Monthly Archives: March 2012

People: Olympic Flame to pass through these streets in Weymouth and Portland!


Olympic Flame to pass through these streets in Weymouth and Portland!

By SailGirl | Monday, March 19, 2012, 21:00

Today the Olympic torch relay route has been confirmed.

The Torchbearer street route for Thursday 12 July starts at Salisbury Cathedral and finishes at Weymouth Beach, going through Portesham, Chickerell, Wyke and on to the Weymouth and Portland National Sailing Academy. At around 6.50pm the Olympic Torch will be transferred to a Cornish pilot gig rowed by Weymouth Rowing Club who will row it to Weymouth Beach in time for the evening celebrations!


The torchbearer street route for Friday 13 July starts at 7.05am at Portland Bill and continues through Southwell, Weston, Easton, Fortuneswell,  and on to Weymouth, passing via Buxton Road, Rodwell Road, Rodwell Ave, Spring Road, Cove Street, Cove Rowe, Trinity Road, North Quay to Newstead Road, Westwey Rd, then on to Preston, Osmington, through Winfrith, Wool, Wareham, Corfe, Swanage and through the rest of East Dorset to Bournemouth Beach Front!


Wendy Morrell from Broadstone in Dorset has been chosen by Lloyds TSB to be part of the Olympic Torch Relay, and as ever Dogs for the Disabled assistance dog Udo will be by her side.

Wendy and Udo, a Golden Retriever, will carry the Olympic torch on Friday 13 July between Portland and Bournemouth in the torch relay preceding the opening ceremony of the London 2012 Olympic Games.


In her teenage years Wendy was diagnosed with complex regional pain syndrome (CRPS) – a chronic pain condition that can affect any area of the body. Then following a knee operation she was diagnosed with Algodystrophy, a condition that affects the growth of bone and cartilage.

Despite using a wheelchair to get around, Wendy was not deterred from leading a full and active life. As well as teaching, Wendy learned to fly and to compete at national level in archery. In 1989 when training with the national archery squad with a view to competing at the Barcelona Paralympic Games, Wendy was hit accidently in the head by a discus, resulting in a brain injury.

Wendy explains; “Following 11 months rehabilitation I remember thinking, what now? My ability to concentrate was diminished, my short-term memory affected and epilepsy triggered as a result of the injury.”

But thanks to Dogs for the Disabled Wendy has gone on to live a full and independent life. Before qualifying with Udo two years ago she was partnered with Caesar, her first Dogs for the Disabled assistance dog, a partnership that was sadly to be short lived as Caesar died tragically of cancer. “Both Caesar and now Udo have made a massive difference to my life and thanks to Dogs for the Disabled assistance dogs I have been able to live a full and independent life, something I never imagined I’d regain when I sustained my injury.”

Wendy was fortunate enough to carry the torch in the build up to the Beijing Olympic Games in 2008 and is very excited to do it again for London 2012. “I’m honoured to carry the torch for a second time and represent Dogs for the Disabled assistance dog owners. Just as Caesar passed on the responsibility of helping me regain my confidence and independence to Udo, I will pass on the Olympic torch, helping to complete its journey to London. It gives me tremendous pride to be involved in what should be a great event.”

In addition to being involved in the torch relays, Wendy has advised LOCOG (theLondon Organising Committee of the Olympic Games) since 2007 on disability related issues, in particular access. Both Wendy and Udo travel across the world to speak at conferences and help improve the lives of people with disabilities and impairments.

Dogs for the Disabled is a pioneering charity that trains assistance dogs for adults and children with physical disabilities and families with a child with autism. Since its inception in 1988 the charity has created over 575 life-changing partnerships and it relies entirely on public donations to continue its work.



Click here for the original article online.




People: Cindy Lange-Kubick: RSDS, the devil that won’t kill you

Cindy Lange-Kubick: RSDS, the devil that won’t kill you

Posted: Tuesday, March 27, 2012 9:00 am

Heather Kuhl hugs her daughter, Rose, outside their home in Lincoln. Heather is planning to leave next month for treatment for RSDS in New Jersey. (KRISTIN STREFF/ Lincoln Journal Star)

First, they put the long, thin needle into your spine. The pain is excruciating, but it’s worth it because you have pain already, after all.

You have pain every minute of every day, despite the 13 medications you take and the pack you wear on your hip with the electrodes attached to your legs to zap the worst of it.

You go to bed in pain. You wake up in pain — 4 a.m. Monday — your feet on fire, your legs like someone is stabbing you, over and over.

You want to scream, but you don’t.

You want to give up, but you don’t.

You have Rose, that’s why. The squirming girl you call Monkey, your little redhead with Down syndrome, sleeping in the bedroom you share.

And you have Anthony, your “little man,” driving already, almost grown up.

So even though you have RSDS — reflex sympathetic dystrophy syndrome, better known as Hell — you hold on.

And you look forward to the long needle in that hospital in New Jersey next month.

Because the needle is followed by the infusion of drugs, and that is followed by something no money can buy: hope.

Hope is why Heather Kuhl drove from her childhood home in north Lincoln to Home Depot on Monday to pick up a drill, a donation to add to a silent auction.

The auction is Thursday night at the Tack Room.

“We don’t know what we’re doing,” says Heather, 41. “We have no clue.”

But the money raised will go toward expenses not covered by insurance for her trip to New Jersey — to see the same doctors who gave her three years without pain.

You can see the pain etched on her face as she holds Rose. She has whole-body RSDS. Face, arms, hands, legs.

“Every place but my back.”

You do not want to get RSDS. I’d never heard of the disorder before I visited a Lincoln woman in 2000 whose friends had organized a fundraiser.

“The pain is so intense, you go crazy,” Bunny Stovall told me that day. Like heated knives, slicing into the sole of her injured right foot, then twisting.

I’ve heard more stories since, all of them terrifying.

An accident, an injury, something that causes nerves to be damaged. Instead of recovery, the pain gets worse. Some victims beg for the damaged limb to be amputated. Some wish for death.

For Heather, it started in 1997. She hurt her wrist and shoulder from repetitive motion at work.

The arm swelled, turned purple. It took six months to diagnose. The treatment — sever the sympathetic nerve — made the RSDS better initially and, by 2001, she was well enough to work again, go back to school and study accounting.

“I wanted to make something of myself,” she says. “I came close.”

Two years later, she was in a wheelchair. This time, the pain was everywhere. She begged her family to let her die.

Then she found out about a pain clinic in New Jersey. They inserted the long needle in her spine, the infusion of drugs followed, and she had nearly three years without pain.

The RSDS came back, a few months before she got pregnant with Rose.

She lives with her parents now, in the house where she grew up.

She has lots of doctors. A GP. A pain doctor. A foot doctor. A chiropractor. A psychologist.

The first time she went to see Dr. Maria Prendes Lintel, the psychologist asked her a question.

On a scale of one to 10, where is your hope?

One, Heather answered.

She asked again, a few weeks ago.


Heather holds Rose. It hurts. It hurts to be touched. She wants her children to touch her.

She’s on her way to pick up that drill. Dr. Maria donated some pottery for the auction. Her chiropractor donated a pillow.

She hates to ask for help, Heather says. “I never know what to say.”

Then she thinks about New Jersey. Angel Flight has paid for her plane ticket. Medicaid will pick up 80 percent of the hospital bill.

“I don’t know if it will work this time,” she says. “I don’t know for how long it will work, but if I could have one day without pain …”

You want to help her.

Reach Cindy Lange-Kubick at 402-473-7218 or

Read more:

Click here for the original article online.


People: The champion cyclist, her mysterious excruciating pain and her unconventional road to recovery

The champion cyclist, her mysterious excruciating pain and her unconventional road to recovery

  • From:The Australian 
  • March 24, 2012 12:00AM

Amanda Spratt celebrates her win in this year’s National Road Race Chaampionships. Picture: Colleen Petch Source: The Australian

Lorimer Moseley

Professor Lorimer Moseley, renowned expert and author on the phenomenon of pain. Picture: Randy Larcombe Source:The Australian

SOME people hit the wall when they just can’t take it any more. But Amanda Spratt hit a ditch. Climbing up a steep mountain road in the French Pyrenees, halfway through the gruelling 10-day Tour de l’Aude in 2008, the champion cyclist was determined to ignore the lightning bolts of pain shooting from her lower back down her right leg, which were so excruciating that she couldn’t feel the pedal beneath her foot.

For as long as the 24-year-old had been riding with the Australian Institute of Sport she’d had this gnawing demon as a passenger, and she’d learnt to put up with it. She didn’t want to be seen as being “soft” during training, she didn’t want to miss out on coming to Europe, and most of all she didn’t want to risk being taken off the program. But now the moment had come when she could take it no more, when the pain had become so overwhelming that she ran off the road and into the ditch.

Back in Australia, Spratt and the physiotherapy team at the AIS battled for months to locate the source of her pain. MRIs and nerve conductor studies on her glutes and hamstrings came back saying everything was fine. Eventually, Spratt was diagnosed as suffering Piriformis syndrome, a rare condition in which the sciatic nerve is compressed. The surgery she had to correct it was judged a complete success, but within weeks the pain was back – more searing than ever. “At first people said it was all part of the recovery but what scared me was that I could tell it was actually worse,” she says. “I could have cycled for about two hours with the pain [before the surgery] but now I could only ride about 45 minutes before it became absolutely unbearable.”

As time passed, Spratt’s condition deteriorated further. No matter how hard she worked in the gym, no matter how strong she became elsewhere, any prolonged cycling seemed to send her body into revolt. At night, her sleep was troubled, even with strong medication. By all conventional medical assessments, there was simply no physical reason for her ongoing agony. The sciatic nerve had been fixed. There was no inflammation around the site. And yet somehow she had become the pain-racked cyclist who couldn’t ride anymore.

GPs’ clinics and hospital emergency departments are full of people like Amanda Spratt, seeking relief from ongoing pain that seems to have no medical basis or cause. About one in five Australians is afflicted by chronic pain – defined as daily pain that continues for three months or more after an initial injury or condition has been treated. When pain becomes persistent or never-ending like this, sufferers will inevitably go on a merry-go-round of X-rays, scans, ultrasounds and even exploratory surgery to identify the problem. Sometimes the cause is never found – by some estimates, 20 per cent of cases fit this criterion – but the “mystery” pain persists in an unrelenting form. Then the cycle continues: painkillers, depression and frustration at not being able to function normally or talk about the suffering with family and friends, whose sympathy has often worn thin. Some are sidelined by their employers – if they’re able to continue work at all. Some may even consider suicide.

Are they going mad? Is it all in their heads? Well, no. And yes. The mainstream medical community has certainly abandoned the once-popular shorthand diagnoses of “hysteria” or “hypochondria” for patients suffering chronic pain without an identifiable cause. But the answer to the second question has become far more nuanced – and exciting – following studies using magnetic resonance imaging, which allows researchers to track how the brain responds to real and imagined stimuli. These have demonstrated that pain can indeed be generated “all in your head”.

Stories are often heard about people feeling “phantom pain” in a limb that’s been amputated, but this is just one of the more bizarre manifestations of a real phenomenon in which the brain keeps telling the body to feel pain. Science is now revealing that the adult brain is not the stable, unchanging entity that generations of physicians, surgeons and healers had assumed it to be. Instead, the central nervous system (which includes the brain) boasts the remarkable ability to change and effectively “rewire” itself. Often the trigger is an episode of acute pain, such as migraine, childbirth or a broken bone. If the brain responds to this trauma by rewiring itself – and the medical community is yet to agree on why it may do so in some cases but not in others – chronic pain can be the result. Behaving like a faulty alarm system, it simply refuses to be switched off once the injury or illness has passed, or becomes so sensitive that it can be tripped into agonising high alert by the slightest stimuli; the brush of a sheet on skin, the touch of your lover or child.

This ability of the brain to rewire itself is known as “neuroplasticity”, a phenomenon thrown into the public spotlight in 2007 by Canadian psychiatrist Norman Doidge’s bestseller The Brain That Changes Itself. But if the book has a positive slant – its subtitle promises “stories of personal triumph from the frontiers of brain science” – it also shows how brains can go rogue by transmitting unnecessary pain signals.

This is why a whole new generation of scientists, doctors and therapists are taking the new understanding of neuroplasticity and asking whether it is the beginning of a revolution that can cure patients such as Amanda Spratt, when all else has failed. After all, they ask, if the brain can change itself, surely it must be possible to convince it to change back?

On a picture-perfect morning, Professor Lorimer Moseley – a renowned expert and author on the phenomenon of pain – was camped with friends on the Wollondilly River, south of Sydney. Walking barefoot through the scrub, he felt a “sharper prickling” around his ankle. Flicking his foot, he discounted the slight stinging as the scratch of a twig, and continued down to the riverbank for his swim. The next thing he remembered was waking up in hospital. Doctors told him he was lucky to be alive – he’d been bitten by an eastern brown snake.

Six months later, Moseley was hiking in a national park near Sydney, and again felt a prickling in his leg – but this time he was soon overwhelmed by waves of agony. A companion called an ambulance, fearing he’d been bitten by a snake again, but when he examined Moseley’s leg more closely he realised he’d just been scratched by a twig. “But the thing is, it really hurt,” Moseley recalls. “I had groin pains for about a week later, just as I had for a week after the real snakebite.”

Moseley’s own misadventures neatly illustrate one of his favourite catchphrases: “Nociception” – the reception of danger signals by the nerves of the body – “is neither sufficient nor necessary for pain”. In other words, it is possible for the body to be harmed and for the brain not to generate pain, and, equally, for the body to be safe but for the brain to launch into agonising panic mode because it has misinterpreted some stimuli as an attack. “The traditional approach to pain,” Moseley says, “has been to say that chronic pain is caused by tissue damage – so to treat it, we need to fix it, cut it out or remove the nerve supply to it.

“The other [more recent] approach is to say that we know chronic pain is not caused by chronic tissue damage, so we can’t treat it but we can teach people to manage it better. I think both approaches are indefensible on biological grounds. The better approach is to say that pain occurs because the brain is trying to protect body tissue – and then to gradually train the brain to stop trying to protect that body tissue.”

Christine Dagg, a 36-year-old retail executive with a penchant for extreme endurance sports, broke her thumb in a mountain biking accident in Africa in 2010. After having it set in a Tanzanian hospital, she and her husband, Wayne, flew straight back to their home town of Sydney, where she had surgery. But after days of intense pain, Dagg’s hand surgeon told her she had developed complex regional pain syndrome, or CRPS – and there were no guarantees that it would ever go away. “At times it felt like needles were being stabbed into my hand; other times, as though my hand was literally on fire – and then moments later, like it had been put in the freezer on raw ice. It was so painful, I genuinely wanted my right thumb to be cut off. I just craved a moment’s reprieve from it.”

In the scale of chronic pain severity, CRPS is about the worst you can get, according to Professor Michael Cousins, head of anaesthetics and pain management at Sydney’s Royal North Shore Hospital. He cites the case in 2008 of a young male sufferer who became so desperate that he convinced his surgeon to amputate his leg in a bid to stop the trauma.

By the time she saw Moseley, Dagg was desperate. She’d taken extended leave and been forced to suspend her plans to fall pregnant with the couple’s first child because of the possible side-effects of the powerful drugs she was taking to manage her pain. “The medications for the pain were really wiping me out, but not really stopping it,” she says. “I was having pain block injections through my throat, into my spine, nerve stimulation, physiotherapy, weekly sessions with a psychologist. It was a slow, frustrating process with no progress, week after week, just a continuation of the pain.”

But then one day Moseley presented her with a strange contraption, and suggested she give it a try. It seemed odd, partly because it didn’t beep or whir, or involve needles or anaesthesia or a polysyllabic prescription. Instead, this “mirror box” consisted simply of a cheap mirror mounted on a light, folding board, with separate sections on either side, one for Dagg’s healthy arm and one for the afflicted arm. “I’m definitely not the sort of person who is into alternative medicine,” Dagg laughs. “If someone had told me previously about a mirror box, I would have thought, ‘That’s just too weird.’ But I was prepared to try anything by then.”

So Dagg did as she was told, removing all jewellery and putting her hands into the separate compartments. Focusing on the mirror between the compartments, she could see two “healthy” arms – one real, and one reflected – while her painful one remained hidden. “And I’ll never forget the moment I looked into that mirror and saw two ‘normal’ hands,” she says. “The pain instantly disappeared. What’s more, it absolutely felt like my ‘bad’ hand was doing all the things my healthy hand was doing.”

Although doctors and scientists have been experimenting with them for more than a century, there is not yet a consensus on why mirror boxes work when they do. And there’s the rub. For every person like Dagg, for whom “mirror therapy” has an almost miraculous effect, there are many others who do not get any sustained pain relief at all. “There are many case studies reporting fantastic results [but] only a few are undertaking empirical research on it,” Moseley says. “The best data on it suggest it is most successful for phantom limb pain… [but] it is not a panacea or magic trick that will solve the complex problem of chronic pain.” Moseley suspects mirror therapy has an impact on what is known as the “virtual body map”, a representation held in the brain of what the physical body “looks” and feels like, which can become conflicted after receiving intense or prolonged stimuli. The person suffering phantom limb pains, for example, may have a brain whose virtual body map still has that severed arm or leg “represented” in a traumatised or cramped position. In the absence of any real stimuli from that region, it may attempt to fill in the messages itself, badly. But conversely, if it receives fresh messages that the limb is healthy and mobile again – through a mirror’s reflection – it may begin to redraw its virtual body map.

“Mirror therapy alone is not really accepted practice,” says Moseley, who uses it instead as one part of a sequential therapy he has developed, called “graded motor imagery”. “But it is quickly gaining fans and scoffers. I think both camps should be open-minded about it. The ability of vision to mess with how the brain perceives our body is well established, so a mirror might be a fabulous tool to tap into that.”

Christine Dagg agrees that mirror therapy, as “magical” as it felt, was really only one part of her recovery from CRPS. “The mirror box, and Lorimer’s books, along with the work I did with the physiotherapist and psychologist at the hospital, all helped me understand why I was in pain – and ultimately, that I just didn’t need to be. It was only my brain ‘causing’ the pain, not physical damage. There was therefore no reason for it to continue.”

She cheerfully admits she briefly became “addicted” to her new therapy, prompting her hospital physio to confiscate it at one point. “The reality was, I couldn’t exactly walk around with a mirror box 24 hours a day,” she says, nursing her seven-week-old daughter, Sylvia. “But it was fundamental in giving me the confidence that I could stop the pain signal; that my brain could switch it off. So I just had to keep working [with other brain image therapies] to get it to switch off permanently. And in the meantime, it was great pain relief.”

While still in its early stages, the research and clinical practices being developed by Moseley and his peers at Neuroscience Research Australia has attracted the support of the Australian and New Zealand College of Anaesthetists’ Faculty of Pain Medicine. “Lorimer’s work is very important,” says Associate Professor Milton Cohen, dean of the faculty. “It shows that new neural connections within the extraordinarily complex brain are not only associated with the development of chronic pain, but can also become disconnected or reconnected through therapy that alters perception. The brain is central to the experience of pain, but the brain’s plasticity – its ability to make these new connections – can also be harnessed towards alleviating, but not eliminating, pain.”

Moseley’s techniques may not work for every example of chronic pain but they illustrate the role of working “outside the square”. That is, not trying to find and fix a “broken part” but concentrating on the whole person.

Cyclist Amanda Spratt confesses she was sceptical when her Australian Institute of Sport physios invited Moseley to provide an assessment of her debilitating condition. “Lorimer was very engaging but I have to admit at the time I was thinking, how is any of this going to help me get back on my bike and back to the level I was competing at?” Spratt says. “Normally [in rehab] you’re very focused on getting back in the gym, strengthening the part of the body that’s been injured, or back on the bike.”

But Spratt was desperate. After fruitless months in rehabilitation, by early 2009 she’d fallen into a psychological and emotional spiral that Milton Cohen insists is not just a by-product of chronic pain but also a destructive contributing factor to it that must be addressed if the patient is to recover.

Moseley says Spratt’s case is a good example of how the brain can change and eventually become hyper-vigilant in its determination to protect its owner from something deemed dangerous: “The brain is like an orchestra,” he says. “The longer it plays the same tune, the better is gets at playing it and the less stimulation it needs to trigger the tune. In a chronic pain sufferer like Spratty, who has experienced pain for a long time, the brain can get so good at playing the tune that simply looking at a bike, or at someone else riding a bike, might be enough to trigger pain.”

Professor Michael Cousins, head of pain management at Sydney’s Royal North Shore Hospital, agrees. “A lot of people, including a lot of doctors, still don’t recognise the fundamental difference between acute pain – which I like to call “good” pain, because it warns you that you have a problem and need to get help – and chronic pain. As a result, it just isn’t on the radar, or it’s a very low priority for them. Personally, I don’t think proper pain relief should just be the primary focus of every doctor, I think it should be considered a human right.”

After assessing the struggling cyclist, Moseley discounted any physical cause for her pain. “Given where she was, and who she was, I knew she would already have seen the best the world has to offer in terms of physicians, surgeons and sports physiotherapists.” He suspected Spratt’s virtual body map might be askew, and suggested a simple test in which participants are shown slides of hands or feet in different positions and asked to identify whether they are right or left, while being timed on their responses. His hunch proved correct. “I was terrible at it!” Spratt recalls, admitting her results were the worst of the athletes who sat the test. But there was a glimmer of a breakthrough, too. “I could almost always identify the left foot correctly, but almost never the right. It kind of became obvious to me something was happening in my brain, that it was having difficulty recognising my right side.”

And so she began a whole new type of rehab. Drawing on Moseley’s “graded motor imagery” approach, a series of photos were taken of Spratt on her bike, focusing on her limbs. She began working regularly through those images, to retrain her brain to identify which of her legs was pedalling or in a different position.

Meanwhile, the closest she got to actually riding her cherished bike was repeatedly watching a video of herself winning a race, years earlier, while visualising how her body would feel as it went through those motions. “It was hard to let go of actually cycling at first,” she says. “But I understood that, because I’d had the pain for so long, my brain had got used to the idea that riding means having pain, and I had to retrain it to think differently. I still find it hard to explain that to some people now. They just don’t get how watching a video or slides can help you heal. But I have the evidence in front of me that it did work.”

Pain experts say one of their greatest challenges – given today’s obsession with silver-bullet medical cures – is to convince patients to try simple, slow therapies instead, particularly when those therapies target the mind rather than the body. And for elite athletes like Spratt, primed through years of training to push through the pain barrier, it can be especially challenging. But by 2010, she wasn’t just racing again – she claimed her first European win at the Grand Prix de Beauraing in Belgium. And in January this year, she pulled away from the pack to claim the women’s crown at the Australian National Road Race Championships in Victoria.

Now she is packing for Qatar in preparation for the World Titles in Holland later in the year – and maybe even a place in the cycling team to represent Australia at the London Olympics. “Cycling is still not pain-free and it may never be pain-free,” she says matter-of-factly. “But nothing out there will hurt me as much as I used to feel. The difference now is, the whole experience has made me much smarter. Knowing what I do now has made me much more confident. And that makes me stronger mentally – and more competitive.”

If there is one thing that now unites pain specialists across Australia it’s that chronic pain should be declared a disease in its own right – and Cousins is leading the push. In 2010 he chaired the National Pain Summit, a meeting of more than 130 medical and healthcare organisations in Canberra, which called on the Federal Government to do just that. “There are anatomical changes we can point to which correlate with the degree of pain,” explains Cousins, “and there are also key psychological and environmental changes. Taken together, these all represent a separate disease entity.”

Recognising chronic pain as a disease in its own right would help liberate sufferers from the round of sometimes pointless medical investigations subsidised by the taxpayer, which are often ordered by doctors who hold to the traditional view that pain is only ever a symptom of a physical problem, says Milton Cohen. He and Cousins argue that instead, Australia urgently needs more pain clinics where sufferers can access an array of health professionals, including psychologists, occupational therapists, physiotherapists, rehabilitation counsellors and social workers. Such clinics have proven highly effective at teaching patients how to manage and reduce chronic pain. Currently, however, there is an average 184-day waiting list to get into a publicly funded service in Australia.

Meanwhile, there may be some exciting treatments on the horizon for blocking pain altogether. Several pharmaceutical companies have begun trials with drugs that inhibit a chemical dubbed “nerve growth factor”, which is believed to encourage the profusion of pain receptors around an injury. Others are experimenting with gene therapy, injecting sufferers with genes responsible for stimulating encephalin, a type of natural opiate produced by the body.

Among the more contentious treatments is the use of ketamine, a powerful anaesthetic and illicit drug being trialled for treatment of CPRS in Australia and overseas, most controversially in Germany, where doctors claim to have cured pain sufferers by putting them into induced comas for several days to “reboot” their brains. That level of drug treatment may be too daunting – or risky – for some, and it fails to persuade Lorimer Moseley, who remains committed to the gentler art of brain wrangling, surrounded by his mirror boxes and artificial limbs.

Patients, Moseley says, surprise him all the time. Like the woman with a 25-year history of debilitating lower back pain who turned up at his clinic a few years ago. He conducted a two-hour examination, explaining that her pain was unlikely to be originating in her back but that her brain was playing a “pain tune” of its own. The following week she arrived for her next session. “She looked like a different person,” he recalls. “And she just announced, ‘Well, my pain’s gone.’?” Moseley allowed himself a moment of smugness: another satisfied customer. But then she continued: “After I came to see you last week, I had an appointment with my sister’s psychic. It took me six months to get in to see her and she was brilliant.”

The patient told Moseley the psychic had discerned things about her that “she couldn’t possibly have known”. And then, as she was walking out the door at the end of the session, the psychic had pulled her aside. “She said, ‘Oh, by the way, there is nothing wrong with your back.’ And it has been fine ever since!” Moseley’s team followed the woman’s progress for the next 13 months; she never regressed, happily reporting that she remained pain-free and active.

Moseley shakes his head in wonder for a moment and I ask if experiences such as this make him doubt his own theoretical framework or practical approach. “Oh no, not at all,” he cries, breaking out of the reverie with customary ebullience. “I mean, if that isn’t evidence of the power of the brain, I don’t know what is.”

Click here for the original article online.


Research: How Your Cat Is Making You Crazy

Granted, this article (below) is not about RSDS/CRPS.  Having said that, when we came across it in our research we found it fascinating and potentially ground breaking regarding a myriad of conditions and could potentially offer help in the long run to a lot of individuals so we thought it was important to share it with all of you.

How Your Cat Is Making You Crazy

Jaroslav Flegr is no kook. And yet, for years, he suspected his mind had been taken over by parasites that had invaded his brain. So the prolific biologist took his science-fiction hunch into the lab. What he’s now discovering will startle you. Could tiny organisms carried by house cats be creeping into our brains, causing everything from car wrecks to schizophrenia?

Michal Novotný

NO ONE WOULD accuse Jaroslav Flegr of being a conformist. A self-described “sloppy dresser,” the 53-year-old Czech scientist has the contemplative air of someone habitually lost in thought, and his still-youthful, square-jawed face is framed by frizzy red hair that encircles his head like a ring of fire.

Certainly Flegr’s thinking is jarringly unconventional. Starting in the early 1990s, he began to suspect that a single-celled parasite in the protozoan family was subtly manipulating his personality, causing him to behave in strange, often self-destructive ways. And if it was messing with his mind, he reasoned, it was probably doing the same to others.

The parasite, which is excreted by cats in their feces, is called Toxoplasma gondii (T. gondii or Toxo for short) and is the microbe that causes toxoplasmosis—the reason pregnant women are told to avoid cats’ litter boxes. Since the 1920s, doctors have recognized that a woman who becomes infected during pregnancy can transmit the disease to the fetus, in some cases resulting in severe brain damage or death. T. gondii is also a major threat to people with weakened immunity: in the early days of the AIDS epidemic, before good antiretroviral drugs were developed, it was to blame for the dementia that afflicted many patients at the disease’s end stage. Healthy children and adults, however, usually experience nothing worse than brief flu-like symptoms before quickly fighting off the protozoan, which thereafter lies dormant inside brain cells—or at least that’s the standard medical wisdom.

But if Flegr is right, the “latent” parasite may be quietly tweaking the connections between our neurons, changing our response to frightening situations, our trust in others, how outgoing we are, and even our preference for certain scents. And that’s not all. He also believes that the organism contributes to car crashes, suicides, and mental disorders such as schizophrenia. When you add up all the different ways it can harm us, says Flegr, “Toxoplasma might even kill as many people as malaria, or at least a million people a year.”

An evolutionary biologist at Charles University in Prague, Flegr has pursued this theory for decades in relative obscurity. Because he struggles with English and is not much of a conversationalist even in his native tongue, he rarely travels to scientific conferences. That “may be one of the reasons my theory is not better known,” he says. And, he believes, his views may invite deep-seated opposition. “There is strong psychological resistance to the possibility that human behavior can be influenced by some stupid parasite,” he says. “Nobody likes to feel like a puppet. Reviewers [of my scientific papers] may have been offended.” Another more obvious reason for resistance, of course, is that Flegr’s notions sound an awful lot like fringe science, right up there with UFO sightings and claims of dolphins telepathically communicating with humans.

But after years of being ignored or discounted, Flegr is starting to gain respectability. Psychedelic as his claims may sound, many researchers, including such big names in neuroscience as Stanford’s Robert Sapolsky, think he could well be onto something. Flegr’s “studies are well conducted, and I can see no reason to doubt them,” Sapolsky tells me. Indeed, recent findings from Sapolsky’s lab and British groups suggest that the parasite is capable of extraordinary shenanigans. T. gondii, reports Sapolsky, can turn a rat’s strong innate aversion to cats into an attraction, luring it into the jaws of its No. 1 predator. Even more amazing is how it does this: the organism rewires circuits in parts of the brain that deal with such primal emotions as fear, anxiety, and sexual arousal. “Overall,” says Sapolsky, “this is wild, bizarre neurobiology.” Another academic heavyweight who takes Flegr seriously is the schizophrenia expert E. Fuller Torrey, director of the Stanley Medical Research Institute, in Maryland. “I admire Jaroslav for doing [this research],” he says. “It’s obviously not politically correct, in the sense that not many labs are doing it. He’s done it mostly on his own, with very little support. I think it bears looking at. I find it completely credible.”

What’s more, many experts think T. gondii may be far from the only microscopic puppeteer capable of pulling our strings. “My guess is that there are scads more examples of this going on in mammals, with parasites we’ve never even heard of,” says Sapolsky.

Familiar to most of us, of course, is the rabies virus. On the verge of killing a dog, bat, or other warm-blooded host, it stirs the animal into a rage while simultaneously migrating from the nervous system to the creature’s saliva, ensuring that when the host bites, the virus will live on in a new carrier. But aside from rabies, stories of parasites commandeering the behavior of large-brained mammals are rare. The far more common victims of parasitic mind control—at least the ones we know about—are fish, crustaceans, and legions of insects, according to Janice Moore, a behavioral biologist at Colorado State University. “Flies, ants, caterpillars, wasps, you name it—there are truckloads of them behaving weirdly as a result of parasites,” she says.

Consider Polysphincta gutfreundi, a parasitic wasp that grabs hold of an orb spider and attaches a tiny egg to its belly. A wormlike larva emerges from the egg, and then releases chemicals that prompt the spider to abandon weaving its familiar spiral web and instead spin its silk thread into a special pattern that will hold the cocoon in which the larva matures. The “possessed” spider even crochets a specific geometric design in the net, camouflaging the cocoon from the wasp’s predators.

Flegr himself traces his life’s work to another master of mind control. Almost 30 years ago, as he was reading a book by the British evolutionary biologist Richard Dawkins, Flegr was captivated by a passage describing how a flatworm turns an ant into its slave by invading the ant’s nervous system. A drop in temperature normally causes ants to head underground, but the infected insect instead climbs to the top of a blade of grass and clamps down on it, becoming easy prey for a grazing sheep. “Its mandibles actually become locked in that position, so there’s nothing the ant can do except hang there in the air,” says Flegr. The sheep grazes on the grass and eats the ant; the worm gains entrance into the ungulate’s gut, which is exactly where it needs to be in order to complete—as the Lion King song goes—the circle of life. “It was the first I learned about this kind of manipulation, so it made a big impression on me,” Flegr says.

After he read the book, Flegr began to make a connection that, he readily admits, others might find crazy: his behavior, he noticed, shared similarities with that of the reckless ant. For example, he says, he thought nothing of crossing the street in the middle of dense traffic, “and if cars honked at me, I didn’t jump out of the way.” He also made no effort to hide his scorn for the Communists who ruled Czechoslovakia for most of his early adulthood. “It was very risky to openly speak your mind at that time,” he says. “I was lucky I wasn’t imprisoned.” And during a research stint in eastern Turkey, when the strife-torn region frequently erupted in gunfire, he recalls being “very calm.” In contrast, he says, “my colleagues were terrified. I wondered what was wrong with myself.”

His bewilderment continued until 1990, when he joined the biology faculty of Charles University. As it happened, the 650-year-old institution had long been a world leader in documenting the health effects of T. gondii, as well as developing methods for detecting the parasite. In fact, just as Flegr was arriving, his colleagues were searching for infected individuals on whom to test their improved diagnostic kits, which is how he came to be asked one day to roll up his sleeve and donate blood. He discovered that he had the parasite—and just possibly, he thought, the key to his baffling self-destructive streak.

He delved into T. gondii’s life cycle. After an infected cat defecates, Flegr learned, the parasite is typically picked up from the soil by scavenging or grazing animals—notably rodents, pigs, and cattle—all of which then harbor it in their brain and other body tissues. Humans, on the other hand, are exposed not only by coming into contact with litter boxes, but also, he found, by drinking water contaminated with cat feces, eating unwashed vegetables, or, especially in Europe, by consuming raw or undercooked meat. Hence the French, according to Flegr, with their love of steak prepared saignant—literally, “bleeding”—can have infection rates as high as 55 percent. (Americans will be happy to hear that the parasite resides in far fewer of them, though a still substantial portion: 10 to 20 percent.) Once inside an animal or human host, the parasite then needs to get back into the cat, the only place where it can sexually reproduce—and this is when, Flegr believed, behavioral manipulation might come into play.

The parasite T. gondii, seen here, may be changing connections between our neurones, altering how we act and feel. (Dennis Kunkel Microscropy, Inc./Visuals Unlimited/Corbis Images)

Researchers had already observed a few peculiarities about rodents with T. gondii that bolstered Flegr’s theory. The infected rodents were much more active in running wheels than uninfected rodents were, suggesting that they would be more-attractive targets for cats, which are drawn to fast-moving objects. They also were less wary of predators in exposed spaces. Little, however, was known about how the latent infection might influence humans, because we and other large mammals were widely presumed to be accidental hosts, or, as scientists are fond of putting it, a “dead end” for the parasite. But even if we were never part of the parasite’s life cycle, Flegr reasoned, mammals from mouse to man share the vast majority of their genes, so we might, in a case of mistaken identity, still be vulnerable to manipulations by the parasite.

In the Soviet-stunted economy, animal studies were way beyond Flegr’s research budget. But fortunately for him, 30 to 40 percent of Czechs had the latent form of the disease, so plenty of students were available “to serve as very cheap experimental animals.” He began by giving them and their parasite-free peers standardized personality tests—an inexpensive, if somewhat crude, method of measuring differences between the groups. In addition, he used a computer-based test to assess the reaction times of participants, who were instructed to press a button as soon as a white square popped up anywhere against the dark background of the monitor.

The subjects who tested positive for the parasite had significantly delayed reaction times. Flegr was especially surprised to learn, though, that the protozoan appeared to cause many sex-specific changes in personality. Compared with uninfected men, males who had the parasite were more introverted, suspicious, oblivious to other people’s opinions of them, and inclined to disregard rules. Infected women, on the other hand, presented in exactly the opposite way: they were more outgoing, trusting, image-conscious, and rule-abiding than uninfected women.

The findings were so bizarre that Flegr initially assumed his data must be flawed. So he tested other groups—civilian and military populations. Again, the same results. Then, in search of more corroborating evidence, he brought subjects in for further observation and a battery of tests, in which they were rated by someone ignorant of their infection status. To assess whether participants valued the opinions of others, the rater judged how well dressed they appeared to be. As a measure of gregariousness, participants were asked about the number of friends they’d interacted with over the past two weeks. To test whether they were prone to being suspicious, they were asked, among other things, to drink an unidentified liquid.

The results meshed well with the questionnaire findings. Compared with uninfected people of the same sex, infected men were more likely to wear rumpled old clothes; infected women tended to be more meticulously attired, many showing up for the study in expensive, designer-brand clothing. Infected men tended to have fewer friends, while infected women tended to have more. And when it came to downing the mystery fluid, reports Flegr, “the infected males were much more hesitant than uninfected men. They wanted to know why they had to do it. Would it harm them?” In contrast, the infected women were the most trusting of all subjects. “They just did what they were told,” he says.

Why men and women reacted so differently to the parasite still mystified him. After consulting the psychological literature, he started to suspect that heightened anxiety might be the common denominator underlying their responses. When under emotional strain, he read, women seek solace through social bonding and nurturing. In the lingo of psychologists, they’re inclined to “tend and befriend.” Anxious men, on the other hand, typically respond by withdrawing and becoming hostile or antisocial. Perhaps he was looking at flip sides of the same coin.

Closer inspection of Flegr’s reaction-time results revealed that infected subjects became less attentive and slowed down a minute or so into the test. This suggested to him that Toxoplasma might have an adverse impact on driving, where constant vigilance and fast reflexes are critical. He launched two major epidemiological studies in the Czech Republic, one of men and women in the general population and another of mostly male drivers in the military. Those who tested positive for the parasite, both studies showed, were about two and a half times as likely to be in a traffic accident as their uninfected peers.

WHEN I MET Flegr for the first time, last September, at his office on the third floor of Charles University’s Biological Sciences building, I was expecting something of a wild man. But once you get past the riotous red hair, his style is understated. Thin and slight of build, he’s soft-spoken, precise with his facts, and—true to his Toxo status—clad in old sneakers, faded bell-bottom jeans, and a loose-fitting button-up shirt. As our conversation proceeds, I discover that his latest findings have become—to quote Alice in Wonderland—“curiouser and curiouser,” which may explain why his forehead has the deep ruts of a chronic worrier, or someone perpetually perplexed.

He’s published some data, he tells me, that suggest infected males might have elevated testosterone levels. Possibly for that reason, women shown photos of these men rate them as more masculine than pictures of uninfected men. “I want to investigate this more closely to see if it’s true,” he says. “Also, it could be women find infected men more attractive. That’s something else we hope to test.”

Meanwhile, two Turkish studies have replicated his studies linking Toxoplasma to traffic accidents. With up to one-third of the world infected with the parasite, Flegr now calculates that T. gondii is a likely factor in several hundred thousand road deaths each year. In addition, reanalysis of his personality-questionnaire data revealed that, just like him, many other people who have the latent infection feel intrepid in dangerous situations. “Maybe,” he says, “that’s another reason they get into traffic accidents. They don’t have a normal fear response.”

It’s almost impossible to hear about Flegr’s research without wondering whether you’re infected—especially if, like me, you’re a cat owner, favor very rare meat, and identify even a little bit with your Toxo sex stereotype. So before coming to Prague, I’d gotten tested for the parasite, but I didn’t yet know the results. It seemed a good time to see what his intuition would tell me. “Can you guess from observing someone whether they have the parasite—myself, for example?,” I ask.

“No,” he says, “the parasite’s effects on personality are very subtle.” If, as a woman, you were introverted before being infected, he says, the parasite won’t turn you into a raving extrovert. It might just make you a little less introverted. “I’m very typical of Toxoplasma males,” he continues. “But I don’t know whether my personality traits have anything to do with the infection. It’s impossible to say for any one individual. You usually need about 50 people who are infected and 50 who are not, in order to see a statistically significant difference. The vast majority of people will have no idea they’re infected.”

Still, he concedes, the parasite could be very bad news for a small percentage of people—and not just those who might be at greater risk for car accidents. Many schizophrenia patients show shrinkage in parts of their cerebral cortex, and Flegr thinks the protozoan may be to blame for that. He hands me a recently published paper on the topic that he co-authored with colleagues at Charles University, including a psychiatrist named Jiri Horacek. Twelve of 44 schizophrenia patients who underwent MRI scans, the team found, had reduced gray matter in the brain—and the decrease occurred almost exclusively in those who tested positive for T. gondii. After reading the abstract, I must look stunned, because Flegr smiles and says, “Jiri had the same response. I don’t think he believed it could be true.” When I later speak with Horacek, he admits to having been skeptical about Flegr’s theory at the outset. When they merged the MRI results with the infection data, however, he went from being a doubter to being a believer. “I was amazed at how pronounced the effect was,” he says. “To me that suggests the parasite may trigger schizophrenia in genetically susceptible people.”

Click here for the original article online.


New Technique: Innovative Pain Device Relieves Chronic Pain Without Drugs

We continue to see more and more articles and message board posts about Calmare Therapy.  Here’s the most recent one we found (below).

Please comment at the end of the article if you have tried this therapy or have any information on it.  On the surface it looks extremely promising and we’d like to gather more information for the RSDS/CRPS community on it.

Innovative Pain Device Relieves Chronic Pain Without Drugs


The Calmare scrambler was invented by Giuseppe Marineo, an Italian scientist. “Calmare” means “to ease” or “to soothe” in Italian.

One of the greatest frustrations of patients and healthcare providers alike is dealing with pain, particularly chronic pain. And nowhere is this more apparent than for cancer patients who endured months or years of chemotherapy, and are left with peripheral neuropathy, a chronic pain condition.

Patients who have agonized through chronic pain say an emerging new treatment has improved their lives – without the use of painkilling drugs. “It’s just a miracle”, Michelle Jacobson, a breast cancer survivor, told a Rhode Island television station.

This non-invasive chronic pain solution is called the Calmare Pain Therapy Treatment, which is licensed to Competitive Technologies, Inc. (OTCQX:CTTC.PK ). Calmare uses a biophysical “scrambler” device which transmits low doses of electricity through electrodes on the skin in order to block pain. In essence, the Calmare scrambler “tricks” the brain into thinking there isn’t pain.

Researcher, bioengineer, professor, and founder of the Delta Research & Development center in Rome, Giuseppe Marineo developed the Calmare scrambler. The device was named after the Italian word “calmare”, which means “to ease” or “to soothe”.

The Calmare scrambler is most often used for chemotherapy-induced peripheral neuropathy, which causes sensations of burning, numbness, aching, coldness, itching, and tingling. However, Calmare is also being used to treat other chronic pain conditions, including lower back pain, neck pain, diabetic pain, fibromyalgia, post-surgical pain, RSD (Reflex Sympathetic Dystrophy), and radiating pain.

The Calmare device was approved by the Food and Drug Administration in 2009, but is only available at 16 private pain clinics in the United States, mostly on the east coast. Wounded soldiers and veterans are also receiving Calmare Pain Therapy at the Walter Reed Army Medical Center and nearly a dozen other U.S. military facilities. The Department of Defense is seeking alternative forms of pain management to discourage the overuse of painkillers, which are widely used by injured veteransreturning from Iraq and Afghanistan.

Medical professionals and clinical studies are reporting promising results from Calmare’s drug-free device.

In a clinical study at the University of Wisconsin, researchers found that Calmare scrambler therapy showed measurable results in helping patients with Chemotherapy Induced Pain Neuropathy. “This technology has consistently shown very impressive results in our blind study,” reports Toby Campbell, MD, chief of Palliative Medicine, University of Wisconsin. 

In a pilot trial of the Calmare device, Massey Cancer Center in Richmond, Virginia found a dramatic reduction in CIPN pain with no toxicity side effect. The 2010 study was published in the Journal of Pain and Symptom Management.

The Mayo Clinic is also requesting volunteers in a clinical trial using Calmare scrambler technology to analyze pain associated with post-herpetic neuralgia.

Click here for the original article online.

Info: Is RSD affected by plastic surgery?

We found this post to the American Society for Aesthetic Plastic Surgery’s message board today and thought it was interesting (see below).

Please comment at the end of this post if you’ve had surgery post RSDS/CRPS and if you’ve experienced any complications from that surgery?



Click here to see the original post online.


Legal: Injured Norfolk Southern worker wins $4.5 million jury verdict against railroad

Injured Norfolk Southern worker wins $4.5 million jury verdict against railroad

By Laurence Hammack | The Roanoke Times

A railroad worker who tripped on a cross tie and injured his ankle has been awarded $4.5 million, one of the largest personal injury jury verdicts in recent Roanoke history.

Following a week-long trial in Roanoke Circuit Court, a jury on Friday ordered Norfolk Southern Corp. to pay the amount to Welsh K. Davis, a former conductor and brakeman for the railroad.

The accident happened in 2008, when Davis was walking along the tracks in the materials yard of the Roanoke terminal, said one of his attorneys, Will Moody Jr. of Portsmouth, who tried the case with his partner, Mike Davis.

Welsh was using a remote control device to couple two freight cars to an engine when he tripped on a cross tie, which had been placed about three feet from the tracks and had steel rails stacked on top of it.

Weeds that had grown up around the tie obstructed Davis’ view and contributed to the accident, Moody said. The lawsuit accused the railroad of having an unsafe workplace, in part because of the weeds.

After tripping on the cross tie, Davis stepped in a depression and rolled his ankle. The injury tore a tendon in his right ankle, for which he had two surgeries.

Davis later developed complex regional pain syndrome, a condition that has left him unable to work and in almost constant pain, Moody said.

“He can barely walk, and when he does it’s with a cane,” Moody said today.

An attorney who represented Norfolk Southern could not be reached immediately.

Because railroad workers are not covered by worker’s compensation, on-the-job accidents fall under the Federal Employers Liability Act, which requires proof that the railroad’s negligence caused an injury.

There have been a number of high-dollar verdicts in Roanoke under the law, including $4.7 million in 1993 to a former NS signalman who injured his back. That verdict was later reversed by the Virginia Supreme Court, and the case ended up being settled for an undisclosed amount.

Click here for the original article online.