoms (again, this would make sense of why the CNS symptoms are palliatively assisted by opiates and other NMDA/glutamate antagonists but I still experience all of the symptoms that are caused by the systemic diastolic and micro-circulatory dysfunction; i.e., lack of muscle recovery and post exertional malaise, abnormal stiffening of the muscles caused by the rapid and abnormal accumulation of metabolic by-products, etc.)
It all fits nicely together. The diastolic dysfunction and micro-circulatory dysfunction cause the neurological dysfunction instead of the reverse, as has been thought for so long.
In short, the use of opiates can be extremely helpful and has a specific scientific basis for why it can be so helpful. Although it’s no easy decision and not to be taken lightly (since it can be hell if you can’t find a doctor who will prescribe these medications,) it can also save lives and can bring a sense of semi-normality. I would suggest that if you can find a supportive doctor to prescribe pain medications, it’s actually worth the trouble. If you have any questions, let me know. I know this is complex but I have all of the scientific papers to document all of the hypotheses that I have presented. Thanks, Keir.
P.S., It’s also important to have extended release so that it functions throughout the night. Without this, the alpha/delta wave anomaly cannot be affected. Short term meds should really only be used for breakthrough pain.