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Fatigue, and specifically thinking about what we know from clues of the history of this patient population and what some of the more biochemically-based findings have been fatigue. There is a syndrome here that was characterized by sleep disorder, tender points and fatigue. The definition of fibromyalgia, with widespread pain clearly being the hallmark of this as opposed to local pain, that in fact persisted for some degree of time.

So we have fairly generalized experience and a fairly persistent process and a fairly significant pain. Here depicted in the typical schema of fibromyalgia. So we are dealing with something which is primarily generalized, that seems to have systemic features, that is persistent in nature, that has a threshold to symptomatology which is lower than we consider normal and there is a semi-hierarchy here - based on the original epidemiological reporting around which the tender points became the anchor for the diagnosis - that suggested that that was the most sensitive and specific problem associated with fibromyalgia.

And that as we moved into some of these other symptoms, our specificity dropped considerably. Our sensitivity remained pretty high. That means that many many more people had these symptoms but they didnít necessarily have the tender points.

We have a little bit of background on the epidemiological side. And I think obviously we havenít really brought to the fore what the critical elements are that produce this symptoms complex. But it also lists fairly frequently associated with typical rheumatic disease complaints of joint pain and the associated findings of either myalgias, arthralgias, and the other central nervous system and perhaps renal abnormalities associated with SLE. Itís clearly been reported that these patients have some kind of fibromyalgic symptoms.

In addition, the trigger issue - which is, what is the environmental stimulus that may get this off the ground - has certainly been linked to infectious etiology such as Lyme, HIV, Hep C, Hep V and other infectious agents as well as chronic psychological.

So, where does this get us? This gets us to three systems, or three organ systems that we have to at least begin to understand something about before we can take a handle on understanding fatigue as it relates to this process. First of all, the skeletal muscle system, which is an important future _ to performance - and in the handout that I prepared for this presentation tonight, there is some discussion of how we measure the ability of muscle to contract and relax periodically. And that is through usually a test-retest model which looks not only at a single manual muscle test, such as the 10-point Kendall or a 5-point manual muscle test, how you might be able to perform on an isokinetic apparatus as a test for the ability to relax and contract over time.

The second organ system that we have to think of, of course, is the central nervous system. And this is one of the domains in which multiple behaviors influence our perception of fatigue or conversely, our perception of performance. I will, of course, speak about that a little bit later.

Then the other has to do with the smooth muscle disorders. They are irritable and there is often bowel dysfunction, feeling of cystitis which is aseptic, migraine headaches and orthostatic hypotension suggesting that we have some disorder, or at least some disregulation of that system as well.

So, do these things cause fatigue? Iíd like us of course to think about pain as a symptom because in fact we know that this is a pain amplification symptom, or series of concerns that our patients have and all the data are very suggestive that a pain process is going on which at some level is perceived to be quite in excess of what we find at the impairment level. Not that there 

Iíd like to now take just kind of a slight switch into talking a bit about fatigue. Fatigue as a complaint, in the clinic, is extremely common. It has been reported in the literature that it is between 14-55% of the chief complaints of people seeking medical advice in 2006. Itís one of the most prevalent symptoms. Itís more frequent in women than in men. Usually a diagnosis can be placed on this symptom in either the medical or psychiatric context. So these are malingerers. These are people who have

So, when we think about fatigue we have to think about the various domains that contribute to it. Itís sort of like cognition. There may be a number of things that contribute to it, just as weíve heard from the previous speaker. Mood is clearly one of them. Patients who are depressed and who are anxious essentially report more fatigue. Itís a highly correlated associated finding. Patients with diminished aerobic capacity have clearly decreased ability to perform both their daily tasks and even their desired activities, their avocational and their most favored routines. Clearly strength, local muscle endurance is a critical component for maintaining performance levels, especially desired performance levels. That is both in terms of peak torque and in terms of

The endocrine metabolic issues, the CRH axis and what we consider the stress neuron, clearly has impact in terms of patients perception of fatigue, or conversely, their sense of their ability to perform. When we talk about fatigue the great preponderance of rheumatic disease literature looks at the use of a visual analog scale. Most of the instruments - Ames, Hack and the others - have incorporated in them one or another visual analog scale. These are very insensitive measures and they certainly tell us that

Serotonin may be the link that helps understand the connection between pain and fatigue. It regulates mood, arousal, aggression and sleep, and learning, nociception , nerve growth factors and appetite. And if this is abnormally low then it may be one of the contributing explanations for why pain is up-regulated and not down-regulated in a relatively mild stimulus. The sleep cycle clearly plays a role here and possibly growth hormone. We know that the replacement of growth hormone in those who are hormone

Sleep deprivation, sleep disruption and sleep disorders in many ways have FMS-like signs and symptoms in terms of fatigue and performance at the motor level. And de-conditioned people clearly have more fatigue and sleep abnormalities, linking the sleep cycle abnormality with more fatigue and inability to perform. The autonomic system may play a role here also because of its abnormal response to tilt-table testing and as a result of that, lack of good orthostatic control may result in pooling using venous lakes or venous capacitance vessels and not permitting skeletal muscles to be adequately perfused thereby creating another abnormality for local muscle perfusion that we have to overcome in this population.

As far as the neuroendocrine system is concerned, we clearly have demonstrated in the exercise literature that Cushingís syndrome, hypercortisolism is associated with poor motor performance and also with muscle atrophy. In addition a decrease in lean body mass. That the ACTH response to CRH, which is increased in this, may in fact be an increased stimulus to cortisol. So as a result of that, that may be a contributor to fatigue and poor motor performance. Iíve already mentioned the

So the findings of pain amplification and perception of high level of exertional fatigue often without true muscle weakness, and sleep disruption are probably the three key elements for understanding the role of fatigue in this patient population. Each one of them by themselves is certainly a contributor to poor motor performance and each has been demonstrated to be one of the pillars of abnormalities that we see in the fibromyalgia syndrome.

So in summary, the current schema: yes or no genetic predisposition. Donít know if thatís going to play a major role here. But when we get into an exciting event or an aggravating event that sets off this cascade of central nervous system hyperactivity, with

As many of you know, there is a lot of technical definitions of fatigue but what it comes down to is: what does it mean to the patient. We so often hear reports like "Iím so tired I canít think, read or even talk to anyone." "Iím often so tired I canít sleep." And "sometimes Iím so tired that in order to brush my teeth I have to move my body instead of my toothbrush." Oh, oh. Thereís no laughing. I thought for sure someone would laugh and I would know somebody was awake in the audience. It actually came

I just want to tell you that there has been a change in the rehabilitative approach to managing fatigue. The old model was simply energy conservation. And for a large part of my career thatís how I conceived it, treating people with rheumatic diseases, that they were debilitated, that they have a chronic illness, that they have a limited amount of energy and all we could do for them was help them manage that little bit of energy more effectively so they could have a .. be able to do the things that they want to do. Most of you are familiar with this. This has been around longer than me, I think. The new model is called Fatigue Management

The other part is when the patient identifies that stress is causing the fatigue, then the patient gets that they need to put stress management techniques into place in order to manage that component. That is a little bit more than what we used to