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Suprise of the Reno Conference- a key to pain and fatigue in ME/CFS?

Discussion in 'Latest ME/CFS Research' started by Cort, Jul 1, 2009.

  1. Cort

    Cort Phoenix Rising Founder

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    Dr Light gave the most exciting presentation at the Reno conference in March. Apparently nobody in the scientific community until recently had any clue how the brain learns when our muscles are overworked. They knew that when the brain believes that damage is about to occur it will flood the body with pain and fatigue signals in an attempt to stop whatever activity is going on. There is little evidence, however, of overt muscle damage in CFS.

    But what if the sensory system that determines if the muscles are damaged is off? What if it is overreacting to even very very small signs of muscle damage - signs that are produced even during mild exercise? What if the brain thinks the muscles in CFS patients are on the verge of collapse and is acting accordingly?

    That is what Dr. light has evidence of - signs that CFS patients have many times the number of receptors that measure such things as lactic acid and ATP than normal people. This suggests that they're reacting to small amounts of muscle activity as if people had just a marathon.

    What a stunning finding! And still very preliminary. More when the last overview of the conference is produced.
  2. Freddd

    Freddd Senior Member

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    Hi Cort,

    I spoke to Dr Light at last years Salt Lake conference. We discussed the lactic acid situation which I have always expected to be found. It was quite illuminating. I used to have terrible muscular burning, for 16 years without letup. After I found the solution I was completely free of that burning pain within 10 days for the last 6+ years. After 40+ years of progressing ME/CFS/FMS including a total systems crash for 16 years I am better than 95% recovered and have only a few symptoms left from residual damage and a car wreck 35 years ago. I can exercise normally and generate new muscle tissue instead of vast pain. I would be pleased to enter a 5k race for formerly diagnosed FMS/CFS patients to demonstrate what I claim. As a systems analyst I figured out the whole of the problem including why it is difficult to diagnose and treat. There are lots of variables and underlying the whole thing are some false assumptions based on early research. Not only do I know what works but also what doesn't work, what prevents a solution and how to increase the odds of success tremendously by elliminating common causes of failure in treament. It's not a secret, just lengthy, so if you would like to know I would be pleased to tell you. My figuring out is on the data and pragmatic level, not the detailed biochemical and physical level addressed by researchers such as the Lights. I'm a data analyst, not a biochemical researcher.
  3. Jody

    Jody Senior Member

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    Hi Freddd, welcome to the forums.

    I'm intrigued. I'd like to hear about what you've discovered.
  4. Cort

    Cort Phoenix Rising Founder

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    Burning muscle feeling - that's my thing to a T after exercise. Hot burning feeling plus irritation, pounding heart, etc. Also feels like my 'skin cannot breath'. I got the B12 thread going in the General treatment section by the way.
  5. Jody

    Jody Senior Member

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    How much exercising are you doing at a time?

    Maybe you need to cut it back, and work your way up slowly?
  6. ChuckG

    ChuckG

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    From Wikipedia:

  7. Cort

    Cort Phoenix Rising Founder

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    I know the importance of lactic acid in causing muscle fatigue has come under question lately; in fact it may have been rebutted. Dr. Light believes that the receptors on our white blood cells are over reacting to very small amounts of lactic acid or other signs of muscle damage. Lactic acid may not cause muscle soreness but it could be associated with it.

    But what accounts for these muscle burning sensations? Burning and really all sorts of odd sensations are often caused by nerve problems. Dr. Natelson thinks the nerves in the muscles may be overreacting. Could the brain - thinking the muscles are damaged - turn on the nerves in the muscles causing pain???

    Jody is definitely right; too much exercise. Cutting back and going slowly -as in moving slowly- seems to be able to build muscle endurance and strength - (very slowly but still....)
  8. Jody

    Jody Senior Member

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    Thank you sir. :)

    I love being right.:D
  9. Dolphin

    Dolphin Senior Member

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    I find the research the Lights are doing interesting. However I'm not convinced by their idea, which they may have picked up from Dr Bateman, that there is nothing abnormal in the muscles but the brain perceives there is. There are plenty of abnormal findings on exercise studies.
  10. Cort

    Cort Phoenix Rising Founder

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    This is my recollection of muscle studies;

    • no consistent increase in lactic acid
    • no inability to generate force (muscle fatigue not weakness)
    • some suggestion that the brain may not be activating all the muscle fibers
    • some evidence that the 'planning stage' in the brain as regards engaging in movement is impaired
    • some evidence of increased oxidative stress in the muscles
    • reduced metabolic functioning in both single and repeat exercise tests for some patients (do not necessarily imply muscle dysfunction however

    I'm sure that I've missed some. There are certainly a lot of possibilities here. Unfortunately most positive studies have not been replicated. As always what we need is more research!
  11. Cort

    Cort Phoenix Rising Founder

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  12. Dolphin

    Dolphin Senior Member

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    Muscle weakness has been considered an integral part of ME. I'm not sure it might be as noticeable in more mildly affected individuals.

    I'm appending Ramsay's description. I've also seen shorter descriptions where people highlighted muscle weakness.

    I look forward to reading the full paper.

    =========
    --------------------------------------------

    The Definitive Description of ME

    MYALGIC ENCEPHALOMYELITIS : A Baffling Syndrome With a Tragic Aftermath. By A. Melvin Ramsay M.D., Hon Consultant Physician, Infectious Diseases Dept, Royal Free Hospital. [Published 1986]

    The syndrome which is currently known as Myalgic Encephalomyelitis in the UK and Epidemic Neuromyasthenia in the USA leaves a chronic aftermath of debility in a large number of cases. The degree of physical incapacity varies greatly, but the dominant clinical feature of profound fatigue is directly related to the length of time the patient persists in physical effort after its onset; put in another way, those patients who are given a period of enforced rest from the onset have the best prognosis.

    Although the onset of the disease may be sudden and without apparent cause, as in those whose first intimation of illness is an alarming attack of acute vertigo, there is practically always a history of recent virus infection associated with upper respiratory tract symptoms though occasionally there is gastro-intestinal upset with nausea and vomiting.

    Instead of making a normal recovery, the patient is dogged by persistent profound fatigue accompanied by a medley of symptoms such as headache, attacks of giddiness, neck pain, muscle weakness, parasthesiae, frequency of micturition or retention, blurred vision and/or diplopia and a general sense of 'feeling awful'. Many patients report the occurence of fainting attacks which abate after a small meal or even a biscuit, and in an outbreak in Finchley, London, in 1964 three patients were admitted to hospital in an unconscious state presumably as a result of acute hypoglycaemia.

    There is usually a low-grade pyrexia [fever] which quickly subsides. Respiratory symptoms such as sore throat tend to persist or recur at intervals. Routine physical examination and the ordinary run of laboratory investigations usually prove negative and the patient is then often referred for psychiatric opinion. In my experience this seldom proves helpful is often harmful; it is a fact that a few psychiatrists have referred the patient back with a note saying 'this patient's problem does not come within my field'.

    Nevertheless, by this time the unfortunate patient has acquired the label of 'neurosis' or 'personality disorder' and may be regarded by both doctor and relatives as a chronic nuisance. We have records of three patients in whom the disbelief of their doctors and relatives led to suicide; one of these was a young man of 22 years of age.

    The too facile assumption that such an entity - despite a long series of cases extending over several decades - can be attributed to psychological stress is simply untenable.

    Although the aetiological factor or factors have yet to be established, there are good grounds for postulating that persistent virus infection could be responsible. It is fully accepted that viruses such as herpes simplex and varicella-zoster remain in the tissues from the time of the initial invasion and can be isolated from nerve ganglia post-mortem; to these may be added measles virus, the persistence of which is responsible for subacute sclerosing panencephalitis that may appear several years after the attack and there is a considerable body of circumstantial evidence associating the virus with multiple sclerosis. There should surely be no difficulty in considering the possibility that other viruses may also persist in the tissues. In recent years routine antibody tests on patients suffering from myalgic encephalomyelitis have shown raised titres to Cocksackie B Group viruses.

    It is fully established that these viruses are the aetiological agents of 'Epidemic Myalgia' or 'Bornholm's Disease' and that, together with ECHO viruses, they comprise the commonest known virus invaders of the central nervous system. This must not be taken to imply that Cocksackie viruses are the sole agents of myalgic encephalo- myelitis since eny generalised virus infection may be followed by a period of post-viral debility. Indeed, the particular invading microbial agent is probably not the most important factor. Recent work suggests that the key to the problem is likely to be found in the abnormal immunological response of the patient to the organism.

    A second group of clinical features found in patients suffering from myalgic encephalomyelitis would seem to indicate circulatory disorder. Practically without exception they complain of coldness in the extremities and many are found to have abnormally low temperatures of 94 or 95 degrees F. In a few, these are accompanied by bouts of severe sweating even to the extent of waking during the night lying in a pool of water. A ghostly facial pallor is a well known phenomenom and this has often been detected by relatives some 30 minutes before the patient complains of being ill.

    The third component of the diagnostic triad of myalgic encephalo- myelitis relates to cerebral activity. Impairment of memory and inability to concentrate are features in every case. Many report difficulty in saying the right word and are conscious of the fact that they continue to say the wrong one, for example 'cold' when they mean 'hot'. Others find that they start a sentence but cannot complete it, while some others have difficulty compre- hending the written or spoken word. A complaint of acute hyperacusis is not infrequent; this can be quite intolerable but alternates with periods of normal hearing or actual deafness. Vivid dreams generally in colour are reported by persons with no previous experience of such a phenomenom. Emotional lability is often a feature in a person of previous stable person- ality, while sudden bouts of uncontrollable weeping may occur. Impairment of judgement and insight in severe cases completes the 'encephalitic' component of the syndrome.

    I would like to suggest that in all patients suffering from chronic debility for which a satisfactory explanation is not forthcoming a renewed and much closer appraisal of their symptoms should be made. This applies particularly to the dominant clinical feature of profound fatigue. While it is true that there is considerable variation in degree from one day to the next or from one time of the day to another, nevertheless in those patients whose dynamic or conscientious temperaments urge them to continue effort despite profound malaise or in those who, on the false assumption of 'neurosis', have been exhorted to 'snap out of it' and 'take plenty of excercise' the condition finally results in a state of constant exhaustion. This has been amply borne out by a series of painstaking and meticulous studies carried out by a consultant in physical medicine, himself an ME sufferer for 25 years. These show clearly that recovery of muscle power after exertion is unduly prolonged. After moderate excercise, from which a normal person would recover with nothing more than a good night's rest, an ME patient will require at least 2 to 3 days while after more strenuous excercise the period can be prolonged to 2 or 3 weeks or more. Moreover, if during this recovery phase, there is a further expenditure of energy the effect is cumulative and this is responsible for the unrelieved sense of exhaustion and depression which characterises the chronic case. The greatest degree of muscle weakness is likely to be found in those muscles which are most in use; thus in right- handed persons the muscles of the left hand and arm are found to be stronger than those on the right.

    Muscle weakness is almost certainly responsible for the delay in accommodation which gives rise to blurred vision and for the characteristic feature of all chronic cases, namely a proneness to drop articles altogether with clumsiness in performing quite simple manoeuvres; the constant dribbling of saliva which is also a feature of chronic cases is due to weakness of the masseter muscles. In some cases, the myalgic element is obvious but in others a careful palpitation of all muscles will often reveal unsuspected minute foci of acute tenderness; these are to be found particularly in the trapezii, gastrocnemii and abdominal rectii muscles.

    The clinical picture of myalgic encephalomyelitis has much in common with that of multiple sclerosis but, unlike the latter, the disease is not progressive and the prognosis should therefore be relatively good. However, this is largely dependent on the management of the patient in the early stages of the illness. Those who are given complete rest from the onset do well and this was illustrated by the aforementioned three patients admitted to hospital in an unconscious state; all three recovered completely.

    Those whose circumstances make adequate rest periods impossible are at a distinct disadvantage, but no effort should be spared to give them the all-essential basis for successful treatment. Since the limitations which the disease imposes vary considerably from case to case, the responsibility for determining these rests upon the patient. Once these are ascertained the patient is advised to fashion a pattern of living that comes well within them. Any excessive physical or mental stress is likely to precipitate a relapse.

    It can be said that a long-term research project into the cause of this disease has been launched and there are good grounds for believing that this will demonstrate beyond doubt that this condition is organically determined.
  13. Cort

    Cort Phoenix Rising Founder

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    Yes there is muscle weakness - no one would say that they are as strong as before; but is the weakness such that it can explain ME/CFS? My understanding of muscle weakness tests and studies is that they have not found this. Check out this paper based on Chaudhuri's findings. I agree the subject is still open.

    http://aboutmecfs.org/Rsrch/CentralFatigueCFS.aspx

    Peripheral vs Central Fatigue - Pathologic fatigue can originate in the periphery (i.e. muscles) or it can be central (brain - induced) in nature or it can be both. Most often it is the result of one or the other.

    PERIPHERAL FATIGUE

    Instead Chaudhuri and Behan and I think most in t he research community believe that a kind of fatigue called 'Central Fatigue' -which originates in the central nervous system - and causes both physical and mental fatigue - is the main player in ME/CFS. Several of the causes of 'Central Fatigue' are central nervous system viruses but also metabolic problems in the brain (eg, lactate -Shungu).

    CENTRAL FATIGUE
  14. Dolphin

    Dolphin Senior Member

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    (Drat! My connection dropped and I lost last post. It was something like the following)

    Thanks for your thoughtful posts, Cort.

    I have just got worried by some things the Lights have said which make out that exercise is good for us but our bodies are giving us the wrong signals. Perhaps this may be true of some with FMS but I'm not at all convinced that it is true for CFS.

    Here's a muscle study (haven't seen full text unfortunately)

    'Functional characterization of muscle fibres from patients with chronic
    fatigue syndrome: case-control study.'

    Pietrangelo T, Toniolo L, Paoli A, Fulle S, Puglielli C, Fan X00f2 G,
    Reggiani C.
    Int J Immunopathol Pharmacol. 2009 April-June;22(2):427-436.
    PMID: 19505395 [PubMed - as supplied by publisher]
    http://www.ncbi.nlm.nih.gov/pubmed/19505395

    Chronic fatigue syndrome (CFS) is a disabling condition characterized by
    unexplained chronic fatigue that impairs normal activities. Although
    immunological and psychological aspects are present, symptoms related to
    skeletal muscles, such as muscle soreness, fatigability and increased
    lactate accumulation, are prominent in CFS patients. In this case-control
    study, the phenotype of the same biopsy samples was analyzed by determining
    i) fibre-type proportion using myosin isoforms as fibre type molecular
    marker and gel electrophoresis as a tool to separate and quantify myosin
    isoforms, and ii) contractile properties of manually dissected, chemically
    made permeable and calcium-activated single muscle fibres. The results
    showed that fibre-type proportion was significantly altered in CSF samples,
    which showed a shift from the slow- to the fast-twitch phenotype. Cross
    sectional area, force, maximum shortening velocity and calcium sensitivity
    were not significantly changed in single muscle fibres from CSF samples.
    Thus, the contractile properties of muscle fibres were preserved but their
    proportion was changed, with an increase in the more fatigue-prone,
    energetically expensive fast fibre type. Taken together, these results
    support the view that muscle tissue is directly involved in the pathogenesis
    of CSF and it might contribute to the early onset of fatigue typical of the
    skeletal muscles of CFS patients.
  15. Freddd

    Freddd Senior Member

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    Hi Jody,

    At the Salt Lake conference I discussed with the Lights the effects of the methylb12, adenosylb12, l-carnitine, methylfolate and alpha lipoic acid on my ability to exercise and the complete disappearance of all kinds of muscle pain including the burning pain of lactic acid in 10 days. I'm not quite back to the ability to do arobic exercise for hours on end that I could do in my 20s, but I'm good for 45 minutes and could easily push that up to a couple of hours now at 61. Only my willingness to spend the time stops me. The exercise intolerance I had for 20+ years is entirely gone. I also adjust to altitude easily again. I'd lost that for 20 years too. Last year it took me 2 weeks to adjust to exercise at 7000 feet from 4500 for the same duration and intensity. This is something those from the flatlands don't run into, but the Lights do out here in SLC.

    I also was able to stop dilantin after 13 years becasue I no longer had the neurological pain and spasms it was controling, again the same set iof supplements.
  16. Jody

    Jody Senior Member

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    Freddd,

    How wonderful to feel younger at 61 than you did at 41. :D

    I'm so glad to hear it.

    I am also experiencing a time when at almost 54, I feel younger than I did at 40.
  17. Freddd

    Freddd Senior Member

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    A friend of mine yesterday commented that I looked 70s 10 years ago and 50s now. I feel younger now than at 39 after I crashed. Other people my age seem so old now. My lady friend is 51 and we seem a good match. We overlap enough on music and period backround that we are not aliens to each other and she can keep up energetically. We hike well together.
  18. Jody

    Jody Senior Member

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    Freddd,

    I love to hear this.

    This is what I'm counting on for myself as well.

    I am determined that though I missed much of my 40's and my early 50's that I will have them anyway, sooner or later. No matter how old I am chronologically when it happens.
  19. Cort

    Cort Phoenix Rising Founder

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    I agree Tom; I've tried to expand my ability to exercise for over 20 years and have ended up concluding that it is impossible to do so and that in fact I should do less exercise than ever. I can only imagine that I'm setting myself up for cardiovascular or other problems - it's very disappointing.

    I think either she was talking about very very low levels of very slowly incremented exercise what she was talking about the fibro end of the spectrum which appears to be able to tolerate much more exercise than the CFS end of the spectrum.

    Oddly enough when I exercise I do believe my muscles get stronger - they certainly get bigger and I feel they can sustain more force. The problem is that the rest of my life falls apart - I just feel like crap! :mad:

    I really don't know if I should periodically engage in aerobic exercise simply to get that part of my body going again and suffer the consequences - which for me are temporary - or if I should just abstain all together. :confused:
  20. Freddd

    Freddd Senior Member

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    Hi Cort,

    For 16 years exercise helped me maintain capacity but could not expand muscle size or strength, just got more pained. After the first rwo years I could barely walk half a block and back. I decided to do something about that and while in the phase 3 Stadol Study I started increasing my walking by 50 feet a day at first, and then about 100 feet per day. In six months I had worked up to being able to walk 4 miles. But it never felt good. I was always hammered. It never made me feel any better and all it was for me was insurance against dropping dead of a heart attack. Because of the pain from the auto crash made worse by the FMS I spent 11 years waking up each morning in tears and terrible pain after a miserable 4-5 hours sleep wishing I could die. This started about 2 weeks after the end of the Stadol study and continued until morphine in pain management. Everything changed first after the mb12 and then after the adb12 even more. I started working doing strength exercises with 1.25 pound weights and 3 reps and working up from there about 3 years before mb12. In 3 years I had worked up to 3 pounds in each hand. After that it took off. Exercise produced normal results after the active b12s and I started recovery. It went slow the first year and picked up speed after I added the adb12. After 3 years I added the carnitine and things really took off. I had been plateaued on the Nordic track at 17 minutes for a year. After the carnitine I was up to 35 minutes in a week and increased the tension. I think that with some coaching through your b12 problems you could happily be doing arobic exercise in a few months. Really. I'm willing to help you if you are willing to try it.

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