Thursday, November 22, 2007
The research into FMS is undergoing a quite fertile period. In this paper I take advantage of several recent papers to look at different theories regarding the origin of pain in this disease. The pain FMS patients suffer from could derive from two places in the body; the central nervous system/brain or in the muscles/tendons themselves. In part one I focus on evidence suggesting that the pain in FMS is due to an oversensitized central nervous system.
Part I: Fibromyalgia is a Brain Disorder
Background: There are several different types of pain disorders; some people have 'hyperalgesia'- an increased sensitivity to painful stimuli, and some people have 'allodynia' - a painful responses to usually non-painful stimuli. FMS patients have both. Where this pain derives from is still not clear but the type of pain found in FMS gives us some clues as to its origin. Researchers know, for instance, that people with allodynia usually exhibit either increased sensitization of their peripheral pain receptors (nociceptors) (peripheral sensitization) located outside of the brain, or increased excitability of neural circuits regulating pain in the brain (central sensitization).
The signal for muscle pain travels via two types of nerve fibers to the dorsal horn of the spinal cord, where it prompts them to release pro-pain substances such as substance P and calcitonin gene-related peptide (CGRP). Substance P is a sensitizer; when it is it released into the neurons of the spinal cord it makes their NMDA receptors hypersensitive to glutamate, when released into the tissues surrounding a wound it makes them more sensitive to stimuli.
NMDA receptor activation and the concomitant release of pro-pain substances such as substance P (SP), nerve growth factor (NGF), brain derived nerve factor (BDNF), and nitric oxide is believed to drive the process of central sensitization. A recent text stated that the 'recruitment of the NMDA receptor appears to be the pivotal event in increasing the sensitivity of the nociceptive (pain) spinal circuits to (painful stimuli)". This is believed to occur when repetitive pain stimuli knock the magnesium block off the NMDA receptors (Staud 2004).
In order for a cell to respond to a substance it must have a receptor for that substance to bind to. Increased receptor activation occurs either when receptors are abnormally sensitive or when high numbers of a receptor are present. High levels of the NMDA receptor on a cell indicate that that cell is hypersensitive to glutamate; i.e. only small levels of glutamate are necessary to prod it into action.
NMDA receptors form ion channels at the excitatory synapses of these nerves. Ordinarily these ion channels are a) closed and b) blocked by extracellular magnesium ions. Two things needed to happen for these ion channels to open, first adequate glutamate needs to be present to open the channel and the membrane of the cell needs to become depolarized in order to flush the magnesium out. The negatively charged cell attracts magnesium ions which then close the NMDA ion channels. If the cell loses its negative charge, the magnesium ions will drift away. The loss of the magnesium ions allow sodium, potassium and most importantly calcium ions into the cell. Once inside the nerve cell the calcium ions activate signaling pathways that call for the production of glutamate, substance P and other pro-pain factors. The neurons in the spinal cord then send a message to the part of the brain called the thalamus which processes it and amplifies the pain response. Prolonged periods of NMDA ion channel activation and the high intracellular Ca2+ levels that accompany it can, by triggering the apoptotic process (cell suicide), result in nerve cell death.
Glutamate is the chief excitatory neurotransmitter in the brain. Ischemia (low blood flows).and low glucose concentrations can stimulate glutamate production. Ischemia is found in several neurodegenerative diseases does. Increased glutamate levels are associated with increased oxidative stress.
The controversy in the central sensitization theory in FMS comes from inability of brain imaging studies, in contrast to other pain diseases, to identify a lesion or wound in the CNS. The one other pain disease in which a CNS lesion is not found, trigeminal neuralgia, involves, interestingly, circulatory problems. In trigeminal neuralgia, increased pressure from a blood vessel applied to a cranial nerve supplying the face causes spasms of severe facial pain.
A recent study that examined how FMS patients responded to exercise provided evidence that central sensitization is at work in FMS.
Staud, R., Robinson, M. and D. Price. 2005. Isometric exercise has opposite effects on central pain mechanisms in fibromyalgia patients compared to normal controls. Pain 118, 176-184.
Many studies have shown that people usually display a decreased response to pain following exercise. The origin of this response is not known but could occur when receptors that monitor muscle movement and contraction (mechanoreceptors) activate anti-nociceptive (anti-pain) receptors. Both FMS (and some CFS patients) appear to have an anomalous response to exercise - following it they report an increased not decreased sensitivity to pain.
FMS patients have long reported that the pain they experience is not located in one place but often occurs body-wide. (Staud indicates it is more intense and widespread in the upper half of the body.) This is the first study to verify this anomaly; it found that the pain thresholds in both exercising and non-exercising muscles were increased after exercise in FMS patients. The pain intensity in the FMS patients did not appear to be particularly high - what was notable is that it increased at all.
Since trauma in the muscles results in local not systemic increases in pro-pain substances it is difficult to imagine how a peripheral process (one located in the muscles) could be at work here. This reaction, therefore, is another indication that a central pain mechanism is at work in CFS. It illustrates that a stimulus centered on one part of the body can, possibly by inducing a hyperexcitable response in the brain, can cause an aberrant response to normal stimuli across the body.
Just what is causing this hyperexcitability is unclear but there is evidence of increased levels of pro-pain substances in the brains of FMS patients.
FMS is Due to Increased Levels of Pro-pain Substances in the Brain
Increased levels of at least three pro-pain compounds associated with NMDA activation (substance P, nerve growth factor (NGF), brain derived growth factor (BDNF)) have been found in FMS. Substance P, the most well-studied pro-pain substance in FMS, is a neurotransmitter and neuromodulator that, besides pain, has been associated with anxiety, stress, neurotoxicity and nausea. Substance P is also involved in the transmission of pain impulses from peripheral receptors to the central nervous system. Releases of substance P cause the area surrounding a wound to become more sensitive to pain. Several studies have found increased levels of substance P in the cerebral spinal fluid of FMS patients.
NGF and BDNF are two neurotrophins that are increased in the cerebral spinal fluid (CSF) of chronic headache patients. Neurotrophins enhance the survival of neurons by blocking the apoptotic process (suicide). They also regulate neuronal plasticity. Alterations in the neural network (neural plasticity) could result in a chronically increased pain state. In vivo studies have indicated that nerve growth factor (NGF) increases the level of the pro-inflammatory neuropeptides CGRP and substance P as well as the growth factor BDNF. One study has found increased levels of nerve growth factor in the CSF of FMS patients.
Like substance P, BDNF appears to be both a neuromodulator and neurotransmitter. BDNF appears to enhance NMDA activity in two ways; first it enhances the production of glutamate and secondly it is able to increase NMDA receptor activity. BDNF is particularly interesting in its ability to induce a long term increase of sensitization in some parts of the brain. Unfortunately, no studies have addressed levels of this important compound in the cerebral spinal fluid of FMS patients. BDNF levels have been assessed in the peripheral blood, however/
The pain in FMS is may not simply be due to increased levels of pro-pain substances. The central nervous system also employs a battery of anti-pain substances designed to turn off or limit the pain response. These may be low in as well.
FMS is Due to Decreased Levels of Anti-pain Substances in the Brain
Sarchielli, P., Alberti, A., Candeliere, A., Floridi, A., Capocchi, G. and P. Calabresi. 2005. Glial cell ine-derived neurotrophic factor and somatostatin levels in ccerebrospinal fluid of patients affected by chronic migraine and fibromyalgia. Cephalalagia 26, 409-415. .
In addition to having high levels of 'pro-pain' factors, FMS patients could also have low levels of 'anti-pain' factors. These are compounds that inhibit the pain response in the spinal cord. One anti-pain factor called 'glial cell line derived neurotrophic factor (GDNF), which works specifically on the sensory neurons, was recently studied in relation to FMS.
GDNF is intriguing in several ways; first it belongs to the transforming growth factor family, one of whose members (TGF-B) is often increased in CFS, and it interacts with the sodium channels in cells. There is some indirect evidence of altered sodium channel activity in CFS (See A Channelopathy in CFS?)
GDNF plays an important role in the regulation of pain in the body. Since GDNF appears able to modify the expression of two NGF regulated pro-pain factors; substance P and the capsaican receptor, low GDNF levels could be at the heart of the sensitization seen in FMS. GDNF also appears to modulate the release of another anti-pain factor called somatostatin. Somatostatin is a key regulatory and anti-inflammatory peptide produced throughout the central nervous system and in most of the peripheral organs.
This study, which appears to be the most complete survey yet of anti-nociceptive factors in FMS, found that levels of both GDNF and somatostatin were markedly reduced in both FMS and chronic migraine patients. That somatostatin and GDNF levels were correlated with each other suggests that GDNF, in particular, plays a key regulatory role in these diseases.
This study suggests drugs developed to increase GDNF and somatostatin could be effective in FMS.
A Shocking 2006 Study Provides More Evidence of Central Nervous System Dysregulation in FM
Usui, C., Doi, N., Nashioka, M., Komatsu, H., Yamamoto, R., Ohkubo, T., Ishizuka, T., Shibata, N., Hatta, K., Miyasaki, H., Nishioka, K. and H. Arai. 2006. Electroconvulsive therapy improves severe pain associated with fibromyalgia. Pain 121, 276-280.
A recent trial involving electroconvulsive therapy (ECT, i.e. electroshock) also suggests that the hyperexcitability seen in FMS is due to lack of anti-nociceptive activity. ECT was found to significantly improve the pain scores in FMS patients with severe pain. Their scores, promisingly, remained low three months after the treatment.
An examination of regional cerebral blood flows after ECT found that it significantly improved blood flows to the thalamus, a part of the brain involved, among other things, in the interpretation of sensory inputs. Chaudhuri and Behan suggested thalamic inhibition may also cause central fatigue in CFS. It is believed that the ECT activated anti-pain nervous system pathways involving serotonin, norepinephrine or dopamine. Prior studies have found reduced serotonin levels in FMS. The recent Pharmacogenomics studies suggest these same pathways may be involved in CFS (Click here). Once again we see evidence suggesting that circulatory problems may play a role in FMS pathophysiology.
More evidence that the brain is involved in FMS comes from a 2005 study that found it may be allied with a disease of exquisite CNS sensitization: migraine.
Migraine and FMS - two sister diseases?
Marcus, D., Bernstein, C., and T. Rudy. 2005. Fibroymalgia and headache: an epidemiological study supporting migraine as part of the fibromyalgia syndrome. Clin. Rheum. 24, 595-601
There are a number of similarities between migraine and FMS; both disease appear to involve an exquisite sensitization to stimuli, both are pain syndromes, and depression and anxiety are common in both. Although migraine is chiefly thought of as headache, recent reports indicate that increased sensitization in the periphery is common as well - almost half of migraine sufferers suffer from allodynia (a painful response to normal stimuli) and about 40% display widespread tender points. A recent study found that about 15% of migraine sufferers fit the criteria for FMS.
Chaudhuri and Behan state there are numerous similarities between CFS and migraine as well. CFS patients share with migraine sufferers such symptoms as headache, confusion, increased sensitivity to light, sounds and smells as well as exacerbated responses to serotonin. Symptom exacerbation during menstruation and muscle pain, disequilibrium and unusual sweating are also often seen in both diseases as are white brain matter abnormalities and reduced cerebral blood flows. Stress, alcohol and caffeine can exacerbate symptoms in both and transient or chronic fatigue is also common in migraine (See A Neurological Channelopathy in CFS?)
This study found that almost half of FMS patients suffered from migraine and 80% suffered from severe headaches. Most intriguingly a finding that headache preceded FMS symptoms in almost half of the FMS patients suggests that sensitization began in the brain and later spread to periphery. Other studies have found an increased incidence of another pain disease possibly allied with FMS, irritable bowel syndrome (IBS), in migraine patients. We just saw that both migraine and FMS patients have low levels of the anti-pain factor BDNF in their spinal cords.
Conclusions - Is FMS a disease in which the central pain producing pathways in the brain and spinal cord are overactive? Several studies have suggested it is; not only have high levels of several pain producing substances (substance P, nerve growth factor) been found in the CSF of FMS patients but reduced levels of an important anti-pain factor, GNDF, have as well. A successful electroshock therapy study suggested that reduced blood flows in the thalamus of the brain may be implicated as well. A possible connection with a disease of exquisite central nervous system sensitization, migraine, further implicates the brain in FMS.
But is central sensitization the answer in FMS? Recent studies that provide evidence of peripheral sensitization suggest that FMS patients may get hit from both sides - the body and the brain. See the next paper in this series for evidence that FMS is disease of the periphery, not the central nervous system
Contact: Cort Johnson at [email protected]
Tuesday, November 20, 2007
ME: A Simple Service Standard.
Greg & Linda Crowhurst Nov 20 2007 (May be reposted)
"When a well-packaged web of lies has been sold gradually to the masses over generations, the truth will seem utterly preposterous and its speaker a raving lunatic"(Dresden James) John le Carre, Absolute Friends, Coronet Books, London 2003, p.334
As only a novel can do, Absolute Friends is a gripping expose of the all pervasive influence of corporate culture upon society; the quote above is a particularly poignant one for ME sufferers.
In the history of medicine has there ever been such a "well-packaged web of lies" as the antics of the Insurance industry; its twenty-odd year attempt, against all the odds, to get ME labeled as a psychiatric condition, instead of the neurological disease that it is? Five time more prevalent than AIDS, much bigger than lung cancer and breast cancer combined, much bigger than multiple sclerosis, diabetes, heart failure, kidney disease, or cystic fibrosis, ME has wrecked our life, my wife and I, for the last 14 years. Effectively, my wife lives the life of a dying person, she is as sick as an AIDS patient close to death or a terminally ill cancer patient and has been like this every day for nearly a decade and a half; with nothing to ease the pain; just me holding her, when I can.
The Insurance Industry, in the meantime, have almost taken over the NHS and just for good measure here in the UK, the Welfare System, the Medical Research Council, all the Royal Colleges, and through the Science Media Centre, the media itself. It is hard to look at my wife in so much pain, so paralysed, so breathless, so numb, too sore to even touch; knowing full well that the reason nothing at all is being done for her, is because of the extraordinary influence of a minority group of UK mental health professionals, who have proven affiliations to corporate industry.
ME, it is to live in a world gone quite mad.
"March you get sore feet. Protest you get a bad throat……Anybody who nails the lies is a radical malcontent.(Absolute Friends p.275)"
Currently you have a name : "ME" that anyone can interpret almost anyway they wish. You have a real physical disease that is not properly validated as such and that is why people’s experience is so devastating and distressing. They have to seek someone who believes in them and their illness. They have to actively seek someone who believes in them and their illness to get any care at all. This is what people with ME are currently experiencing :
q· Denial of how very physically ill they are.
q· Playing down of the symptoms and the disease process.
q· Lack of appropriate biomedical tests.
q· Confusion over the clinical definition and a dearth of appropriate treatment of ME.
q· Potential abuse by medical professionals and carers who do not know or choose not to know the truth of this neurological illness.
q· Misinterpretation and misrepresentation of the facts of the disease.
Plus a complete lack of support; on so many levels, it is an absolutely unacceptable level of service provision to such chronically ill and disabled people. The Government funds only psychiatric research. The Medical Research Council erroneously classifies ME as a mental disorder, as does the Institute of Psychiatry.
A true ME service can only be built upon truth, not lies or silent denial. We want the best outcome potential, to:
q· Help sufferers with the things that can be helped.
q· Support sufferers with the things that cannot be helped
q· Help sufferers to live at peace, to the best of their ability, within a complex and ravaging illness.
ME sufferers want peace of mind; they want to know clearly what is wrong with them. They want to understand their symptoms, they want to know if any of them can be alleviated. They want an accurate diagnosis and a realistic prognosis; otherwise they cannot adjust their life accordingly. You cannot get on with your life, basically, if all the time you are waiting to get better. People need to be able to accept how ill they are and this is an emotional and practical process that cannot be dealt with if the illness and the full range of devastating symptoms are not validated in the first place. It is like standing on a pile of sand with no firm foundation upon which to build. Sufferers want adequate and appropriate services, in order to maximise the opportunities of their life and to minimise the stress and distress of the illness. The key factor, says my wife, is being able to accept that you are ill, there is no treatment and currently there is no cure; you have to learn how to live with that harsh reality. You also need hope that it will not always be like this, that the government will do something sincere, validating and appropriate about it, by funding biomedical research and biomedical clinics with biomedical clinicians, who will develop the service as research discovers new ways forward.
It has taken us 14 years to identify five core components that are essential in any ME service or policy statement; if a single one of them is missing then people with ME are likely to be harmed. In our opinion, any service for people with ME should honour the WHO definition of ME, should be underpinned by a clear definition and criteria, should know and understand all the symptoms and the multi-system dysfunction and should be willing to create the clearest picture of people’s circumstances, so that they can get the best treatment and support available. As these services are currently not available, they need to be created, because ME sufferers are entitled to it.
Here is a framework against which to judge any service or policy announcement, such as the recent NICE guideline in the UK.
1. Honour the fact that ME is a serious neurological disease (WHO ICD 10. G93): The WHO definition is the one piece of evidence and validation that people with ME already have, to prove they are ill with a recognised disease. Quite simply it is the truth, from which all service effort must flow. If you come from any other position, for example that ME is a psychiatric disorder, what you say may even sound reasoned, on paper at least, but all that flows from this flawed perspective will be skewed, twisted and even deadly, if it is built upon the wrong reasoning that ME is a mental health disorder.
If a service does not accept the WHO definition that ME is a neurological illness, it will allow various interpretations of what ME is, to be acceptable.
There are very real vested interests in portraying ME as a psychiatric syndrome, as opposed to a seriously debilitating physical illness, with multi system dysfunction, as highlighted by Ian Gibson MP in his Parliamentary Inquiry (2006). Ifpractitioners do not believe ME is a physical neurological illness, then all the patient’s symptoms can be misinterpreted and not honoured ; this is so dangerous.
2. Respect the fact that ME is a multi-system disease affecting all systems of the body and each person’s individual experience of this disease. Over and over again one reads about how incredible it is that ME patients manage to survive at all, so dreadful and serious are the symptoms. Patently though, this is not being respected by policy makers; who, having considered the biomedical evidence, would dare recommend rehabilitation or Graded Exercise Therapy as THE core treatment strategy, as NICE do, in their recently published Guideline? Only by taking into account the full biomedical research can a full and true picture of the severity of the illness and symptoms in ME, be arrived at and a safe care pathway created.
3. Validate the ME sufferer's experience by using appropriate criteria for assessment and adequate biomedical testing using up to date equipment and methods. The Byron Hyde, the Sarah Myhill, the Paul Cheney; the level of assessment and testing that they carry out in their clinics - this must be made available to ME sufferers across the board. What other illness of this severity or disability would settle for less?
By not using a clear definition and by not advocating appropriate clinical criteria and state of the art biomedical testing, a service will only spread confusion for doctors patients and paramedical staff alike about what is ME. Clear diagnostic criteria, such as the Canadian Criteria, are essential for doctors to be able to properly identify the disease and not confuse it with "fatigue" conditions.
4. Identify the full need and aim to treat/support the whole range of symptoms, with honest prognosis. Survey after patient survey paint an horrific picture of multiple serious symptoms that affect all the body systems; ME sufferers are in sheer physical torment most of the time. Can these symptoms be treated? We don’t know. After 14 years of unbelievable suffering, my wife is more or less left to just get on with it. Patients and medics alike will not understand the experience of people with ME fully without proper emphasis and guidance on the vast range of symptoms. Proper aids and equipment will not be developed or provided unless there is a complete documentation of the often confusing symptoms. In order to have the symptoms of ME fully treated and honoured, full biomedical clinics and clinicians need to be in place. The psychiatric skew on this illness needs removing as it badly influences the perception and the reality of service provision.
5. Competently provide ongoing support: It is frightening how little support people with ME receive. These seriously ill and disabled patients every day have to put up with clumsy or inadequate, if any, support that does not take into account the light, the touch, the sound, the drug and chemical sensitivities. The pain, the paralysis, the numbness, the inability to bear being touched. The screaming crawling sensations, the itching burning agony, the inability to breathe, to talk, to think; and the post exertional malaise.
Support needs are so complex, there are so many issues on so many levels to take into account, especially with severe ME. On our website: www.metrainingco.org.uk we have posted a detailed guide to supporting the severely affected. Competent support can only be in place if the illness is recognised, defined, outlined fully, tested in depth and treated appropriately. It can only be available if there is a genuine commitment to training based on the four previous criteria. It will only be available when ME is fully honoured as the severe, neurological, multi-system, dysfunctional, disabling disease that it is. It will only be available when there is appropriate investment to provide for it.
Conclusion: People with ME need to set the agenda, not government or the insurance industry. We desperately need to reclaim our power, sufferers and carers, and take a stand against the blatant lies, the widespread injustice and the distortion of the truth of ME.
We need to build proper services that honour, respect, validate, treat and support people with ME today.
<a href="http://technorati.com/tag/CFS" rel="tag"><img style="border:0;vertical-align:middle;margin-left:.4em" src="http://static.technorati.com/static/img/pub/icon-utag-16x13.png?tag=CFS" alt=" " />CFS</a>
Research out of the University of Michigan Health System is shedding new light on why people with the chronic pain condition fibromyalgia report that they do not respond to the types of medication that often relieves other people. U-M researchers say that may be because patients with fibromyalgia were found to have reduced binding ability of a type of receptor in the brain that is the target of opioid painkiller drugs such as morphine. The study included PET - positron emission tomography - scans of the brains of patients with fibromyalgia and a control group of people without the often-debilitating condition.
You're not crazy. There IS a reason you're in pain.
Monday, November 19, 2007
Telegraph Doctor Supports One Click NICE Judicial Review.
Dr James LeFanu writes in the Daily Telegraph: NICE policy contradicts verdict of those with ME/CFS. Devastating disturbance of brain function in patients. CBT/GET no good. Daily Telegraph asks patients to write in with the evidence. Contact details provided.
READ THE NEWS ON ONE CLICK
- - - -
MAY BE REPOSTED
RE: 'Doctor's Diary' - Monday 19 November 2007
NICE (the National Institute for Health and Clinical Excellence) clearly have a difficult job to do but as Dr James le Fanu correctly points out they are making a complete mess of trying to help people with ME/CFS.
The problem lies with the way in which a misguided medical profession decided to rename and redefine ME (myalgic encephalomyelitis) as CFS (chronic fatigue syndrome). In doing so they have created a spectrum of illnesses ranging from those who have a recognised neurological condition to those who have a type of chronic fatigue that is indistinguishable from a psychiatric illness.
For NICE to then conclude that everyone under the umbrella of ME/CFS should be automatically offered cognitive behavioural therapy and/or graded exercise therapy - treatments which patients often report are ineffective, or may even make them feel worse - makes no practical or economic sense at all.
No wonder NICE is once again being challenged in the courts and in parliament.
Dr Charles Shepherd
Hon Medical Adviser, ME Association
NB: The 'Doctor's Diary' item by Dr James le Fanu can be viewed on the MEA website at: http://www.meassociation.org.uk
* * *
The problem with lumping all sorts of fatigue together under the name CFS is that it confounds research. As in any case of mixing apples and oranges, what applies to one does not apply to others. One reason they haven't been able to find a cure for CFS is that CDC hasn't been trying very hard. Another is that the mish-mash of people who really have ME and people who really have depression and people who have everything else in between guarantees that they won't find a treatment that works for everyone, because we don't all have the same disease.
Maybe if we went back to the name and definition of ME for those of us who have the neurological problems to justify that diagnosis, we could get the help we need. But, since 1988, it has been almost impossible to get an ME diagnosis in the US because of the CDC decree that those symptoms must be called CFS. I am convinced that I have the post-viral disease that used to be called ME, but finding a doctor who will call it that has been impossible. Most of them just don't like to buck the establishment.
Sunday, November 18, 2007
1. BPS Slams NICE Guidelines - One Click NICE Judicial Review.
The One Click Group would like to thank the British Psychological Society (BPS) for issuing this press release relating to the proposed One Click Judicial Review of the CFS/ME NICE Guidelines. If BPS members refuse to treat ME/CFS labelled patients with CBT/GET because they consider these psychosocial treatments to be inappropriate for their needs, NICE is in terrible trouble with these Guidelines, the like of which it has never known. This is yet another evidence nail driven straight into the heart of these appalling Guidelines. See the BPS press release published in full on One Click.
(emphasis added by Karen)
The disbelief and skepticism that chronic fatigue syndrome (CFS) patients experience from family, friends and colleagues can be disheartening. But when that skepticism comes from the health care professionals whom patients seek out, desperately hoping for validation and treatment options, it can be devastating. And even when patients do manage to find a medical professional who believes CFS is real and who wants to help, the providers often don't know how to treat this complex illness.
Read the complete article at
It's a long article (9 pages) about sleep (and the Sleep Number bed), but well worth reading. http://www.nytimes.com/2007/11/18/magazine/18sleep-t.html?th&emc=th
I swear by my Sleep Number bed!
The Sleep Number bed, while expensive, paid for itself the first year -- I was able to work that many more hours as a result of the better quality sleep I was finally getting.
Researchers have proven that you can create fibro-like symptoms in healthy volunteers by depriving them of sleep; the "fibro" goes away when they're able to resume normal sleep. I had the same experience -- near the beginning of this relapse, I was tested for fibro and told I didn't have it; after another year of inadequate sleep, I did. And after a week on the Sleep Number bed, the "fibro" was under control. Technically, I still have it because I still react to pressure on the test points, but that's a long way from being in constant pain, even when lying down doing nothing.
If you haven't tried a Sleep Number bed, I recommend you do -- you can sleep on it for 30 nights and return it owing only the delivery charge if it really doesn't work for you. But in a recent discussion among people I know and trust, the consensus seemed to be "you'll have to pry it from my cold, dead hands". Especially if you have either CFS or fibro, it's worth a try. Improving the quality of your sleep is the first step to improving the quality of your life. My first specialist told me that, and my experiences in this relapse have proven him correct -- when no one was doing anything to help me sleep, I got worse. When my sleep problem was fixed, my immune system kicked in and fought off the virus. What I'm dealing with now is the damage done by years of sleeping less in a week than some people sleep in one night. But doctors kept arguing with me that I was imagining things, and wouldn't accept my proof that I really was awake all night (like a scarf that was a ball of yarn when I went to bed the first time, and completed by morning). They just kept handing out the "logic" that "sometimes we think we're awake when we're really asleep" and ignoring my explanations of how I knew I wasn't really asleep. There's a few zillion e-mails I wrote in the middle of the night in that four-year period that prove I wasn't asleep at times I said I wasn't asleep.
Dr. Murphree believes that it takes at least as long to recover from sleep deprivation as it did to dig that hole. In which case, I still have a few more years before I've reached what he thinks will be maximum recovery. Maybe it'll be enough to work those extra hours necessary to be self-supporting. Or maybe some of the damage is permanent because the problem wasn't addressed in time.
And, yes, tonight is one of those nights where the pain is so bad that even my pain pills aren't helping. I proved, once again, that the advice that walking would make my pain better is wrong -- walking on my aching knee made it feel much worse. By the time I got home from a brief shopping excursion, I was limping so badly I barely made it up the stairs. Fortunately, a friend drove me, and he carried my stuff upstairs so I only had to climb up once. Now I wait and hope the pain simmers down enough that I can get a little sleep tonight. Because sleepless nights make the pain worse, starting another vicious cycle: can't sleep because of pain, pain worse because I can't sleep, can't sleep the next night because of pain, pain worse because I can't sleep...
But, there again, doctors seem to believe that because I'm female, I'm a wimp where pain is concerned, and that I call the least little thing "severe", so they disregard both the pain and my description of, at times, passing out because the pain is so bad. Which is actually a blessing, because it gives me a minute of relief.