Monthly Archives: December 2006

Understanding and Treating Complex Regional Pain Syndrome


October 2006
Understanding and Treating Complex Regional Pain Syndrome
Devon Schuyler

“We’re lost in the woods here about the causes of complex regional pain syndrome [CRPS], because the definitive trials could cost millions and the NIH is not funding pain research now,” said R. Norman Harden, MD, director of the Center for Pain Studies, Rehabilitation Institute of Chicago.

What to do? The Reflex Sympathetic Dystrophy Syndrome Association estimates that the CRPS affects between 200,000 and 1.2 million Americans. The underlying causes of the syndrome have yet to be defined, and no definitive diagnostic test exists even though CRPS was first described in the late 19th century by the neurologist Silas Weir Mitchell. Mitchell referred to the cluster of symptoms he noticed in some of the Civil War soldiers who were under his care as “causalgia.”1 The soldiers persistently complained of severe, burning pain long after their wounds had healed.2 They also experienced swelling, redness, and temperature fluctuations at the injured site, typically a limb.

More than a century later, in 1994, the International Association for the Study of Pain (IASP) gave the syndrome its official name-complex regional pain syndrome-and developed clinical criteria for diagnosis.3 Confusion about CRPS remains, however, and may be part of a larger shortcoming related to overall pain management. “Physicians know very little about pain in general and even less about CRPS,” said Anne Louise Oaklander, MD, PhD, associate professor of neurology at Harvard Medical School in Boston.

DIAGNOSTIC CRITERIA
CRPS has 4 diagnostic criteria. The first-which is not necessary for diagnosis-is the presence of trauma or a cause of immobilization. Second is continuing pain, allodynia, or hyperalgesia in which the pain is disproportionate to any known inciting event. Third is evidence of edema, changes in skin blood flow, or abnormal sudomotor activity in the region of pain. Fourth is the exclusion of other conditions that would account for the degree of pain and dysfunction.

The IASP further divides CRPS into CRPS I, in which major nerve damage is not present, and CRPS II, in which major nerve damage is present. CRPS II replaces Mitchell’s old term “causalgia,” while CRPS I replaces the term “reflex sympathetic dystrophy,” which was introduced in 1946 by a Boston physician named James Evans.4

At least one neurologist rejects the IASP criteria, specifically for the diagnosis of CRPS I. “You diagnose CRPS I only when there is no medical explanation for the symptoms,” said Jose Ochoa, MD, PhD, professor of neurosurgery and neurology at the Oregon Health and Science University and director of the Neuromuscular Unit at Legacy Good Samaritan Hospital and Medical Center in Portland, Oregon. He said that such a diagnosis of exclusion is illogical. In his view, it means that the clinician simply has failed to diagnose the true cause of pain-whether it be nerve injury, arthritis, phlebitis, hysteria, or malingering.

But most physicians accept the criteria, although it is possible that the definitions could change as clinicians gain a better understanding of the syndrome. “In time, we may recognize half a dozen different kinds of CRPS, not just two,” said Ricardo A. Cruciani, MD, PhD, vice chair of the Department of Pain Medicine and Palliative Care at Beth Israel Medical Center in New York City.

A CLINICAL DIAGNOSIS
Diagnosis of CRPS is clinical, based on the patient’s history and examination findings. “This is a disease that really puts a premium on the clinical diagnostic skills of the neurologist because there is no MRI scan or electromyography study that can make this diagnosis,” said Oaklander.

Neurologists should look for focal signs of nerve injury, such as weakness, loss of pin sensation, reflex changes, or Tinel signs, explained Oaklander. They can check for mechanical allodynia with a light touch and for temperature allodynia using test tubes of warm and cool water. The clinician should also take note of trophic changes to the skin, nails, and hair and look for signs of autonomic disturbance, such as neurogenic edema or the differences in temperature or color in the patient’s limbs.

Thermography or a spot temperature measurement can be used to document vasomotor autonomic disturbances. Changes in perspiration can be assessed by dragging a smooth-handled instrument across the skin of the affected and unaffected side; the instrument will glide more easily over sweaty skin than dry skin.1 The clinician may also note decreased range of motion, weakness, dystonia, tremor and, in some cases, myoclonic activity.1

Bone scans and sympathetic nerve blocks do not aid in diagnosis, but some clinicians will use a 3-phase bone scan to reveal whether CRPS has resulted in osteopenia and use a sympathetic nerve block to determine whether the sympathetic nervous system is involved-which it is in about 20% of cases, according to Cruciani. In addition, Oaklander said that she will occasionally do a somatic nerve block to identify exactly which nerves have been damaged. Radiographs should be used only in cases where an orthopedic problem is suspected to be the cause of the syndrome.

POSSIBLE CAUSES
CRPS is usually triggered by an injury such as a fracture, sprain, crush injury, or penetrating injury. Oaklander pointed out that even something as innocuous as having blood drawn can lead to CRPS, as can undergoing a surgical procedure. “Damage to cutaneous sensory nerves has been shown to be the culprit, but we don’t understand why only very rare patients are left with problems after such routine procedures,” she said.

What exactly goes wrong in CRPS is poorly understood. It has alternatively been explained as a hypersensitization of the CNS, an inflammatory process, and a disorder of the sympathetic nervous system. According to Cruciani, constant pain signals from the periphery may lead to changes in the posterior horn of the spinal cord, such as an increase in the number of N-methyl-d-aspartic acid (NMDA) receptors that bind glutamate, an increase in the number of certain types of sodium channels, or a change in the expression of the calcitonin gene-related peptide. An increase in proinflammatory cytokines also has been identified. “All of these changes at the molecular level may have a correlate in the excitability of the somatosensory cortex,” he said, explaining that plastic changes in this area have been correlated with chronic pain.

One hypothesis is that the pain of CRPS I is caused by undetected nerve injuries. In an effort to identify these injuries, Oaklander undertook a skin biopsy study of 18 adults with CRPS I and 7 osteoarthritic patients with disabling leg pain, swelling, and disuse. “We found anatomical evidence that patients with CRPS I had fewer sensory nerve endings in the epidermis of their painful CRPS-affected area than in nearby control areas,” reported Oaklander.5

It is not clear, however, whether these nerve changes are the cause of CRPS I or a consequence. Harden, who also is associate profes-sor in the Department of Physical Medicine and Rehabilitation at Northwestern University Feinberg School of Medicine, Chicago, argued that the changes are probably a consequence: “The most likely explanation is that these people have this intense vasoconstriction from the disease . . . and this causes a dying back of the nerves,” he said. Oaklander agreed that cause and effect remain unclear but pointed out that her study found no evidence of nerve losses in the control group with other painful injuries.

SOMATIZATION?
One of the biggest controversies in CRPS is the role of the mind. Some experts maintain that CRPS often has a psychogenic cause, such as depression. “Fifty percent of people with chronic pain are depressed,” said Cruciani. It’s unclear, however, whether depression is a cause or a consequence of the syndrome. Sociologic considerations also may play a role, especially if the patient has a financial incentive to be disabled.

“I would say that it is a biomedical disease, a psychological disease, and a sociologic disease,” said Harden. “It is all of those things in every patient; it’s just to be determined in what measure.”

By contrast, Robert J. Schwartzman, MD, chair of Neurology at Drexel University College of Medicine in Philadelphia, remarked that “it’s never, ever psychiatric. When you have severe pain that totally wrecks your life, you’re depressed.”

Oaklander took a slightly different approach, pointing out that if the patient’s chronic pain can be attributed to a psychogenic cause, the condition is not CRPS. She also cautioned neurologists not to attempt to make psychiatric diagnoses. She pointed out that the country’s current disability system discourages patients from recovering. She echoed the idea that there might be economic reasons why patients maintain their disability. However, she said that she did not encounter malingering any more frequently among patients with CRPS than among patients with any other medical condition.

TREATMENT STRATEGIES
Treatment of CRPS usually involves several specialists, all of whom must have expertise in the syndrome. For example, Cruciani, who works at a referral center for patients with CRPS, reports that his team includes neurologists, anesthesiologists, rehabilitation experts, psychiatrists, and a psychologist. “You have to have a team that’s knowledgeable about CRPS and how to treat it,” said Harden. “If you don’t have that kind of team in place, you fail.”

Treatment of CRPS is far from straightforward. The FDA has not approved any pharmacologic or interventional treatments. The most common therapies, however, are medication, physical rehabilitation, and nerve blocks. Some patients also undergo spinal cord stimulation, drug pump implantation, or other surgery.

Medication. Many of the drugs used in CRPS are chosen based on their success in treating other types of neuropathic pain disorders, such as diabetic retinopathy and postherpetic neuralgia.6 For example, opioids, the anticonvulsant gabapentin (Neurontin), and tricyclic antidepressants have not been evaluated for treatment of CRPS but are often used because randomized clinical trials have shown them to be effective in treating other neuropathic conditions.

Although opioids are the gold standard for treating acute pain, their use is highly controversial in CRPS.6 “We know that opioids cause hyperalgesia,” said Harden. “If you have a drug that causes hyperalgesia and a disease that is characterized by hyperalgesia, how logical is it to use that drug in that disease?” Oaklander agreed that it was theoretically possible for opioids to worsen CRPS, but she said that this should not prevent physicians from prescribing opioids for certain patients who have CRPS. She did, however, caution that the lowest effective dose should be used. Some pain specialists advocate the use of methadone for the management of CRPS, according to Cruciani. Another possibility is an opioid in combination with an NMDA antagonist such as memantine (Namenda).

The best-studied treatment for early CRPS is the bisphosphonate drugs. Placebo-controlled studies have shown improvements in active movement and motor function with intranasal calcitonin,7 intravenous clodronate,8 and intravenous alendronate (Fosamax)9; one placebo-controlled study showed no improvement with intranasal calcitonin.10 Clodronate may be the most effective because it acts on several inflammatory mediators.6 However, Oaklander pointed out that bisphosphonates have not been tested for use in chronic CRPS.

Another common treatment for CRPS is systemic corticosteroids. In a study of 23 patients, 30 mg/d of oral prednisone was significantly more effective than placebo was.11 “We use that strategy to break the cycle of pain when a patient goes into a flare,” said Cruciani.

Several studies have looked at topical medications for CRPS. One study found topical dimethyl sulfoxide to be as effective as an oral free radical scavenger.12 Topical lidocaine patch also was effective in an open-label study.13 Experimental medications for CRPS include thalidomide, which has not yet been studied in controlled trials; etanercept (Enbrel); ketanserin; and ketamine. In a highly controversial procedure, Schwartzman sent 31 patients to Germany to be treated with anesthetic doses of ketamine that produce a coma lasting 5 days. Schwartzman reported that 10 of those patients are now cured, including 1 who has been in remission for 9 years. Adverse effects included hallucinations and flashbacks; potential complications include memory loss, pneumonia, blood clots, and stroke. Harden said that most clinicians view the ketamine coma treatment as questionable, but that its true value would remain unknown until randomized controlled trials are performed.

Schwartzman also has developed a 10-day course of intravenous ketamine that is delivered on an outpatient basis. Positive results were achieved in an open-label study.14 He said that he and his team have used the treatment in about 150 outpatients.

Cruciani pointed out that ketamine has been helpful in the treatment of postherpetic neuralgia. He cautioned that the drug has significant adverse effects and that most patients would be unable to tolerate it in doses high enough to control the pain of CRPS.

Physical rehabilitation. Most experts stress the importance of physical rehabilitation, including both physical and occupational therapy. Rehabilitation should be started immediately or as soon as medication has had a chance to relieve the most severe pain.

“The most important thing is physical therapy,” said Cruciani. “Not only do physical therapy and exercise improve CRPS in the affected limb, they also prevent it from migrating to other parts of the body.” Cruciani refers patients with CRPS of the lower extremities to physical therapists and patients with CRPS of the upper extremities to occupational therapists. The goals of physical rehabilitation include minimizing edema, normalizing sensation, promoting normal positioning, and decreasing muscle guarding.15

Nerve blocks. Nerve blocks for CRPS usually contain local anesthetics-either alone or in combination with clonidine, NSAIDs, corticosteroids, bretylium, or guanethidine.16 There are no universally accepted guidelines for the use of lumbar sympathetic or stellate ganglion nerve blocks, and the quality of published reports is generally poor.16 However, some clinicians do use nerve blocks in select cases, especially if pain is severe enough despite treatment with oral medication to interfere with physical or occupational therapy. If a nerve block is effective in decreasing pain, the clinician may want to consider repeating the treatment. However, there is no convincing evidence to support the use of long-term treatment with nerve blocks.16

“Sympathetic nerve blocks can relax the blood vessels and give temporary relief, but meta-analysis shows that there’s no evidence of long-term disease modifying benefits,” said Oaklander, who advised that patients receive only a few.

Spinal cord stimulation. Many experts recommend the use of spinal cord stimulators in CRPS, especially for patients who are responsive to sympathetic blocks.17 Research on the stimulators is far from conclusive, however. In the one randomized trial conducted on spinal cord stimulation for CRPS, patients assigned to spinal cord stimulation plus physical therapy had a significant reduction in pain compared with those assigned to physical therapy alone.18 Harden argues that 1 trial is not enough to go on for clinical decision making. “The study suggests that perhaps spinal cord stimulation works a little bit better than physical therapy alone, but it’s unclear what the nature of the control treatment was.” He said that given the risks and high cost of implanting a surgical device, more studies are needed. “You should not be charging $40,000 for an implanted device like this without more evidence,” he said.

Still, many experts find the devices to be beneficial. “We use a lot of spinal cord stimulation,” said Cruciani. He said that the treatment works well in the limbs but is less effective for pain in the center of the body. In addition, Oaklander said that she often recommends the stimulators but cautioned that they are expensive, invasive devices that do not help all patients. She conceded that more research is needed to determine how the devices work and which patients are most likely to benefit.

Implanted drug pumps. Implanted drug pumps are even less well studied than spinal cord stimulators, with most research consisting of case reports.19 “The implanted pumps that deliver opioids can be useful for someone with pain that responds best to treatment with an opioid but who develops intolerable adverse effects from taking it as a pill,” said Oaklander. “We also consider baclofen pumps for patients with intractable CRPS dystonia that’s too widespread to be treated with botulinum toxin [Botox] . . . so there is a very specific and limited number of patients for whom that might be an appropriate treatment.” Cruciani, by contrast, said that he has many patients on the pumps in his group practice. He pointed out that in addition to opiates, clonidine, baclofen, and bupivacaine independently or in combination could be administered by pumps. He also has treated several patients with ziconotide (Prialt), a new drug that has been advocated for patients whose pain is resistant to opioid therapy or who develop intolerable adverse effects from opioids.

Surgery. A number of surgical approaches have been attempted in an effort to cure CRPS. “The most effective treatment for painful nerve injury is surgery, when indicated,” said Ochoa, such as in the case of surgery to decompress a trapped median nerve, manage a neuroma, or manage a tumor or disk compressing a nerve.

Cruciani agreed that surgery is essential when a clear surgical cause can be found. However, he estimated that only about 10% of CRPS cases can be addressed surgically. “It tends to be the exception more than the rule,” he said. Some surgeons have performed sympathectomy in an effort to resolve pain, but results of published reports are not encouraging. In some cases, the procedure may lead to a worsening of pain.16

PROGNOSIS
Most experts agree that with treatment, most patients can expect their CRPS to improve. “There’s a misconception that personal injury lawyers would like to promulgate, which is that CRPS is lifelong and completely disabling,” said Harden. With proper treatment, patients could get on with their lives, he said. Because patients go into remission as opposed to being cured, patients need to stay active, engage in physical and occupational therapy, and possibly take medication and continue with other treatments that have helped, he added.

Cruciani estimated that with treatment, about 20% of patients go into remission. “Then you have about 40% to 50% of patients who are stabilized. Although they continue to have pain and are uncomfortable, they can function to a certain degree. Then you have 30% for whom it doesn’t matter what you do; they’re miserable.”

Oaklander pointed out that she never sees geriatric patients with CRPS; the average age of most patients is about 40, and the prevalence decreases as patients age. “These kind of epidemiologic data are consistent with a disease that does not last forever,” she said. “It’s one of the things that keeps me optimistic.”

REFERENCES
1. Harden RN, Bruehl SP. Diagnosis of complex regional pain syndrome: signs, symptoms, and new empirically derived diagnostic criteria. Clin J Pain. 2006;22:415-419.
2. Mitchell SW. Injuries of the Nerves and Their Consequences. Philadelphia: JB Lippincott & Co; 1865.
3. Merskey H, Bogduk N, eds. Classification of Chronic Pain: Descriptions of Chronic Pain Syndromes and Definitions of Pain Terms. 2nd ed. Seattle: IASP Press; 1994.
4. Evans JA. Reflex sympathetic dystrophy. Surg Clin North Am. 1946;26:780-790.
5. Oaklander AL, Rissmiller JG, Gelman LB, et al. Evidence of focal small-fiber axonal degeneration in complex regional pain syndrome-I (reflex sympathetic dystrophy). Pain. 2006;120:235-243.
6. Rowbotham MC. Pharmacologic management of complex regional pain syndrome. Clin J Pain. 2006;22:425-429.
7. Gobelet C, Waldburger M, Meier JL. The effect of adding calcitonin to physical treatment on reflex sympathetic dystrophy. Pain. 1992;48:171-175.
8. Varenna M, Zucchi F, Ghiringhelli D, et al. Intravenous clodronate in the treatment of reflex sympathetic dystrophy syndrome. A randomized, double blind, placebo controlled study. J Rheumatol. 2000;27:1477-1483.
9. Adami S, Fossaluzza V, Gatti D, et al. Bisphosphonate therapy of reflex sympathetic dystrophy syndrome. Ann Rheum Dis. 1997;56:201-204.
10. Bickerstaff DR, Kanis JA. The use of nasal calcitonin in the treatment of post-traumatic algodystrophy. Br J Rheumatol. 1991;30:291-294.
11. Christensen K, Jensen EM, Noer I. The reflex dystrophy syndrome response to treatment with systemic corticosteroids. Acta Chir Scand. 1982;148:653-655.
12. Perez RS, Zuurmond WW, Bezemer PD, et al. The treatment of complex regional pain syndrome type I with free radical scavengers: a randomized controlled study. Pain. 2003;102:297-307.
13. Devers A, Galer BS. Topical lidocaine patch relieves a variety of neuropathic pain conditions: an open-label study. Clin J Pain. 2000;16:205-208.
14. Goldberg ME, Domsky R, Scaringe D, et al. Multi-day low dose ketamine infusion for the treatment of complex regional pain syndrome. Pain Physician. 2005;8:175-179.
15. Harden RN, Swan M, King A, et al. Treatment of complex regional pain syndrome: functional restoration. Clin J Pain. 2006;22:420-424.
16. Nelson DV, Stacey BR. Interventional therapies in the management of complex regional pain syndrome. Clin J Pain. 2006;22:438-442.
17. Hord ED, Cohen SP, Cosgrove GR, et al. The predictive value of sympathetic block for the success of spinal cord stimulation. Neurosurgery. 2003;53:626-632.
18. Kemler MA, Barendse GA, van Kleef M, et al. Spinal cord stimulation in patients with chronic reflex sympathetic dystrophy. N Engl J Med. 2000;343:618-624.
19. Kanoff RB. Intraspinal delivery of opiates by an implantable, programmable pump in patients with chronic, intractable pain of nonmalignant origin. J Am Osteopath Assoc. 1994;94:487-493.

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Donated motorized chair gives woman independence

Donated motorized chair gives woman independence

By TIFFANY DE MASTERS
tdemasters@thespectrum.com

ST. GEORGE – After being enslaved by a 60-pound wheelchair, Melissa Williams was given a piece of her independence back when strangers gifted her a motorized chair.

A new cart, costing $5,600, was delivered to Williams’ home a couple of days ago.

Williams, 37, Pasco, Wash., suffers from Reflex Sympathetic Dystrophy, a painful disease which disturbs the sympathetic nervous system and can cause swelling and loss of use of an affected area.
Her legs have been a target of this disease, which has confined her to a wheelchair, crutches or a walker.

“There’s a smile you have when you have independence,” Williams said. “I lost that. It was really wonderful to get that back.”

Jeff Harbach, one of the owners of the local business, David Gabriel Furniture, 1770 E. Red Cliffs Drive, said the chair originally belonged to his mother, Arlene Harbach, who died of brain cancer in 2004.

She was unable to use the chair because her cancer advanced so quickly.

Over the last couple of years, Harbach and his family didn’t know what to do with it.

“We never really felt right about selling it so it just stood around,” Harbach said.

The solution for the chair didn’t come up until a few months ago, when Harbach’s mother-in-law, Linda Urza, told him about Williams.

Urza, Richland, Wash., works at River Stone Dental where Williams has been going for dental work for 15 years.

She has known Williams for five years and has watched her go from a perfectly healthy person to not being able to do anything for herself. She said Williams ended up in a wheelchair. Then she could no longer push it because of the deterioration of muscle in her arms.

“She (Williams) has digressed so rapidly that she can’t use her hands,” Urza said. “I wanted in anyway to ease her burdens.”

Urza offered money to Harbach but after discussing it with his sisters, Harbach said they wanted to give it to Williams.

“We were excited to do it,” he said. “We knew that if we weren’t going to sell it we wanted to give to someone who could use it.”

Urza said everyone had to do something to make this happen.

“Everyone did something so she could have this miracle,” she said.

David Mease, Harbach’s brother-in-law and co-owner in David Gabriel Furniture, was part of helping getting the chair wrapped and finding shipping.

Mease said it was good to let Williams know that there are people in the world who still give.

“The neat thing is how it brings everybody together. It’s touching for all of us,” Mease said. “I’ve never met her, but it’s as if I’ve known her all along.”

Now that Williams has the chair, she has gained parts of her freedom back. Before, she said she had to coordinate with people to come over so they could open her doors and go out to the mailbox.

She said she can now take her service dog for a walk or go to the grocery store around the corner.

“It’s a blessing that there’s people still in the world willing to do that for people and expect nothing in return,” Williams said.

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Gift of wheels



Gift of wheels

Published Friday, December 22nd, 2006
By John Trumbo, Herald staff writer

Melissa Williams received a Christmas gift Thursday that was beyond her wildest expectations.

Two Federal Express employees drove up to her front door in Pasco at 10:45 a.m. and unloaded a new motorized wheelchair that had been shipped overnight from St. George, Utah.

The 200-pound package was a gift from people whose mother acquired it earlier this year. But she died of brain cancer without having used it.

Williams and the wheelchair connected through the good will and initiative of Richland’s Linda Urza, who works in the office of Williams’ dentist.

Urza said she knew about Williams’ debilitating condition, called reflex sympathetic dystrophy, and was surprised how quickly it had advanced. She also knew that her son-in-law in St. George had access to the motorized wheelchair and might be willing to donate it to Williams.

After making several phone calls, the donation was set.

“He said family members decided it would be a blessing to give it as a gift” to a total stranger, she said.

Urza flew to Las Vegas on Nov. 20 to meet family members and take the wheelchair to St. George, where a trucking company was to ship it to the Tri-Cities.

Urza’s son-in-law and son, who owns a furniture store in St. George, arranged through Federal Express to transport the heavy wheelchair at a discounted rate. But the shipping company executives had a better idea — they’d do it for free, and deliver it overnight at no extra charge.

Williams, 37, was aware the gift was on its way, but didn’t expect it to arrive until the day after Christmas.

“It was a total surprise that it came today.” said Williams, who is thrilled to have the battery-powered machine.

“The way I had to get around before was in a 60-pound manual wheelchair like hospitals use,” she said.

But Williams no longer has the strength to push herself in the manual wheelchair, and she has not been able to convince her insurance company to pay for a power chair like the one she received Thursday.

“The insurance company says I already have a wheelchair and they won’t replace it unless it is over 5 years old or totally broken,” she said.

“My doctors have written letters of my medical need (to the insurance company), and they still deny it,” she added.

The new wheelchair, which Urza said still had the $5,600 price tag on it, will allow Williams to be more independent and not have to coordinate her schedule with others when she wants to go somewhere.

“It is absolutely fabulous for my Christmas,” Williams said.

“It’s amazing the generosity other people are willing to do,” she added.

Urza said the way the gift came about amazed her too.

“I mentioned it to one person and it went from there. It was the right people at the right time who were able to make a big difference in her life,” Urza said.

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Imaging could furnish proof of chronic pain


Imaging could furnish proof of chronic pain
Emotional, legal boost for patients
By Carey Goldberg, Globe Staff
December 19, 2006

Researchers foresee a day when people tortured by chronic, unexplained pain will be able to prove that they really hurt — evidence that could help sufferers be taken more seriously and could even lead to better treatments.

Recent studies suggest that prolonged, ongoing pain leaves a signature in the brain that can be detected using advanced imaging techniques. In other work, researchers at Massachusetts General Hospital and elsewhere have found that excruciating nerve damage can be detected in bits of skin the size of a pinhead. And genetic tests may someday prove useful, researchers believe: Certain genes appear to be linked to lower pain thresholds and a tendency to develop chronic pain.

Most of the research remains years from helping patients, but as it comes to fruition, “what it means is that no longer can they say, ‘it’s all in your head,’ ” said Jim Broatch , who leads an advocacy group for people with a specific chronic pain disorder.

Clinical proof of pain could make an enormous difference for patients — emotionally, with unsympathetic relatives and colleagues, and legally, in battles with insurers and employers, researchers say.

And as science uncovers more of the objective signs of pain, that knowledge may help with diagnoses, treatment, perhaps even the development of new drugs, they say.

Late last month, German researchers reported that they had turned up microstructural changes in the brains of people who had suffered for years from lower back pain.

The study of 40 patients, presented at the Radiological Society of North America conference in Chicago, used a type of brain scanning called Diffusion Tensor Imaging, which can detect long-term changes in the nerve pathways in the brain.

The scan identified three areas involved in pain processing that showed signs of heightened activity. It was as though pathways that had started as single-lane roads had been expanded into four-lane superhighways, as more and more signals traveled along them, said researcher Juergen Lutz .

“With these objective and reproducible correlates in brain imaging, chronic pain may no longer be a subjective experience,” Lutz said in a press release.

Other work focuses on the theory that people who have chronic pain might have something wrong with their pain-killing system.

Last month, University of Michigan researchers reported findings that patients with fibromyalgia, a chronic pain disorder, have abnormally low levels of natural opiate-like painkillers in parts of their brains.

The study, presented at a rheumatology conference, “also just validates that these people are in pain,” said researcher Richard E. Harris . “They’re trying to turn on their analgesic system but it’s not enough to reduce the pain.”

Brain imaging of pain is still too experimental for clinical use but that is coming, Harris said. “I’d say it will probably be five or 10 years until we can have a patient walk into a doctor’s office and say, ‘I have pain,’ and the doctor says, ‘I want to refer you out to a specialist who does imaging to verify that or find out where your pain is located,’ ” whether in the brain, spinal cord, or elsewhere, he said.

Proving the presence of pain through genetic testing is probably even further away , Harris and others said. Several studies have established a link between a gene and pain disorders, including one that can affect the jaw; a mutation in that same gene seems to predispose people to low pain-killing opioid activity in the brain and low pain thresholds, published research suggests.

Other work is much further along. At Mass. General, for example, Dr. Anne Louise Oaklander is already measuring “the objective correlates of pain” by counting the numbers of pain-sensing nerve endings in tiny skin samples from patients with unexplained pain. Paradoxically, patients with previously unexplained pain tend to have fewer such endings.

Such skin biopsies allow researchers to diagnose “small fiber neuropathies,” the nerve damage that is sometimes a side effect of diabetes and other diseases. The nerve endings are so tiny that they have been largely invisible, Oaklander said, but skin biopsies are “opening a window into the pain system, allowing us to see when it is damaged.”

Oaklander’s work recently helped a college athlete who suddenly began experiencing an unbearable burning sensation in his palms and on the soles of his feet, according to a paper slated for publication in the February issue of the journal Anesthesia & Analgesia.

Greg Palladino , a lacrosse goalie at Southern New Hampshire University, was on a team trip to Bermuda last year when he began suffering a pain that only submersion in ice would alleviate. It was as though broken glass were running through his veins, he told his doctors.

He returned home and was treated repeatedly at area hospitals for weeks. Despite extensive tests, the doctors were baffled, said Palladino’s father, Steven. Medicine failed to help, and he lost 55 pounds in weeks.

When Oaklander was called in, she did a skin biopsy that showed conclusively that Palladino’s “erythromelalgia” — his red, burning appendages — stemmed from severe damage to small nerve fibers that apparently came on because of an auto immune reaction. For some reason, his body had started attacking its own nerve cells.

The biopsy gave doctors the confidence to put Palladino on enormous doses of steroids to stop the auto immune attack, and he has almost completely recovered, his father said.

Palladino was — in a way — lucky that he had tissue damage that could be detected; many patients, Oaklander said, have very real pain that is caused by undetected problems in their nervous system, afflicting them with “an invisible disability that leaves no traces.”

“It’s a wiring problem,” she said. “It’s like when your oil light on your dashboard goes on, and you think, ‘My car must be low on oil,’ but you pull over and check your oil and it’s fine, and you realize it’s an electrical problem. These are people who have electrical problems in their pain system, and their neurons are firing as much as if they had a broken leg, only their leg is fine.”

For patients with chronic unexplained pain, the lack of physical proof of their suffering compounds the problem, pushing some as far as suicide.

“You feel like you’re malingering, you feel like you’re crazy,” said Mary Beth Ludington , patient representative for Jim Broatch’s group, the Reflex Sympathetic Dystrophy Syndrome Association, which helps people with pain disorder. “I used to feel like a wimp until I was diagnosed. Then it was: ‘Hallelujah! I’m not crazy and I’m not a big wimp! There’s a reason for this, and a name.’ It really validates the suffering that a lot of people go through.”

Carey Goldberg can be reached at goldberg@globe.com.
© Copyright 2006 Globe Newspaper Company.

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Living in constant pain


Living in constant pain

By John Barnhart
Wednesday, December 13, 2006 10:54 AM EST

Ricky Baker lives in constant pain.

“I always was an outside person,” said the 47-year-old Bedford County resident. “I’ve worked all my life, since seven or eight years old. All I knew was work.”

He used to work for the city of Salem as a small engine mechanic. At the same time, he had his own business doing small engine repair, landscaping and mowing.

Now, he can’t work with his hands. Some days, he can’t even get out of bed. He formerly wore a size nine shoe but now wears size 13 shoes because his feet are swollen. He can’t put a boot on because his ankles lock.

He has pain and muscle spasms in his legs and must keep the left leg, which won’t bend at the knee, level with the hip. When he gets around, he needs either a crutch or a wheelchair.

Baker has Complex Regional Pain Syndrome/Reflex Dystrophy Syndrome (CRPS/RSD). According to the RSDS Association, a national organization that focuses on this syndrome, it was first described by a Philadelphia doctor named S. Weir Mitchell. Mitchell had been a surgeon in the federal army during the War Between the States and noticed that some men continued to complain about severe pain long after a wound, typically to the arm or leg, had healed.

Normally, CRPS/RSDS, with its hallmark of continual excruciating pain, occurs after some physical trauma and 15,000 Americans develop it each year. However, according to Jim Broatch, the RSDS Association’s president, nobody knows what causes it. Even a simple injury can trigger it and many can’t think back to a specific incident.

“Even now, we don’t know why some people get it and some don’t,” Broatch said in a phone interview.

Baker can’t remember for sure. He recalls having surgery on his shoulder. The syndrome later started in that shoulder, spread to his neck and the opposite shoulder and eventually spread down his left side to his leg, then to his right leg.

It’s hard for him to focus his thoughts because of the constant pain.

Another feature of the syndrome is hypersensitivity to touch. Baker said that the shower spraying on his legs sometimes makes them feel like they are being set on fire.

It took him 10 years to get his problem properly diagnosed, a tremendously frustrating process. He finally got a diagnosis after doing Internet research and discovering a description of what he was experiencing. He took this to his doctor and the doctor agreed.

The long wait created a problem. Baker said that he had already deteriorated too much.

“The sooner it gets caught, the better off the people are,” Baker said.

Broatch noted that there is no gold standard for diagnosing CRPS/RSDS. He said it’s called a syndrome because it’s a collection of signs and symptoms. This is why it often spreads from the point where it started to other limbs by the time it’s finally diagnosed.

Baker said that the pain first started with bad headaches. At one point, a doctor thought his problem was from pulled muscles in his neck.

As it progressed, his legs began “locking up.” There were times when he would crawl in bed and sleep all night with his legs cramped to his chest. Occasionally, it would go away, only to come back worse than ever. They swelled, were discolored and felt hot all the time.

By 1995, he was unable to work.

“I cried my eyes out,” Baker recalled. “I felt like it was the end of my life.”

Baker sleeps only two or three hours per night. The pain never goes away and sometimes it’s so bad it leaves him sweating and sick. He is constantly on pain medication and has to change medications from time to time because their effectiveness starts decreasing.

“I take over 30 some pills a day,” he said.

Broatch said that CRPS/RSDS is hard to treat.

“Anyone can have trouble getting treatment because there are no medications indicated for this condition,” he said.

According to Broatch, this makes it especially difficult for sufferers who depend on Medicaid to pay for the drug costs.

The pain is so bad and so unrelenting that sufferers sometimes commit suicide. Baker said that he was in Lewis Gale Hospital in Salem at one point and was ready to jump out of a third floor window. Then, he said he saw a Bible, picked it up, hugged it and spent the night hugging it.

“That’s what saved me, the Bible,” he said.

For more information about CRPS/RSDS, go to the RSDS Association’s Web site at www.RSDS.org or call 877-662-7737 toll-free.

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Loss of Consortium – Six Figure Settlement Offer


Loss of Consortium – Six Figure Settlement Offer

Editor: John Bisnar
Firm: Bisnar | Chase
December 11, 2006

Last week in a mediation in San Jose, California, a defendant’s insurance company offered our client a six figure settlement in a legal malpractice claim. Our client alleged that the defendant attorney, while representing his wife and consulting with both he and his wife regarding her claims, negligently failed to advise him of his right to a loss of consortium claim. The claim was eventually lost due to the passage of time. The settlement conference ended without a resolution of the case. The defendant’s attorneys contented that they did not have sufficient authority to pay our client’s settlement demand. At not time did the defendant’s attorneys contend that their client did not commit malpractice.

The legal theory of “Loss of Consortium” is generally the deprivation, in some degree, of the care, comfort, affection, companionship, cooperation, service and/or sexual relations of a spouse due to an accident or injury. Our client’s wife suffered a severe electrical shock from a defective toaster that malfunctioned causing the severe shock. The wife, who is now our client as well, was so severely injured that she is unable to engage in or enjoy, the normal activities of life.

One of the results of the severe electrical shock the wife suffered was contracting Reflex Sympathetic Dystrophy Syndrome (RSD). RSD is a severe, painful, chronic, neurological syndrome also know as Complex Regional Pain Syndrome. RSD is characterized by extreme sensitivity to touch, severe burning pain, pathological changes in bone and skin, excessive sweating and tissue swelling. The wife’s case against the toaster maker (defective product) and the operator of the cafeteria where the toaster (premises liability) was located, is set for trial in January 2007.


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Doctor opens pain center; Wide range of treatments offered in Flint Twp.



Doctor opens pain center; Wide range of treatments offered in Flint Twp. FLINT

TOWNSHIP THE FLINT JOURNAL FIRST EDITION
Wednesday, December 13, 2006

By Shena Abercrombie
sabercrombie@flintjournal.com • 810.766.6307

FLINT TWP. – Dr. Spencer T. Bertram recently joined the Great Lakes Pain Consultants group and opened an office in Flint Township in October.

The office, at 1059 Professional Village Drive, suite E, is one of three pain management centers in the group.

The office is an extension of the Bay City office of Great Lakes Pain Consultants, which is operated by Dr. Theron Grover, said Jean Smeets, a registered nurse who works with Bertram.

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