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By Melanie Fridl Ross

GAINESVILLE, Fla. - The cause of fibromyalgia, a common syndrome characterized by severe fatigue and heightened sensitivity to muscle and tissue pain, has evaded easy explanation. Now University of Florida researchers will use $1.2 million in federal grant money to try to pinpoint the biological basis of the chronic disorder, which primarily afflicts women.

Two five-year studies are planned. In one, scientists will take magnetic resonance images of the brains in patients with fibromyalgia and in those without to determine which regions activate when pain occurs. In the other, patients with fibromyalgia will be evaluated to see how strenuous muscle activity affects their pain. The project is an attempt to clarify how the body processes pain in people with the disorder, said Roland Staud, M.D., director of the Musculoskeletal Pain Research Center at UF and the studies' principal investigator.

"Whereas chronic, widespread pain is very preventable in patients with arthritis or in those with systemic lupus or inflammatory bowel disease, fibromyalgia is assumed to develop over many years, and the question is to understand the mechanisms that lead patients from being just sensitive to pain, dysfunction and suffering," said Staud, also an associate professor of medicine in the division of rheumatology and clinical immunology at UF's College of Medicine.

"We know this is something that happens over time - the evidence that is currently available shows it probably takes years - nevertheless, it's unknown to this day what the decisive factors are. The psychological hallmark of all this is many of these patients are distressed, which is understandable. When you have chronic pain and nobody seems to understand why you have chronic pain, you become distressed and depressed and anxious, and so on."

Fibromyalgia syndrome afflicts up to 30 million people in the United States, mostly women in their 30s and 40s. The often disabling medical condition, characterized by widespread body aches and pains and uncontrollable fatigue, is difficult to treat. It is often accompanied by other problems, such as headaches, sleep disorders, cognitive impairments and an irritable bowel.

Traditional treatments don't adequately manage chronic pain in patients with the disease. Meanwhile, typical blood tests and body imaging fail to reveal the root cause of fibromyalgia's typical symptoms.

"The intrinsic question is what factors drive pain in fibromyalgia?" Staud said. "What makes this pain better, what makes that pain worse? We only have very anecdotal evidence, that is, patients who say 'When I overdo things I have more pain.' The exercise testing we'll use, for example, is a precisely defined activity that may be related to increases in pain. We'll also be able to see whether rest decreases fibromyalgia pain sensations and changes patients' spinal pain processing."

Meanwhile, related research already under way at UF will continue, Staud said. In particular, UF researchers seek to learn more about what triggers fibromyalgia's hallmark symptom: sudden and debilitating pain flares, which frequently interfere with patients' ability to work or enjoy normal day-to-day activities. As part of the study, they will take blood samples, then hunt for abnormalities in chemical messengers in the brain and assess whether proteins known as cytokines, certain metabolic processes, or abnormal immune system functioning play a role in the occurrence of pain flares.

Ultimately, scientists hope to use the findings to identify new treatments for fibromyalgia patients and for other chronic pain sufferers, Staud said.

"Health-care providers would really like to understand the biology of chronic pain," he said. "We're looking particularly at inflammatory mediators that may be related to increases in pain sensation. So I think at the end we hope to better understand how to prevent and treat these pain flares and suffering and disability in this particular patient population."

UF researchers restore spatial deficits caused by stroke in rats

By Sarah Carey GAINESVILLE, Fla. - Building on years of basic science that helped pinpoint a region of the rat brain that affects spatial awareness, University of Florida researchers are now testing the ability of antibodies to restore brain function after a simulated stroke. Scientists studying rats with spatial neglect syndrome - a cognitive disorder associated primarily with stroke in people - found that injections of molecules known as monoclonal antibodies into damaged regions of the animals' brains encouraged existing neurons to sprout new growth, and restored normal spatial perception as assessed by observing behavior over a period of weeks. The National Institute of Mental Health recently awarded Roger Reep, Ph.D., and James Corwin, Ph.D., of Northern Illinois University, a three-year grant renewal totaling $989,000 for their ongoing research. "What we've found is that the regions of the brain in which neglect syndrome occurs in humans have corresponding regions with similar function in rats," said Reep, Ph.D., a professor of physiological sciences with UF's College of Veterinary Medicine and a member of UF's McKnight Brain Institute. "This means we can investigate mechanisms of neural repair, and so there's hope for developing a therapy to promote recovery in humans. That's the key insight." UF scientists used monoclonal antibodies, which interfere with the tendency of a naturally occurring protein to block neuron growth, in the laboratory. Researchers elsewhere already had shown the approach could restore movement in rats with spinal cord injuries. Never before, however, has the antibody, known as IN-1, been studied in relation to spatial neglect syndrome. "In binding to the protein, the antibody keeps the protein's growth-inhibiting characteristics from working as they would naturally in that particular region of the brain following brain injury," said Joe Cheatwood, a graduate student in Reep's laboratory. "Our work is not directly clinical, but is designed to be hopefully translational, in that someone designing a clinical trial in people would be able to know what to expect for cognitive problems such as those seen in our neglect model," he added. It has long been known that people who have suffered a stroke typically lose not just physical function but also spatial awareness - how the world looks and one's relationship to it - because regions on one side of the brain are suddenly dysfunctional, Reep said. These patients have a condition known as hemispatial neglect, a neurological disorder almost always associated with damage to the right side of the brain. Researchers say roughly half of those with a right hemisphere injury, about 25 percent of all victims of major stroke, experience the phenomenon known as neglect syndrome. Every 45 seconds, someone in America has a stroke. About 700,000 Americans will have a stroke this year and more than 167,000 of them will die. Stroke is America's No. 3 killer and one of the leading causes of disability, according to the American Stroke Association. Reep and his colleagues believe that an area of the brain known as the dorsocentral striatum receives and processes information important to attention and spatial perception. For more than 20 years, Reep and Corwin, an associate professor of psychology at Northern Illinois University, have studied the circuitry of the rat brain that corresponds to the human brain's make-up. Of particular interest are the neurological connections from the cerebral cortex to the dorsocentral striatum, a previously unknown network of relationships that are ultimately linked to the brain's ability to perceive space and direct attention, and that has proven crucial for recovery from neglect. During this period, Reep has worked extensively with a rodent model developed with Corwin and fellow McKnight Brain Institute neurologists Kenneth Heilman, M.D., Robert Watson, M.D., and Edward Valenstein, M.D. "We realized over time that the striatum was the location of changes that lead to temporary recovery that can be induced by pharmacological agents," said Reep, whose studies on brain circuitry span a 20-year period, with funding provided primarily through the National Institutes of Health. Reep said it is rewarding to see the longtime efforts of basic science pay off. "What people generally think is that when you have a stroke, youget irrevocable damage, but our question has always been, what kinds of compensatory changes is the rest of the brain capable of making?" Reep said. "If you create the right environment, using, say, stem cells and antibodies, what parts of the brain are capable of repair?" Spontaneous recovery from hemispatial neglect does not occur in rats, and is seldom seen in humans, Reep said, adding that when the human brain is damaged through a stroke, physiological changes occur in surrounding tissue. Reep's team has simulated this effect in rats and diagrammed its findings with sophisticated imaging techniques that use digital superimposition and color coding to visualize the ways in which various neuron connections intermingle. That aspect of the researchers' work was highlighted last year in the journal Brain Research. Reep also presented his findings at the most recent annual meeting of the Society for Neuroscience. "The next step for this work is to combine a stroke model with the use of antibodies and stem cells, in an attempt to create the most favorable conditions for restoration of lost neural connections and behavioral recovery of function," Reep said.