Monthly Archives: February 2008

The Childhood RND Educational Foundation


The Childhood RND Educational Foundation was formed to educate health professionals and the lay population about the characteristics and treatment of RND and other amplified musculoskeletal pain syndromes in children.

Amplified Musculoskeletal Pain by any name is intensely painful. It disturbs the life of the child and family and causes intense suffering and disability.

This video follows the pre-diagnosis, diagnosis, and treatment of a young girl with the RSD form of this disorder as well as discussing and showing children with a variety of other Amplified Musculoskeletal Pain syndromes.

This intense exercise program, shown in detail here, has been shown to be successful 92% of the time.

Dr. David Sherry is the Director of Clinical Rheumatology at Children’s Hospital of Philadelphia, and Professor of Pediatrics at the University of Pennsylvania.







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Beating Back the Stigma of Pain Treatment

Beating Back the Stigma of Pain Treatment

Paula Abdul’s Stardom May Help Cut Negative Perceptions About Chronic Pain, Painkiller Use


Paula Abdul arrives at the Lili Claire Foundation 10th annual benefit dinner in Los Angeles on Saturday, Oct. 13, 2007. (Matt Sayles/AP Photo)

If celebrity gossip were the stock market, Paula Abdul’s shares would be on a solid uptick.

Her hit program “American Idol” started Tuesday — with no writers needed — and TVguide.com reports that she’s in talks to sing at the Super Bowl halftime show.


Abdul, who has endured more than her share of bad Hollywood gossip, also has a condition not shared by many fellow celebrities. She’s one of millions of Americans who suffer from chronic pain.

Acknowledging Her Pain

In a 2005 interview, Abdul was straight up with People magazine, confirming that she had taken powerful drugs before — Oxycontin, Vicodin, Soma — but all in an excruciating trial-and-error process to beat her chronic pain.

Abdul claimed to suffer from a condition called Regional Sympathetic Dystrophy, or Complex Regional Pain Syndrome. The condition, she said, started with a cheerleading neck injury that sent her body into a mysterious chain reaction of pain symptoms that spiraled into intolerable pain over decades.

Chronic pain may be mysterious, but it’s not uncommon. About 10 percent of people suffer from pain that lasts longer than a year, according to 2002 statistics from the American Pain Foundation. For people with neuropathy, spinal cord injuries, rheumatoid arthritis and other diseases, chronic pain can last for decades — and sometimes require drugs with side effects that can leave people drowsy, nauseous, or suffering from memory lapses to make life tolerable.

Getting Acceptance

“We don’t want sympathy at all, we just want empathy; we want understanding,” says Mike K. Buckley, 51, a retired firefighter in Massachusetts who suffers from chronic pain.

In the summer of 2002, Buckley pulled a fire hose toward a blaze in full gear. With just one unnatural turn, two discs in the middle of his back bulged into his spinal cord.


This single injury has sent him to the emergency room 20 times in the past four years, every time in a bout of excruciating pain.

Buckley stayed at work for three years, even after a T-bone car accident injured a third disc in his spine, making his chronic pain condition inoperable.

“Oh you’re taking Oxycontin? Are you addicted?” Buckley remembers his fellow firefighters asking. “I used to joke with people: I wished I was just getting high off of this!”

In fact, most chronic pain patients won’t get high with a well-managed dose of opioids like Oxycontin, says Dr. Elliot Krane, professor of anesthesia and pediatrics at Stanford University in Palo Alto, Calif.

“All of us have had patients on grams and grams — rather than milligrams — of morphine or hydropmorphone, for example, who have been very functional,” said Krane, “whereas the same dose would render the opioid-naïve patient comatose.”

Prescription Woes

Prescriptions for opioids took off in the 1980s and 1990s with the realization that short-term painkillers could help chronic pain patients in the long term, says Dr. Joe Shurman, chairman of pain management at Scripps Memorial Hospital in La Jolla, Calif.

Unfortunately, in the late 1990s, the drug Oxycontin left a wake of reports of prescription painkiller overdoses and abuses skyrocketed.

“It gives everybody with pain a bad rap,” said Buckley, whose doctors have tried Vicodin, Oxycontin and epidural injections to fix his pain before finally finding a prescription for methadone, which he says works. Each time a chronic pain patient switches drugs, he or she may take a couple of weeks to adjust to the mental and physical side effects.

“A lot of us just take it to get through the day, and a lot of times the pain wins,” said Buckley.

Buckley had to retire in January of last year after a fall down some stairs, which Buckley says weren’t compliant with the fire code. Though he says he still spends most of his days at a seven on the 1-10 pain scale used by doctors, Buckley may have been lucky that doctors even believed he was in pain.


Convincing Peers and Doctors

“I guess I wasn’t screaming enough; I told them I was in pain, but I guess I should have been yelling at them,” said Janice Dallas, a Type 1 diabetic who suffers from “fire and lightning” pain due to a degenerative nerve disease called neuropathy.

“It started out in ’94 with neuropathy, it wasn’t diagnosed until 2000,” said Dallas. Part of Dallas’ six-year wait for a diagnosis was an odd condition: She felt pain in her trunk, as opposed to the more common areas of hands and feet.

But part of Dallas’ challenge to get diagnosed might have also been doctors’ heightened scrutiny of anything that might resemble drug-seeking behavior.

In response to the rising Oxycontin abuse, the U.S. Drug Enforcement Administration started the official Action Plan to Prevent the Diversion and Abuse of Oxycontin in 2003.

The plan led to high-profile cases of doctors going to jail for prescribing certain opioids. Now doctors are hesitant to prescribe heavy-duty pain killers like Oxycontin. “It’s shifting to being underprescribed,” said Shurman.

But perhaps high profile cases of chronic pain — like Abdul’s — could eventually help normalize the stigma and fear that come along with the proper use of prescribed painkillers.

“Unless you’ve really experienced pain you can’t get rid of, you don’t understand our world,” Buckley said.

Unlike Buckley, Abdul had a chance of ending her world of pain. In her interview with People, Abdul says after more than 25 years of unsuccessful treatments she’s feeling better than ever. According to the Associated Press, Abdul and her doctor report she’s only taking low-side effect medication of Enbrel for arthritis and Pamidronate for complications of her chronic pain.

Buckley still feels supportive of Abdul’s trial in the spotlight.

“When it comes down to it celebrities are people just like us and have to deal with this pain that changes their whole world.”






Click Here For The Original Article Online.

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Disease shock after bunion op

Disease shock after bunion op


A mum only found out she had a muscle wasting disease after going into hospital for a routine foot operation.

X-rays after surgery on Kathleen Metcalfe picked up that she had reflex sympathetic dystrophy (RSD), a malfunction of the nervous system.

The mum-of-one now has to use a wheelchair for long distances and is unable to work after the diagnosis in April last year but is hoping to put the condition “on the map” and speak to other sufferers.
Kathleen, who was told she was one of only a handful of people in the North East to have RSD, said: “I’ve now found out what I used to take for granted.

“I used to just put my coat on and go out the door, but I can’t do that anymore. I can’t walk that much and I need the help of a wheelchair.”

Kathleen, who used to be a cleaner at Sunderland Magistrates’ Court, found that being on her feet all day aggravated a bunion on her left foot.

The pain became so intense that she decided to go ahead with a bunion operation at Sunderland Royal Hospital in February 2007.

But just weeks later she started suffering from constant burning pain in her toes and the bridge of her foot.
Discolouration and swelling also took hold, meaning that Kathleen, of Melrose Crescent, Seaham, was unable to use her foot as she once had.

If her condition reaches the next stage of the illness, the muscle may begin to waste away.
She explained: “I would advise anyone to have the bunion operation as it needs to be done and the surgeon there is superb.

“What happened to me was just unforeseen. Nobody knows what could have caused it as not much is known about RSD. I think I must have a unique foot.”

The results of the X-ray, coupled with Kathleen’s symptoms, led doctors to diagnose reflex sympathetic dystrophy (RSD), which is also known as complex regional pain syndrome (CRPS).

It occurs when the part of the sympathetic nervous system that controls blood flow and sweat glands is disturbed and becomes overactive.

It can be triggered by infection, pressure on a nerve, heart attack, stroke or surgery, but it’s usually brought on by injury.

Kathleen, who is married to Bill and is mum to Leanne, 25, says she would like to speak with other sufferers and perhaps set up a support group.

She said: “I was at a tribunal a couple of weeks ago to do with being refused mobility and the doctor there said that it’s rarely known in the North East. When I heard that, I decided to put it on the map and let people know it exists.”

If anyone wishes to speak to Kathleen about RSD they can contact her on 581 4306.

Click Here For The Original Article Online.

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Norepinephrine-induced nociception and vasoconstrictor hypersensitivity in rats with chronic post-ischemia pain

Norepinephrine-induced nociception and vasoconstrictor hypersensitivity in rats with chronic post-ischemia pain

Dimitris N. Xanthosa, e, Gary J. Bennettb, c, d, e and Terence J. Coderrea, b, c, e, f, Corresponding Author Contact Information, E-mail The Corresponding Author
aDepartment of Psychology, McGill University, Montreal, Que., Canada
bDepartment of Neurology & Neurosurgery, McGill University, Montreal, Que., Canada
cDepartment of Anesthesia, McGill University, Montreal, Que., Canada
dFaculty of Dentistry, McGill University, Montreal, Que., Canada
eCentre for Research on Pain, McGill University, Montreal, Que., Canada
fMcGill University Health Centre Research Institute, McGill University, Montreal, Que., Canada
Received 21 August 2007; revised 9 October 2007; accepted 30 October 2007. Available online 14 January 2008.

Abstract

Painful hypersensitivity to norepinephrine (NE) has been reported in various chronic pain conditions that exhibit sympathetically-maintained pain (SMP), particularly CRPS-I and II. We investigated the parallels between the nociceptive and vascular sensitivity to NE in rats with chronic post-ischemia pain (CPIP), an animal model of CRPS-I induced by hind paw ischemia–reperfusion injury. Intradermal injections of NE to the affected hind paw induced dose-dependent nociceptive behaviours in CPIP rats, but not sham animals. These behaviours were blocked by α1– and α2-adrenergic receptor antagonists, or a nitric oxide (NO) donor. Using laser Doppler flowmetry, we detected vasoconstrictor hypersensitivity in the ipsilateral CPIP hind paw, as compared to responses in sham animals or the contralateral hind paw. The vasoconstrictor hypersensitivity was also attenuated by adrenergic antagonists. Intradermal injection of [Arg8] vasopressin (AVP) or the endothelial NO synthase (eNOS) inhibitor, l-NIO, to the affected paw also induced nociceptive behaviours in CPIP rats, but not sham rats. These results suggest CPIP rats display abnormal nociceptive responses to adrenergic and non-adrenergic vasoconstrictive agents. Furthermore, the nociceptive responses to NE in CPIP rats are paralleled by enhanced vasoconstrictive responses to NE, and are relieved by α-adrenergic antagonists or a vasodilator. We conclude that persistent tissue ischemia and hypersensitivity to sympathetic vasoconstriction are important mechanisms for pain in CPIP rats, and that either reducing vasoconstriction or enhancing vasodilatation may be effective methods of relieving the pain of CRPS-I.


Click Here For The Original Article Online.

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Topical Application of Nitric Oxide Donor Isosorbide Dinitrate…


Topical Application of Nitric Oxide Donor Isosorbide Dinitrate Appears to Improve Symptoms of Complex Regional Pain Syndrome

Complex regional pain syndrome (CRPS) is a disorder that causes

chronic, often severe pain. The syndrome follows a seemingly minor soft tissue injury or fracture.

Up to now, little has been found to help relieve the symptoms patients experience with CRPS: change in tissue blood flow, skin temperature, edema (swelling from fluid), and sweating, among others. Although some analgesics may relieve some pain, some patients do end up having affected limbs amputated.

The authors of this study wanted to see if improving the blood flow to the affected limb would reduce damage that may result in the need for amputation. To do this, researchers recruited five women, average age 49.6 years, to be treated on the affected hand with nitric oxide donor isosorbide dinitrate ointment (ISDN), which would cause dilation (widening) of the blood vessels, allowing for improved blood flow. The ointment was applied four times a day for 10 weeks.

The researchers measured skin temperature, comparing the affected side with the non-affected side, and patients used a weekly diary using the Visual Analog Scale> to rate pain from one to 100, with 100 being the worst possible pain. The pain intensity was assessed with the McGill Pain Questionnaire. Hand and arm strength, and elbow extension were also measured.

At two weeks following the start of the study, the researchers found an increase of approximately 4 degrees Celsius in the affected hand. The muscle force in the elbow remained the same in four patients, but deteriorated in one. Three patients complained of headache during the first two weeks of treatment.

The authors concluded that, although reliability of the study is limited because of the small size (five patients), the treatment does appear to affect body temperature where applied and may prove to be a viable treatment for CRPS.

George Groeneweg, BS, et al. Vasodilative Effect of Isosorbide Dinitrate Ointment in Complex Regional Pain Syndrome Type 1. In Clinical Journal of Pain. January 2008. Vol. 1. No. 24. Pp. 89-92.

Click Here For The Original Article Online.

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Swiss study in mice may lead to new pain drugs




Swiss study in mice may lead to new pain drugs

Wed Jan 16, 2008 2:49pm EST

By Julie Steenhuysen

CHICAGO (Reuters) – Enhancing a natural pain-filtering mechanism in the spine helped relieve chronic pain in mice without the unwanted side effects of current pain relievers, Swiss researchers said on Wednesday.

They honed in on a specific molecule that helps prevent chronic pain signals from reaching the brain, without blocking normal pain messages that alert people to danger.

And they said their experiments in mice may point the way to better drugs in humans.

“Our approach addresses primarily chronic pain,” said Hanns Zeilhofer of the University of Zurich in an e-mail.

He said analgesics such as aspirin can cause stomach ulcers, while opioids such as morphine make patients sleepy and are addictive.

Zielhofer’s idea was to find a way to trick the body into intercepting pain signals before they cause havoc in the brain.

“We know that normally the spinal cord acts as filter for pain signals. It prevents most of the pain signals from reaching the brain, where pain becomes conscious,” said Zeilhofer, whose study appears in the journal Nature.

Zeilhofer’s team focused on a molecule called GABA that that can inhibit pain signals.

A class of drugs called benzodiazepines, which include diazepam — better known as Valium — bolsters the action of this GABA molecule in the central nervous system. The drugs are used to treat things like anxiety and insomnia, but when injected near the spine, these drugs also relieve pain.

“Problem is, they must not be used in chronic pain patients because of undesired effects that they have in the brain,” Zeilhofer said in an e-mail. “They make patients sleepy, they impair memory and can cause addiction.”

But benzodiazepines target at least four different GABA receptors that mediate pain control.

“These receptors turned out to be predominately present in the spinal cord and occur in the brain at much less density,” he said. By targeting just two of the GABA spinal receptors, they might be able to make a drug that could be used for chronic pain without losing potency or making people sleepy.

To test this, the researchers used genetically engineered mice to target only the GABA receptors in the spine. Then they irritated nerves in the paws of mice, making them more sensitive to touch and measured how fast the mice pulled away when gently touched.

“When we treated the mice with the right drugs, their sensitivity to this touch became normal again,” Zeilhofer said. And it worked without unwanted sedation or impaired motor function.

“Normal pain, however, was retained. This is important because normal pain has a protective function as it warns us of tissue damage,” he said.

They also used brain scans on rats to see how the drugs worked in certain pain centers that control both the sensation of pain and the feelings of anxiety that pain can produce. The scans showed the drugs reduced pain in these brain regions.

Zeilhofer said the study showed that targeting specific GABA receptors may provide a promising new target for drug development. “The next big challenge will be to develop drugs which work in humans,” he said.

(Editing by Maggie Fox and Cynthia Osterman)





Click Here For The Original Article Online.







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Relief for Worst RSD May Lie With Ketamine Coma

PAIN MEDICINE
ISSUE: 1/2008 | VOLUME: 34:01

Relief for Worst RSD May Lie With Ketamine Coma
By David Rosenfeld

LAS VEGAS—For the most severe cases of reflex sympathetic dystrophy (RSD), inducing a five-day coma may be the only effective treatment.

The method is akin to rebooting the central nervous systems of patients whose nerve cells have gone haywire. The FDA has yet to approve coma therapy, which is induced by administering large bolus injections of ketamine and midazolam at up to 50 times the normal dose. But that has not stopped U.S. doctors from pioneering the use of a “ketamine coma” in American patients treated at hospitals in Germany and Mexico.

For the better part of four years, Robert Schwartzman, MD, chairman of the Department of Neurology at Drexel University College of Medicine in Philadelphia, and colleagues have been studying the effects of ketamine treatment, including induced comas, in patients with RSD. Their results suggest that the coma therapy may provide long-term and perhaps permanent relief in as many as half of the most severe cases.

Ketamine first won FDA approval in 1970 as an anesthetic. It quickly became known on the street as “Special K,” a powerful hallucinogen similar to LSD and PCP. Clinicians in the United States can legally give the drug to patients with RSD—also known as complex regional pain syndrome (CRPS) type I—who are under conscious sedation. In this group, relief typically lasts no more than six months, Dr. Schwartzman said.

Potent Agent

Ketamine is the most potent clinically available inhibitor of N-methyl-D-aspartate (NMDA) receptors. These receptors permit the transfer of electrical signals between neurons in the brain and the spinal column. Studies support the idea that RSD results from a dynamic change in the physiology and structure of central pain neurons mediated by NMDA receptors. When these receptors malfunction, enzymatic and metabolic cascades occur in pain cells, and the degree of pain is magnified out of proportion to the physical injury causing it.

In a study of infusions of low-dose ketamine (Pain Physician 2005;8:175-179), Dr. Schwartzman and colleagues found that a critical factor in central sensitization seems to be the release of magnesium on the NMDA receptor, with an influx of calcium and the initiation of intracellular cascades. As an NMDA antagonist, ketamine blocks central sensitization. Drugs such as dextromethorphan, amantadine and memantine (Namenda, Forest Pharmaceuticals) also could be used, but they appear to have a low potential for blocking the sensitization process.

Ketamine has long been known to be able to prevent RSD/CRPS following surgery, said Scott Reuben, MD, professor of anesthesiology and pain medicine at Tufts University School of Medicine in Boston and director of pain management at Baystate Medical Center in Springfield, Mass.

“If it [ketamine] can prevent CRPS, the thought was, ‘can we use it to treat it?’ ” said Dr. Reuben, who serves as an adviser to the Mexico study. “This is just the stepping stone. Unfortunately, all we have are case reports and retrospective studies. We need prospective studies.”

Only the Worst Patients

RSD affects between 200,000 and 1.2 million Americans, according to the Reflex Sympathetic Dystrophy Association. The disorder develops without any apparent explanation in 1% to 2% of patients with fractures and in 2% to 5% of patients with peripheral nerve injuries. The RSD group claims that roughly 50,000 new cases develop each year.

For the Mexican and German research, doctors chose patients with the most severe cases of RSD who had tried everything—including blocks and hyperbaric chambers—for their pain.

Frustrated physicians from around the world refer patients to Dr. Schwartzman. “I only see the worst patients,” said Dr. Schwartzman, who took on the challenge of RSD after being unable to cure one of his patients with the condition. “Some have gone through up to 100 doctors.”

Failure in More Than Half

Dr. Schwartzman has sent a total of 38 patients to Germany for treatment with the ketamine coma, which was discovered serendipitously by Ralph-Thomas Kiefer, MD, and Peter Rohr, MD, in Tübingen. The two physicians had induced a coma in a patient with RSD and severe head trauma. When the patient awoke, the pain syndrome had vanished.

The five-day coma is induced with large bolus injections of ketamine (1-1.5 mg/kg) and midazolam (2.5-7.5 mg). The coma is maintained with infusions of ketamine (3-7 mg/kg per hour) and midazolam (0.15-0.3 mg/kg per hour), which are tapered toward the end.

Every patient in whom a coma is induced does well initially, Dr. Schwartzman said, but the pain returns in 55% to 60% of cases. Still, of the 38 patients treated in Germany, at least 12 have had minimal or no pain for more than five years. Three of the 12 required occasional subanesthetic boosters of ketamine.

“We’re blocking the RSD,” Dr. Schwartzman said. “The maintaining thing is still there. If you don’t block the maintaining problem, the same molecular genetic cascade occurs.”

A study of the full ketamine coma in the patients treated in Germany will soon appear in Pain Medicine. Of the 20 patients featured in the study who underwent the therapy, 16 experienced complete remission lasting at least six months. “While the trial suggests improvements in pain reductions,” the researchers concluded, “a randomized controlled study will be necessary to prove its efficacy.”

The coma’s side effects—precipitous weight loss, sleep disruption, anxiety, weakness and the usual complications of critical care medicine—are potentially serious. The bottom line, Dr. Schwartzman said, is that “the procedure has proven to be very safe but clearly has inherent risks.”

South of the Border

A study in Mexico has started, with a protocol similar to that used in the German study; patients are sent to the San José Technological Hospital, which is affiliated with the Tec de Monterrey School of Medicine in Monterrey, Mexico, a few hours’ drive from the Texas border. Patients pay about $20,000 for the treatment, which is not covered by insurance.

Leading the Mexican medical team is Fernando Cantœ Flores, MD, an anesthesiologist and specialist in pain management who was trained at the University of Texas.

The study was originally approved in the United States by the institutional review boards of the University of South Florida and Tampa General Hospital, but the FDA refused to grant an exemption to its international new drug application. Rather than embark on a process that would likely cost $3 million and delay treatment for their patients, the study was moved to Mexico. A review board in Monterrey also approved the study.

So far, eight patients have been treated in Mexico. The main difference from the German study is that pain thresholds are measured with a force gauge. The German study relied on self-reporting.

Low-Dose Conscious Sedation

A less dramatic treatment option for severe cases of RSD is a subanesthetic infusion of low-dose ketamine (10-30 mg per hour titrated according to side effects such as amnesia, blurred vision and vomiting). Dr. Schwartzman has performed close to 200 of these—about one each week for the past four years—at Hahnemann University Hospital in Philadelphia. The treatment costs about $10,000, and insurance companies will not pay for it. Dr. Schwartzman estimated that he performs 95% of all such procedures in the country. He also treats about 10 outpatients per week with lower doses in his clinic.

The infusions succeed in 70% to 80% of cases. But even in the most responsive patients, pain typically returns after approximately six months. A study published in Pain Medicine (2004;5:263-275) found similar results.

A two-hour infusion of low-dose ketamine can also be used to manage RSD or as a booster after treatment with the coma. Pretreatment with 0.2 mg of I.V. glycopyrrolate (the only other drug needed) is administered along with a ketamine drip at 100 mg per hour, supplemented with 5- to 40-mg I.V. bolus injections of ketamine. An average adult will require a total of 400 to 600 mg of ketamine over a two-hour period.

For patients with the most intractable cases of RSD, the full coma treatment may still be the only hope. In a study published online in Pain Medicine in July 2007 (online early article), Dr. Schwartzman and his German colleagues found that an “awake” version of the ketamine infusion at higher doses (50-500 mg per day) over a 10-day period in four patients with extreme RSD did not relieve pain.

Cause for Optimism

Shannon Stocker, MD, an Orlando, Fla., RSD patient, underwent coma therapy in Mexico. Dr. Stocker said the concern she felt about going into the treatment was “overwhelmed by a desire to get better because the pain was so bad it was worth all the risk. The burning pain was constant. But when there was anything like raindrops, it felt like ice picks stabbing me.”

The ketamine coma may be the key to curing other conditions directly related to either RSD or similar nerve dysfunction. As a result of her RSD, Dr. Stocker had skin ulcers all over her arms, which began to clear up while she was still in the coma.

Jim Broatch, executive director of the RSD Syndrome Association, called ketamine therapy “promising” but added that more data are needed. “We’re saying the jury is still out.”

Dr. Schwartzman has now written more than 60 articles on RSD and spoken about the disorder at more than 100 conferences, including the 2007 annual meeting of the American Academy of Pain Management, at which he delivered the keynote address.

The success of the various ketamine protocols has made him optimistic about the prospects for patients with previously intractable RSD. “It’s wonderful to be able to successfully treat someone in severe pain,” he said. “That’s why you go to medical school.”