Hope is faith holding out its hand in the dark.  -George Iles

Tuesday, September 29, 2009

Getting to the Roots of Fibromyalgia Pain

Dr. Daniel Clauw is a rheumatologist and professor of anesthesiology and medicine at theUniversity of MichiganMedical School. A study he co-authored in 2002 found that fibromyalgia patients process pain differently from other people.

Q. Fibromyalgia is so hard for most people to understand. How do you explain it?

A. Fibromyalgia is real. But the pain isn’t occurring because of damage or inflammation in muscles and joints. It’s the result of differences in the way the brain and spinal cord process and transmit pain. It’s as if the volume control is turned up on pain.

Q. How so?

A. When I lecture on fibromyalgia, I point out to people that they’ve been sitting for 30 minutes. During that time, nerve endings in the back and buttocks have been firing constantly, sending messages to the spinal cord and the brain that there is pressure in those regions of the body. Since it’s not harmful, the brain sends back messages to ignore it. But if those descending messages aren’t as strong as they should be, a person may feel the pressure as painful, even when it shouldn’t be.

Q. So patients are hypersensitive?

A. A lot of what we’ve learned is that people are at different places on the bell-shaped curve of pain sensitivity. Some of the biggest naysayers contend that fibromyalgia isn’t a discrete disease because its presence or absence depends on where you draw the line on pain sensitivity. But in fact, we judge lots of diseases that way. There is a normal range for blood pressure and blood sugar. Outside that range, if it’s too high or too low, it causes problems.

Q. If there are no objective tests for fibromyalgia, how can you prove that patients are truly processing pain differently?

A. There are three lines of evidence.

In 2002, Richard Gracely and I published a study in Arthritis and Rheumatism that provided the first objective corroboration. We did brain scans on people with and without fibromyalgia while applying carefully calibrated pressure to the thumb. The fibromyalgia patients showed much greater activation in the brain with the same level of pressure. To evoke the same response in people without fibromyalgia, we had to use twice the pressure.

Since then, three other studies have shown hyper-reactivity in parts of the brain that are involved in processing pain. These are the regions that tell us where the pain is and how much of it we’re experiencing — the primary and secondary somatosensory cortices, the thalamus and the posterior part of the insula.

Q. For the sake of argument, couldn’t you make a case that if patients simply believe something is more painful, they will have more activity in these brain regions? After all, thought itself is represented by activity in the brain.

A. Only in part. There have been imaging studies of people under hypnosis, in which patients were tricked into thinking that pain was increased or reduced. You see some changes on brain scans, but not the same widespread hyper-reactivity that you see consistently in fibromyalgia patients.

Q. You said there were three types of evidence. What’s the second?

A. Rick Harris in our group is using a type of brain imaging that allows you to look at the levels of [brain chemicals called] neurotransmitters. We’re particularly interested in glutamate, a neurotransmitter that increases pain transmission. He’s found that levels are higher in the brains of people with fibromyalgia.

At the same time, patients have lower levels of neurotransmitters that reduce pain transmission, including norepinephrine and serotonin. There are 5 to 10 of these substances that turn up the response, and 5 to 10 that turn it down. It’s a yin-yang effect.

One of the other big advances in the fibromyalgia field is the discovery that substance P and nerve growth factor — chemicals that increase pain transmission — are two to three times higher in the spinal fluid of fibromyalgia patients. All these imbalances may be responsible for their hypersensitivity.

Q. Do these screening techniques provide the type of objective tests doctors are looking for?

A. You could use them to confirm a diagnosis, but they’re not specific for fibromyalgia. The same responses are found in other chronic pain states, such as migraine headaches.

Q. That would tend to confirm that fibromyalgia pain is real, not imagined.

A. The other thing that’s sobering is that imaging studies of patients show brain atrophy in regions that are involved in pain processing, suggesting that if you have chronic pain syndromes too long, you get permanent changes in brain structure. Early diagnosis and treatment may be very important.

Q. Do genes contribute to fibromyalgia?

A. That’s the third line of research. It shows that chronic pain is strongly genetic. There have been twin studies in the last year from huge twin registries in Sweden, looking at fraternal and identical twins, raised together or apart. The researchers have then teased out the relative contributions of genes and environment — nature and nurture — and found that 50 percent of the risk of developing chronic pain is genetic and 50 percent is environmental.

But the really cool thing is a 2004 study by Lesley Arnold at the University of Cincinnati. She identified a group of people with fibromyalgia. She then examined their first-degree relatives and found that the relatives were eight times more likely to have fibromyalgia than family members of people without the disease. That’s enormous. If you do exactly the same type of family study on people withrheumatoid arthritis or lupus, the odds of having a first-degree relative with the disease is between two and three times greater, not eight.

Even if family members didn’t have fibromyalgia, they tended to have more pain in general, suggesting that the volume control problem runs in families.

Q. Have specific genes been identified?

A. Four different gene variants are found in higher levels in patients with fibromyalgia, including a variant of the COMT gene. This gene is associated with pain sensitivity in a number of pain conditions. There was just a nice study in Arthritis and Rheumatism showing that in a big database of people with osteoarthritis of the knee, the presence or absence of this gene variant was strongly associated with pain sensitivity, especially in women. The gene is known to be estrogen-sensitive.

Q. If COMT is estrogen-sensitive, could that help explain why women are more likely than men to suffer from fibromyalgia?

A. Possibly, but it would require more research to make that determination.

Q. If 50 percent of the risk for fibromyalgia is genetic and 50 percent is environmental, what are the environmental factors that trigger the disease?

A. Almost any biological stress can trigger pain in people who are predisposed — infections, surgery, car accidents, falls, prolonged stress. There was a really good study last year by a group in the U.K. They looked at a population of 50-year-olds with chronic widespread pain and compared them to a group without. Because of the British national health system, they were able to go back and examine medical records for the same patients from 42 years earlier. At age 8, the patients who later developed fibromyalgia were 1.5 to 2 times more likely than controls to have been in a car accident or to have had prolonged hospitalization.

It’s a cool time to be a pain researcher.

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