FIBROMIALGIA TERAPIA
COMBATTERE LA FIBROMIALGIA SCEGLI L'ARGOMENTO CON I TAGS
Una traduzione un po'maccheronica,meglio di nulla......Romy |
Notizia interessantissima dal sito NFA: QUOTE FOR IMMEDIATE RELEASE 4 January 2007 “Fibromyalgia: Show Me Where It Hurts” New Study Links Fibromyalgia to Reduced Brain Dopamine ORANGE, Calif---- 4 January 2007---- The National Fibromyalgia Association today announced that a new study published in the January issue of The Journal of Pain provides new scientific evidence demonstrating for the first time that there is a fundamental difference between the brains of fibromyalgia patients and healthy individuals not afflicted with the disorder. The study’s lead author, Dr. Patrick Wood, is a nationally recognized researcher and authority on the cause and treatment of fibromyalgia. This groundbreaking study supports Dr Wood’s “Dopamine Theory of Fibromyalgia,” which proposes that people with fibromyalgia produce less dopamine—a natural chemical in the body that functions as a neurotransmitter—in the very areas of the brain where dopamine is needed to process painful bodily sensations. The reduction in the activity of dopamine neurons, believed to result from a combination of environmental factors, including chronic stress, as well as genetic factors, serves as the strongest evidence yet that dopamine-related issues may be the root cause of fibromyalgia. “This study provides a whole new perspective on the pathology of fibromyalgia symptoms,” says Wood. STUDY The research study used positron emission tomography (PET) to compare the capacity of fibromyalgia patients to synthesize brain dopamine in comparison with healthy controls. A total of seven female fibromyalgia patients and eight healthy controls were recruited for the study at Louisiana State University Health Sciences Center, where Dr. Wood serves as assistant professor and directs both the Fibromyalgia Research Program and the Fibromyalgia Care Clinic. The results of the study demonstrate that patients with fibromyalgia have significantly reduced dopamine synthesis in multiple brain regions. “It’s all in your head!” For years, people with fibromyalgia have been told that their illness and symptoms were imaginary, or “all in their heads!” Indeed, fibromyalgia has divided the medical community on the subject of its legitimacy due in large part to the lack of a known cause or genetic markers,. According to the National Fibromyalgia Association, an estimated 10 million Americans are affected by the disorder. Genetic factors and exposure to chronic stress have been increasingly suspected as key factors associated with fibromyalgia. Treatment typically focuses on addressing fibromyalgia symptoms, which include widespread pain, fatigue and sleep disturbance. “One of the reasons fibromyalgia is considered so controversial is because we simply don’t know the cause,” explained Dr. Wood. “Our treatment of the symptoms has been sort of a ‘shot in the dark’ because we don’t really understand what it is we are treating.” However, based in the results of this study, there is reason to bring more emphasis on those treatments that may affect brain dopamine activity. “In effect,” Wood said, “we may begin to treat the source of the disorder, and not just its symptoms.” “Fibromyalgia: Show Me Where It Hurts” Dr. Wood’s research involving the Dopamine Theory of Fibromyalgia is featured in a recently released film entitled “Fibromyalgia: Show Me Where It Hurts,” which premiered at the National Fibromyalgia Association's 2006 National Patient Conference in March. A trailer of the film can be viewed on the National Fibromyalgia Association’s website: www.FMaware.org. In light of the latest results and the small initial sample size, Dr. Wood and the National Fibromyalgia Association (NFA) are urging further studies to determine the extent to which the lack of dopamine might be associated with the pain and other symptoms that characterize fibromyalgia. "Further research on Dr. Wood’s Dopamine Theory could help answer questions that could directly benefit people with fibromyalgia,” said Lynne Matallana, founder and president of the National Fibromyalgia Association, the largest nonprofit association serving people with fibromyalgia and other chronic pain illnesses. Matallana, who was diagnosed with fibromyalgia in 1995, appears in “Fibromyalgia: Show Me Where It Hurts.” For the complete text of the study, visit: http://journals.elsevierhealth.com/periodicals/yjpai/current ABOUT THE NFA: The National Fibromyalgia Association is a non-profit 501©(3) organization whose mission is to develop and execute programs dedicated to improving the quality of life for people with fibromyalgia by increasing the awareness of the public, media, government and medical communities. The NFA publishes a quarterly magazine, Fibromyalgia AWARE and hosts an award-winning website at www.FMaware.org. ---#---- Media Contact: Corin Walson (714) 921-8850 Email: cwalson@walsonpr.com How to Print this Article National Fibromyalgia Association 2200 N. Glassell St., Suite A, Orange, Ca 92865 Phone: 714-921-0150 Fax: 714-921-6920 |
Mi chiamo Patrizia, sono un'insegnante di Educazione Fisica e fino a 5 anni fa ero in ottima salute. Che dire... dopo vari interventi alle spalle (retaggi di sport agonistico) mi sono ritrovata nell'ottobre 2002 con la Fibromialgia. Mi sono subito chiesta: "MA COS'E'"? Patrizia (Padova), 47 anni - marzo 2004 |
Mi chiamo Paola, la mia storia di FM ha inizio nel dicembre 2002. Paola (Monza), 41 anni - febbraio 2004 |
|
Research on Fibromyalgia Increased 24-hour urinary cortisol excretion in patients with post- traumatic stress disorder and patients with major depression, but not in patients with fibromyalgia.
|
FibroMoves Keeps Her Moving Reprinted from FMOnline Since January 2001, I have been struggling with fibromyalgia. Although this pain syndrome affects all aspects of my life, I have been proactive in dealing with it.
I joined and became an active member of the local fibromyalgia support group. Also I discovered a wonderful program called FibroMoves. This is a warm water aquacize program designed specifically for fibromyalgia suffers. It allows me to exercise, because I can no longer walk even short distances without experiencing pain. The cardio workout helps me keep in shape.
We lost the program at one pool, so I contacted another pool manager and asked her to dedicate an hour per week to us. As she was agreeable, I volunteered to lead the classes until we were able to find an instructor. That didn’t happen, so I have almost finished the training to become a qualified CALA instructor. CALA was flexible so that I could participate within my limitations yet achieve my goal.
We now have a FibroMoves class every day with 33 participants attending classes at three pools. My FibroFriends who attend the sessions say it has a positive effect on their lives, not just physically but emotionally and mentally, too. http://www.fmaware.org/site/News2?page=NewsArticle&id=6084 |
Exercising and In Control Reprinted from FMOnline When I was diagnosed with fibromyalgia in 1997, I had no idea how the disease would progress. I had pain in my hips which eventually moved to neck, legs, feet and arms, and easy movement was quite difficult. Instinctively I knew that I had to “get moving.”
I joined a gym and began working out. I worked mainly on a treadmill, because I found that stretching my leg and hip muscles was crucial. But I realized that wasn’t enough.
This past December I joined Curves. The machines give me an integrated full-body workout and the recovery boards address cardiovascular needs. Besides feeling better, I have lost one dress size and feel more in control of my illness! http://www.fmaware.org/site/News2?page=NewsArticle&id=6088 |
Understanding Chronic Pain and Fibromyalgia: A Review of Recent Discoveries
by Robert M. Bennett MD, FRCP Professor of Medicine, Oregon Health Sciences University
I have seen over 5,000 fibromyalgia patients over the past 20 years; most want to be reassured that their symptoms are the product of a "real disease" rather than figments of a fertile imagination--commonly ascribed to the psychological diagnosis such as somatization, hypochondriasis, or depression. The good news is that contemporary research is hot on the track of unraveling the changes that occur within the nervous system of fibromyalgia patients. The basic message is that fibromyalgia cannot be considered a primarily psychological disorder, but as in many chronic conditions, psychological factors may play a role in who becomes disabled and may even up-regulate the central nervous system changes that are the root cause of the problem.
What is the problem? The problem is: disordered sensory processing.
What is Fibromyalgia? Fibromyalgia is a chronic pain state in which the nerve stimuli causing pain originates mainly in the muscle. Hence the increased pain on movement and the aggravation of fibromyalgia by strenuous exertion.
Pain is a universal experience that serves the vital function of triggering avoidance. A few unfortunate individuals have a congenital absence of pain sensation; they do not fare well due to repeated bodily insults that go unnoticed. As a physician I see patients with an acquired deficiency in the pain sensation (e.g. diabetic neuropathy or neurosyphilis) who develop a severe destructive arthritis--a result of repeated minor joint injuries that are overlooked. Thus pain sensation is a necessary part of being human. Pain sensation is a fact of life. Even the primitive amoeba takes avoiding action in the face of adverse events. In such primitive life forms, pain avoidance is purely reflex action, as they do not have the complexity of a highly developed brain to feel pain in the sense that humans do: (1)The unconscious reflex avoidance reaction that is so rapid that it occurs before the actual awareness of the pain sensation (as in all life forms), (2) the actual experience of the pain sensation (that can only occur in highly complex organisms). This is an important point, as it implies that different parts of the brain are involved in these two consequences of the pain reaction.
Over the last few years a number of important research discoveries have started to clarify the enigma of chronic pain. Many of these new findings have a special relevance to the chronic pain of fibromyalgia. The cardinal symptom of FM is widespread body pain. The cardinal finding is the presence of focal areas of hyperalgesia, the tender points. Tender points imply that the patient has a local area of reduced pain threshold, suggesting a peripheral pathology. In general, tender points occur at muscle tendon junctions, a site where mechanical forces are most likely to cause micro-injuries. Many--but not all--FM patients have tender skin and an overall reduction in pain threshold. These latter observations suggest that some FM patients have a generalized pain amplification state. There has been a recent plethora of experimental studies apposite to the pathophysiological basis of both the peripheral and central aspects of pain.
The Pathophysiological Basis for Chronic Pain The International Association For the Study of Pain (ASP) defines pain as follows: "Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage." This definition explicitly affirms that pain has both a sensory and an affective-evaluative component, and furthermore acknowledges that it may occur in the absence of obvious visceral or peripheral pathology. To fully understand chronic pain, one must integrate the sensory and affective/evaluative elements of the pain experience. It is equally misguided to focus on the psychological aspects of pain, as it is to address only the sensory component and ignore the affective dimensions. However, for the sake of clarity, each of these two constitutive elements will be considered separately.
The Sensory Component Pain is generally envisaged as a cascade of impulses that originates from nocioceptors in somatic or visceral tissues. The impulses travel in peripheral nerves with a first synapse in the dorsal horn and a second synapse in the thalamus, and end up in the cerebral cortex and other supraspinal structures.
This results in an experience of pain and the activation of reflex and later reflective behaviors. These reflex and reflective behaviors are aimed at eliminating further pain. The expectation is that this nocioceptor driven pain will be successfully abolished, allowing healing and a return to a pain-free state. The problem with chronic pain is that the linear relationship between nocioception and pain experience is inappropriate or even absent, and the expected recovery does not occur.
It is a common misconception to view the nervous system as being "hard-wired"; that is, stimulation of a nerve ending (say a needle prick) always produces the same behavioral and affective response. This concept implies that the same intensity of pain stimulus will always elicit the same degree of nerve stimulation and hence the same subjective experience of pain. It is now understood that the concept is wrong. Some 30 years ago, Melzeck and Wall proposed that pain is a complex integration of noxious stimuli, affective traits, and cognitive factors. In other words, the emotional aspects of having a chronic pain state and one's rationalization of the problem may both influence the final experience of pain. Mendell and Wall provided the first experimental evidence that the nervous system was not hard-wired in 1965. They noted that a repetitive stimulation of a peripheral nerve, at sufficient intensity to activate C-fibers, resulted a progressive build-up of the amplitude of the electrical response recorded in the second order dorsal horn neurons. If the system had been hard-wired, each stimulus would have elicited the same response in the second order neuron. They termed this phenomenon "wind-up." It is now appreciated that the phenomenon of wind-up is crucial to understanding the problem of chronic pain via the mechanism of "central sensitization."
Central sensitization refers to an increased activation of second order neurons in the spinal cord, resulting from injury or inflammation-induced activation of peripheral nocioceptors. Sensory input from muscle, as opposed to skin, is a much more potent effector of central sensitization. This may be the clue to the role of muscle pain in the total spectrum of fibromyalgia. A common example of central sensitization is post-herpetic neuralgia. Previous injury to a peripheral nerve leads to an amplification of both nocioceptive and non-nocioceptive impulses. The mechanism responsible for the abnormal perception of non-nocioceptive impulses in post-herpetic neuralgia is an increased excitation of second order nocioceptive neurons in the dorsal horn of the spinal cord. A special example of central pain occurs when there is pathology within the central nervous system. This occurs in a thalamic stroke--severe unilateral pain, often accompanied by strong emotions, that occurs in the absence of any nocioceptive input.
There are two forms of second order spinal neurons involved in central sensitization. (1) Nocioceptive--specific neurons--respond only to nocioceptive stimuli, and (2) Wide dynamic range neurons--respond to both nocioceptive and non-nocioceptive afferent stimuli. Both may be sensitized by nocioceptive stimuli leading to central senitization but wide-dynamic range neurons are generally more intensely sensitized than nocioceptive-specific neurons. Nocioceptive and non-nocioceptive peripheral nerves often converge onto the same wide dynamic range neuron (see figure). Once sensitized by ongoing nocioceptive impulses from peripheral nerves, wide-dynamic range neurons will respond to non-nocioceptive stimuli just as intensely as they did prior to sensitization. This results in sensitizations like a light touch to be experienced as pain (i.e. allodynia). Sensitization of wide-dynamic range neurons by prior pain stimuli provides the pathophysiological foundation for nonnocioceptive pain.
There is emerging evidence that afferent activity from Golgi tendon organs and muscle spindles can be converted into pain signals under the influence of central sensitization. For instance, some patients with strokes and spinal cord injuries develop severe pain on movement. Benc has proposed the term "proprioceptive allodynia" to describe this phenomenon. He describes such individuals as "while not experiencing pain at rest, they develop excruciating burning and tingling, often difficult to describe, that appear only when trying to hold an object, move a limb, stand or walk." Thus everyday muscle activity may cause pain and impair function in some individuals with central sensitization. At a physiological level, pain on movement implies that proprioceptive afferents are projecting onto second order wide-dynamic-range spinal neurons that have been sensitized by previous nocioceptive activity. Thus the central nervous system of subjects who have ongoing pain (e.g. arthritis) or have had previous pain experiences (e.g. post injury pain) may be permanently altered due to changes that can now be understood at the physiological molecular and structural levels. At a clinical level this is seen as persistent pain in survivors of serious illness who experienced high levels of pain during hospitalization, persistent pain after breast surgery, or the occurrence of fibromyalgia after automobile accidents. The reason why the phenomenon of central sensitization only occurs in a minority of individuals is not currently known. At a molecular level, there are many studies demonstrating the important role of excitatory amino acids such as glutamate and neuropeptides such as substance P in the generation of central sensitization. Substance P and CRGP are important neurotransmitters in lowering the threshold of synaptic excitability, which permits the unmasking of normally silent interspinal synapses and the sensitization of second order spinal neurons. Substance P, unlike the excitatory amino acids, can diffuse long distances in the spinal cord and sensitize dorsal horn neurons in spinal segments both above and below the input segment--with resulting pain signal generation from non-nocioceptive afferent activity. Clinically this will lead to an expansion of receptive fields; e.g. the spread of pain from to uninjured areas after an automobile accident.
The Psychological Component It was seen in the preceding section that chronic pain could occur in the absence of ongoing tissue damage--this is an example of the sensory component of pain. It was also noted that one component of pain is a reflex avoidance behavior that can occur before the conscious appreciation of pain. In terms of brain physiology this implies that more primitive parts of the brain contain several discrete nuclei (e.g. the thalamus, cingulate gyrus, hippocampus, amygdyala, and locus ceruleus) that interact to form a functional unit called the limbic system. This is the part of the brain that subserves many reflex phenomena, including the association of sensory input with specific mood states (e.g. pleasure, fear, aversion etc.). These facts form the physiological basis for considering the emotional aspect of pain. Interestingly, the electrical stimulation of the brain during neurosurgical procedure does not induce pain sensations in pain-free subjects. However, in past pain patients it often reawakens previous pain experiences. It is surmised that such stimulation re-activates cortical and subcortical pain circuits that were previously dormant. It is not known whether there is a single cortical structure that subserves pain memory. Currently it appears that different cortical and subcortical structures are involved in the pain experience. For instance, removal of the somatosensory cortex does not abolish chronic pain, but excision of lesions of the anterior cingulated cortex reduces the unpleasantness of pain. The anterior cingulated cortex is involved in the integration of affect cognition and motor response aspects of pain and exhibit increased activity on PET studies of pain patients. Other structures involved in cortical pain processing include the prefrontal cortex (activation of avoidance strategies, diversion of attention and motor inhibition); the amygdala (emotional significance and activation of hypervigilance); and the locus ceruleus (activation of the "fight or flight" response).
All these structures are linked to the medial thalamus, whereas the lateral thalamus is linked to the somatosensory cortex (pain localization). One example of limbic system activation is the hypervigilance that accompanies many chronic pain states, including fibromyalgia.
The emotional component of pain is multifactorial and includes past experiences, genetic factors, generals state of health, the presence of depression and other psychological diagnosis, coping mechanisms, and beliefs and fears surrounding the pain diagnosis. Importantly, thoughts as well as other sensations can influence the sensory pain input to consciousness as well as the emotional coloring of the pain sensation. The term given for this modulation of pain impulses is the "gate control theory of pain." Thus thoughts (beliefs, fears, depression, anxiety, anger, helplessness, etc.), as well as peripherally generated sensations, can both dampen or amplify pain. Indeed, in many chronic pain conditions (that lack any effective therapy for the sensory/pain component), a reduction of pain and the resulting suffering can only be affected by modulating the psychological aspects of pain. As the psychological contribution to pain varies enormously from patient to patient, this approach has to be individualized. However, there are some general principles that are worth noting. There are important consequences of having pain that will not go away (as is the expected experience for most pain in most people). The unsettling realization that the problem may well be life-long generates a varied mix of emotions and behaviors that are often counterproductive to coping with a chronic problem. Many of these changes (which are partly reflex in origin) would be appropriate for dealing with acute self-healing pain events, but become a liability when dealing with chronic pain. The end result of chronic pain is often depressive illness, marital discord, vocational difficulties, chemical dependency, social withdrawal, sleep disorders, increasing fatigue, inappropriate beliefs, and a radical alteration in their previous personality. Varying degrees of functional disability are a common accompaniment of chronic pain states. The reasons for dysfunction are multiple and vary from individual to individual. Pain often monopolizes attention (causing lack of focus on the task at hand). It is usually associated with poor sleep (causing emotional fatigue). Movements may aggravate pain (causing a reluctance to engage in activity). Fear of activity often leads to deconditioning (which predisposes to muscle and tendon injuries and reduced stamina). Pain causes stress, which may result in anxiety, depression, and inappropriate behavior (causing disability due to secondary psychological distress). The modern era of psychological imaging is providing an important new framework for understanding these "emotional" responses. http://www.fmaware.org/site/PageServer?pagename=fibromyalgia_science Fibromyalgia tends to be treated rather dismissively, sometimes with cynical overtones. When I trained in London some 30 years ago, this diagnosis was never mentioned, even though I trained with one of the foremost rheumatologists in the world at the time. In the United States fibromyalgia has become a semi-respectable diagnosis within the last 10 years, but even so it has some critics. The problem for doctors is that fibromyalgia is not a problem that can be understood according to the classic medical model. This is the model that is used in all medical training. It is based on the correlation of specific tissue pathology with distinctive symptoms (e.g. tuberculosis of the lung causing a chronic cough). Elimination of the causative agent (e.g. the tubercule bacillus) cures the disease. This model has led to the most major advances in medicine that we benefit from today. |
|
Inviato da: Izhar Hadyan
il 26/04/2024 alle 03:19
Inviato da: frim
il 25/04/2024 alle 13:08
Inviato da: niel
il 25/04/2024 alle 13:07
Inviato da: jasy
il 25/04/2024 alle 13:06
Inviato da: cara1001
il 23/04/2024 alle 19:02