Fibromyalgia, Pain and What It Means

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Biology 202
2004 Second Web Paper
On Serendip

Fibromyalgia, Pain and What It Means

Erica Graham

Introduction
Fibromyalgia is a musculoskeletal syndrome whose main symptoms consist of chronic pain and fatigue. The pain is generally widespread, but diagnosis is dependent on the existence of 11 of the 18 specifically designated tender points on the body (1), which are generally located at the intersection points of various muscles and tendons (2). A tender point is generally defined to be an area of hyperalgesia, which is another way of saying that a painful stimulus is perceived to be much more painful than it actually is. In the case of those suffering from fibromyalgia, even slight pressure to a tender point or any surrounding area has the capacity to cause intense pain. The fatigue experienced in fibromyalgia is quite similar to that suffered by patients with chronic fatigue syndrome. Therefore, it is the occurrence of excruciating pain given moderate pain experience that distinguishes the two. Although widespread body pain is sometimes a symptom of chronic fatigue syndrome, it tends to be more intense and localized in origin (i.e. tender points) in cases of fibromyalgia. Thus, it is this aspect of the illness on which I will focus.

A Sensory Experience
There are two components of physical pain in humans. The first component is sensory. Our nervous system provides a way in which different parts of the body can recognize and react to pain. Painful information that originates within the nervous system is referred to as noxious stimuli. These noxious stimuli are received by pain receptors, called nocioceptors, which are located in the somatic or visceral tissues of the body. The nocioceptors are either chemical, mechanical or thermal in nature, and they function by transmitting impulses to the rest of the brain, notifying it of the existence of pain (3). This, in theory, will trigger natural responses that will remove the pain over time and permit healing, restoring the body to its natural state of equilibrium, free of pain.

Deficiencies occur when the brain's ability to free the body of pain is lacking or slowed. Intuitively speaking, persistent painful stimuli will not allow the brain sufficient time to respond effectively to the nocioceptive impulses. Thus, as the impulses are created and travel through to the brain, the stimuli build up and consequently amplify the intensity of pain. Neurologically, this idea helps to explain the concept of central sensitization, which occurs when the nocioceptors' response to noxious stimuli is amplified greatly. Under normal circumstances, about one-fifth of nocioceptors are triggered to regulate everyday pain impulses. However, when injury or inflammation of tissue occurs, the majority of them are activated. Therefore, under the influence of prior injury and post-healing, the amplified state of both nocioceptive (i.e. noxious) and non-nocioceptive impulses remains. Hence, continuous pain can result in the sensitization of nocioceptive-specific neurons in the presence of such input. Another type of neuron, called wide dynamic range(WDR) neurons, responds to both painful and painless stimuli. Because both types of impulses are heightened upon tissue injury, the WDR neurons can also be sensitized, thus reducing the individual's threshold for pain, as any stimulus can be treated as a noxious one. This is especially significant with respect to WDR neurons, since their response to noxious stimuli is greater than nocioceptive-specific neurons (3). This process is one proposed cause of chronic pain in fibromyalgia patients, particularly since the locations designated as tender points and the surrounding areas are more prone to minor, almost insignificant, injury (2).

Contributing to the body's (dys)regulation of pain impulses are neurotransmitters. More specifically, people suffering from fibromyalgia generally have much greater quantities of substance P, which is a chemical that excites pain responses in the nervous system and further works to sensitize neurons receiving nocioceptive information (2),(4). In addition, these individuals tend to have lower amounts of serotonin and norepinephrine, both of which play a partial role in the reduction of pain (3),(5).

Determining the origins of chronic pain is a relatively sketchy process, particularly when injury or other easily noticeable factors cease to exist. I think that the notion of setpoints would be put to good use in this circumstance. Because our bodies are used to operating at equilibrium, any and everything they can do to maintain such an equilibrium puts us at ease (4). However, everyone operates at a different equilibrium, and that level for fibromyalgia sufferers is perhaps even lower than the average person's, with respect to pain processing in particular. Given this reasoning, an individual operating at the fibromyalgia pain equilibrium, versus one at "normal" equilibrium, will have an increased number of nocioceptors reporting pain at any given point. This is interesting given the results of a study in which people with the syndrome, upon application of mild pressure to their thumbs, exhibited increased brain activity in twelve areas, whereas control subjects had activity in two (6). Given a specific threshold setpoint for pain, it is rather plausible that the results of this study can be generalized to the wider population of people with fibromyalgia. If our bodies possess a pain setpoint which regulates the minimum number of nocioceptors that are activated at any given point, it follows that given a higher setpoint in a fibromyalgia patient, any noxious stimulus, regardless of severity, would activate a higher number of nocioceptors. This would thus increase the magnitude of the pain signals being sent to the brain, and therefore activate more parts of the brain. As a result, even at rest, there is an increased state of pain response in comparison to that in an individual without chronic pain.

The same logic may apply to the existence of greater amounts of substance P in the system. The setpoint for the substance is higher in suffering patients, and as a result, internal signals that excite its release fire more often. Similarly, if the equilibrium amount of serotonin and norepinephrine are lower, pain impulses will not be inhibited as easily.

A Perceptual Experience
Pain is not only a sensory experience in humans, but a perceptual one as well. Simply put, people feel pain. This feeling of pain is as important as the existence of the pain itself. Like the sensory impulses, awareness of pain, in addition to the subsequent physical and emotional effects that it has on the individual, is contingent upon past experiences with pain, genetic factors and cognitive dispositions. In other words, there are many other factors, both conscious and unconscious, that can affect the intensity and magnitude of the pain impulses and the individual's awareness of them. This concept refers to the gate-control theory of pain, in which a person's thoughts or emotions at the time of pain processing can either reduce or amplify their perception of that pain (2),(3).

I find it is very important to separate the overall pain experience into two separate components. The main reason for this is the I-function. Because the I-function is the part of the brain that consciously experiences, it is rather easy to differentiate between pain exclusive of the I-function and that which is inclusive. Sensory pain being the former, if the same chronic pain were to occur in an individual who possessed a disconnection between the I-function and the parts of the body being affected, which are linked to the rest of the brain, the intensity of the existing pain would be reduced, but rather the awareness of that pain and the emotional consequences that frequently accompany it. Therefore, it goes without saying that pain perception varies on an individual basis. However, in the case of those suffering from fibromyalgia, because the equilibrium threshold for pain is lowered, the conscious experience is greater with respect to the amplitude of the pain, and it is the resulting emotions stemming from this experience that feed into whether that conscious state of pain is consistent, lessened or exacerbated. It seems that people in general experience a feedback loop of emotion when it comes to pain, to the extent that the I-function goes through a process of assessing pain, developing a proportional response/reaction, which in turn may or may not benefit the individual and their perception of what is occurring. This is true even more so in cases of persistent and intense pain.

Observations
I think the concept of chronic pain and pain in general is an interesting one. In gathering information for this topic, I have come to question the true origin of pain. I think that observing that which is happening on a neurobiological level, and the impact that it has, raises a question of where one should look to solve the problem. What exactly is pain if it cannot be felt? I think that the I-function plays a major role in identifying any kind of pain, arguably more so with chronic pain; it is, after all, the I-function that recognizes the pain not just as a continuous stream of impulses but as a problem. I think the gate-control theory would be put to good use, specifically because it seems to account for those cases in which a person can experience serious injury and not feel any pain. If the I-function is preoccupied, or focused elsewhere, the statement, "there is a problem" does not exist in consciousness. I am sure that we all, although maybe not consciously, possess the ability to eliminate the perceptual effects of noxious stimuli. I think that this capability, with respect to chronic pain, could possibly beneficial. However, I do think that our awareness of pain is necessary to the extent that if the idea "there is a serious problem" needs to be available in consciousness for the purposes of medical attention or some equivalent, we can actually act accordingly before extreme damage is done to our bodies. As a result, I believe we are notified of any pain, chronic or otherwise, as a warning to protect ourselves – both our bodies and I-functions included – from existing threats.


References

1) An Overview Of Fibromyalgia , from the Mayo Clinic

2) Understanding Chronic Pain and Fibromyalgia: A Review of Recent Discoveries , from the National Fibromyalgia Association

3)The Neurobiology of Pain , from The National Pain Foundation

4) The Neuroscience and Endocrinology of Fibromyalgia , report from a workshop held at the NIH, from the National Institute of Arthritis and Musculoskeletal and Skin Diseases

5) Fibromyalgia: Not All in Your Head, Newsweek article written on the subject, posted by the National Fibromyalgia Association

6) New Brain Study Finds Fibromyalgia Pain Isn't All in Patients' Heads, from Science Daily


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