Max
06-20-2008, 04:36 PM
Understanding Chronic Pain and Fibromyalgia:
A Review of Recent Discoveries
by Robert M. Bennett MD, FRCP
Professor of Medicine, Oregon Health Sciences University
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.
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.
I will try to convey to you what we mean by "disordered sensory processing." Even a superficial understanding of this topic will change the way you think about the fibromyalgia problem. Furthermore, recent advances that have been made at the molecular level hold out the promise of more effective treatment for fibromyalgia pain.
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."
http://www.fmaware.org/site/PageServer?pagename=fibromyalgia_science
A Review of Recent Discoveries
by Robert M. Bennett MD, FRCP
Professor of Medicine, Oregon Health Sciences University
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.
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.
I will try to convey to you what we mean by "disordered sensory processing." Even a superficial understanding of this topic will change the way you think about the fibromyalgia problem. Furthermore, recent advances that have been made at the molecular level hold out the promise of more effective treatment for fibromyalgia pain.
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."
http://www.fmaware.org/site/PageServer?pagename=fibromyalgia_science