Monthly Archives: January 2008

An unusual presentation and outcome of complex regional pain syndrome

J Can Chiropr Assoc. 2006 March; 50(1): 20–26.
An unusual presentation and outcome of complex regional pain syndrome: a case report
Heather M Shearer, BA(Hon), DC* and Astrid Trim, BSc, DC, FCCSS(C)**

*Clinical Sciences Resident, Graduate Education and Research, Canadian Memorial Chiropractic College, 6100 Leslie Street, Toronto, Ontario M2H 3J1. Phone 416-482-2340 ext: 287
**Faculty, Canadian Memorial Chiropractic College, Private practice, Mississauga, Ontario
Correspondence may be sent to Dr. Heather M. Shearer at the above address or by e-mail:<!– try{initUnObscureEmail ("e_id2577538", '‘ + reverseAndReplaceString(‘ac.ccmc/ta/reraehsh’, ‘/at/’,’@’) + ‘‘)}catch(e){} //–>
Author responsible for negotiations concerning the manuscript.
A 44 year-old woman presented to a chiropractic clinic with swelling and point tenderness over the right metacarpals and right shoulder and elbow pain of insidious onset. Examination revealed right wrist and hand swelling, diminished grip strength, and reduced wrist and cervical ranges of motion. A bone scan, radiographs, and clinical examination led to the diagnosis of complex regional pain syndrome (CRPS). Following chiropractic care, the patient had improved grip strength, functional abilities, and pain reduction. The primary characteristics of CRPS include motor, trophic and sensory changes, usually in a peripheral limb following some form of trauma. Due to the varied symptom presentation, it may be unclear which conservative therapies will be most beneficial in the treatment of CRPS. A multidisciplinary approach to treatment should be pursued with these patients. More investigation of therapies such as chiropractic care as it relates to the pathophysiology of CRPS is needed.

Keywords: pain, neuropathy, chiropractic

Complex Regional Pain Syndrome (CRPS) represents a revised taxonomic system for two forms of neuropathies. CRPS Type I describes regional sympathetic dystrophy (RSD) and may occur without a definite nerve lesion. Type II represents causalgia, which involves cases in which a definite nerve lesion occurred.1 The taxonomy for the syndromes was developed in 1994 by the International Association for the Study of Pain (IASP) and was introduced based on patient history, symptoms, and examination findings.2 T he word complex was chosen to represent the varied clinical presentation of the syndromes.

The primary characteristics of the syndrome include motor, trophic and sensory changes, usually in a peripheral limb following some form of trauma to the region. Some features include persistent pain at disproportionate levels to the injury, evidence of edema, and alterations in blood flow and motor activity.1

The clinical picture of CRPS Type I has been described as occurring following a range of trauma, from sprains, bruises, soft tissue trauma to fractures or surgery of the affected limb.3 Additional inciting events may include stroke, myocardial infarction, and shingles.4 Although CRPS is usually associated with trauma, it has been reported that no precipitant could be identified in ten percent of diagnosed cases.5 Sensory changes most commonly appear early. Physical examination may reveal a hypersensitivity to light touch and pinprick testing. Autonomic abnormalities of swelling, hyperhydrosis, and skin blood flow are reported as common diagnostic criteria.6 Temperature differences have often been used to describe the temporal aspect of the syndrome. Acute presentations have been described as having warmer symptomatic limbs, while chronic patients are described as being in a cold end-phase.4 Others who have not found the temperature changes to be a reliable indicator of disease stage have disputed this temporal classification.5 Other commonly reported findings include muscle weakness, joint stiffness, impaired accurate movements, and severity of symptoms disproportionate to trauma, and regional osteoporosis in chronic patients.4

As noted above, CRPS Type II occurs following a traumatic peripheral nerve lesion. All symptoms are very similar to those of CRPS Type I including extreme hypersensitivity, distal extremity swelling, and symptoms spreading beyond peripheral nerve distribution.3

Case Study

A 44 year-old woman presented to a chiropractic clinic with swelling over the dorsum of the right hand, point tenderness over the 4th and 5th right metacarpals, and right shoulder and elbow pain. According to the patient, the symptoms had been present for several weeks and were of insidious onset. During the subsequent month, the patient developed progressive weakness of the right hand and wrist and was having difficulty performing daily activities such as brushing her hair and teeth, and writing. She also reported occasional paresthesia in the right hand and arm. The swelling persisted and the patient noted that the affected hand had decreased range of motion and increased temperature in comparison with the asymptomatic hand. At the time of the initial examination, the patient rated her pain as 9/10. Her medical history was unremarkable aside from being post-menopausal since the age of 39.


At the initial examination, there was visible swelling in the right wrist and hand. All right wrist ranges of motion were reduced by 50%. Grip strength was 4kg and 23kg in the right and left wrists, respectively. An upper limb neurological examination was unremarkable. There was significantly decreased cervical flexion, left rotation, and right lateral flexion. Right shoulder abduction was diminished by 10–20%. Adson’s test was positive and restrictions were noted in motion palpation of the right first rib, clavicle, sternoclavicular joint, and cervicothoracic joints.

Right wrist radiographs revealed a generalized osteopenia in the carpals, distal radius, and in all five proximal metacarpals. Patchy osteoporosis was evident in all of the right carpals (See Figures 12). Although the lateral aspect of the lunate is not clearly visualized in Figure 1, bright light examination of the original films revealed an intact cortical margin in this area. Left wrist radiographs were unremarkable. The patient was referred to her general practitioner for blood work. Blood tests revealed a mildly elevated platelet count and erythrocyte sedimentation rate and the rheumatoid factor was negative. The patient was subsequently referred to a rheumatologist. A bone scan performed at three months post-onset revealed increased activity in either the metacarpals or carpal bones at the base of the right first, second, and third metacarpals (See Figures 34). There was milder non-specific diffuse increased uptake in the remaining right wrist region and medial half of the right clavicle. Based on these findings, a medical diagnosis of shoulder-hand syndrome was made by the rheumatologist.

Figure 1 Figure 1

Right wrist with patchy osteoporosis.

Figure 2 Figure 2

Multiple lucencies in the right carpal bones.

Figure 3 Figure 3

Wrist bone scan with increased uptake in right wrist.

Figure 4 Figure 4

Full-body scan with increase uptake in the right upper limb and SC joint.

The patient was treated by a chiropractor two to three times weekly for the initial three weeks, then one to two times per week for another five weeks. The goal of the treatment was to restore first rib, clavicular, sternoclavicular, and lower cervical joint biomechanics using spinal manipulative therapy. Soft tissue therapy was also performed on the scalenes, trapezius and levator scapulae musculature. Initially, no hand or wrist treatment was provided due to the level of pain. After one week, the patient reported improved right hand dexterity and was able to grip a pencil and utensils. She also noted having improved cervical flexion and increased circulation throughout the right arm. By the completion of three weeks and 10 treatments, she had returned to work full-time. Right hand grip strength increased to 10 kg, and cervical ranges of motion were full with only minor pulling occurring with left and right rotation. Shoulder ranges of motion were full and pain-free. Right clavicle and first rib motion was improved but remained tender. Adson’s test was negative. At this point, acupuncture was added to the treatment regime. Acupuncture was performed twice per month while she continued with chiropractic care once to twice per week. Following two months of care, the patient had resumed most of her exercise program, and was able to garden and work full-time. Chiropractic and acupuncture treatments were then alternated weekly for several months to achieve the best, ongoing results. Acupuncture was the chosen modality for pain control. In accordance with Traditional Chinese Medicine patterns, the two common wrist points used were “heart 7” and “triple energizer 5”. Both acupuncture and chiropractic care continued for several months.


A follow-up appointment with the rheumatologist occurred at five months. He re-confirmed the diagnosis, although he did remark that it was an unusual presentation of the shoulder-hand syndrome. Due to the improvement in both the hand and shoulder symptoms he recommended the patient continue with her current therapy and exercises. He also suggested the patient take Actonel due to her moderate osteopenia, and noted that it may aid in her CRPS symptoms. The patient chose not to take the medication.

An evaluation performed at nine months post-onset revealed that pain intensity levels had decreased to 1–2/10. The pain was described as a dull ache in the right wrist and shoulder only. Cervical spine and shoulder ranges of motion were unremarkable, as were all orthopaedic tests. Palpation revealed mild hypertonicity of the right scalene, and tenderness of the right clavicle and first rib. At this time, the wrist symptoms had greatly improved since the initial examination. Active and passive wrist flexion was full, while there was 30% decrease in active extension. Tenderness was reported at the base of the right metacarpals and the carpals. Motion palpation of the wrist was tender, with restrictions noted at the radiocar-pal joint and midcarpal region. Grip strength was equal bilaterally. Right wrist mobilizations were initiated by the chiropractor at this point.

At the one-year follow-up, the patient had full cervical and shoulder ranges of motion. Right wrist ranges of motion were full with pain at end-ranges and pain with passive wrist extension. Grip strength was equal bilaterally.

At two-year follow-up, the patient reported some mild residual difficulty with prolonged writing, leading to pain in the right thumb and forearm. Cervical ranges of motion and orthopaedic testing were unremarkable. Mild tenderness was noted over the right first rib and trapezius musculature. Right wrist ranges of motion were full, with mild pain at the end range of extension. Grip strength was equal bilaterally with normal colour and muscle appearance in comparison to the left hand.


Although the new taxonomy for CRPS has been in place for several years, it is evident that many clinicians continue to be unfamiliar with the new terminology. A literature search revealed the use of various synonymous terminology including Sudek’s atrophy, reflex sympathetic dystrophy, shoulder-hand syndrome, alygodystrophy, and CRPS. In fact, the taxonomy used often varies depending on the country concerned, the specialty treating the patient, or the personally favored terminology. Part of the confusion stems from the variety of applied diagnostic criteria and until further clarity is gained with respect to the clinical presentation of CRPS, it is important that clinicians continue to be very specific and complete when describing the clinical presentation of CRPS.

The pathophysiological mechanism for CRPS remains poorly understood. Early theories focused on hyperactive sympathetic responses causing the symptoms. Proponents of this theory cite the salient response to sympathetic blockades as evidence of the pathogenesis.6 Others have argued that because blockades are not effective in all patients, other possible pathological mechanisms need to be explored.

Another proposed theory gaining support is the possibility of an exaggerated sensitivity to sympathetic nervous system neurotransmitters. A denervation hypersensitivity of the peripheral B-adrenergic receptor is thought to occur following nerve injury. The lowered adrenergic outflow from sympathetic neurons is compensated for by latent receptor up-regulation. Increased receptor function, synaptic efficacy and exaggerated response to otherwise normal neurotransmitter loads is the result. The end result is symptoms which are attributed to an over-active sympathetic nervous system.4

Recent investigations have reported that an exaggerated inflammatory response may also be a possible disease mechanism.5 Localized neurogenic inflammation may be related to increased vasodilation, acute edema, and sweating. Clinical findings which indicate that there may be an inflammatory process in the pathogenesis of early CRPS include joint effusions measured with MRIs, increased synovial protein concentration, hypervascularity, and neutrophil infiltration.3

The lack of a gold standard test for the diagnosis of CRPS may lead to over diagnosis of this condition. As such, CRPS can be a difficult condition for both patients and clinicians. Other neuropathic disorders, undifferentiated arthritis, rheumatism, inflammatory arthropathies, and unilateral vascular occlusive disorders should all be considered as possible differentials. In order to discern between various diagnoses, the clinical and imaging findings must not be examined in isolation. Taken together, the findings will quickly help to narrow down the differential diagnoses. For example, the inflammatory ar-thropathies which affect the hand and wrist include rheumatoid arthritis, psoriatic arthritis, and gout. Infection should also be considered another differential. Some of the radiographic findings of CRPS include normal joint spaces and margins. This assists in differentiating CRPS from infection or rheumatoid arthritis. In addition, the clinical pictures would be notably different for all three diagnoses. Although the clinical findings between CRPS and gout do have several similarities, the radiographic findings for both this and psoriatic arthritis are not consistent with those of CRPS.

Several authors cite the misdiagnosis of dysfunctional postures as CRPS Type I, and that a multidisciplinary approach for the diagnosis and treatment of both conditions is needed.8 Currently we must rely on a detailed history and physical examination in order to make the appropriate diagnosis. Certain key information must be ascertained. This includes any history of inciting trauma, and history of sensory, autonomic, and motor changes. The physical examination should reveal any neurological changes, distribution of pain, swelling, sweating, and trophic changes.

In a prospective study, the symptoms and progress of 829 CRPS-diagnosed subjects were examined over an eight-year period. It was concluded that patients could not be subdivided into temporal stages based on the temperature of the affected limb. Instead, it was suggested that patients be categorized by either primarily warm or cold forms. Those with colder limbs were more inclined to have been suffering from CRPS for a longer period of time.5 Due to the inconsistencies of presenting symptoms among acute and chronic sufferers, it has also been suggested that the syndrome be classified as either mild, moderate, or severe.7 The current diagnostic criteria require that the following four criteria be satisfied:2

  • The presence of an initiating noxious event or a cause of immobilization.
  • Continuing pain, allodynia, or hyperalgesia with which the pain is disproportionate to any inciting event.
  • Evidence at some time of edema, changes in skin blood flow, or abnormal sudomotor activity in the region of the pain.
  • This diagnosis is excluded by the existence of conditions that otherwise would account for the degree of pain and dysfunction.

In the IASP classification, Merskey and Bogduk noted that only criteria 2 and 4 had to be satisfied.

Paraclinical testing is important to provide information regarding autonomic, sensory, and motor changes. Bone scintigraphy is useful in providing information about vascular bone changes, especially in later disease stages. Plain radiographs need only be taken at the chronic stage, when bone mineralization status can be evaluated. Quantitative sensory testing (QST) and autonomic function testing for these patients has been reviewed in the literature, although it is beyond the scope of this paper to discuss the details of the testing.3,7

Not only has the taxonomy of this syndrome changed, the therapeutic approach has also been greatly modified. Sympathetic blockades were a common diagnostic tool and form of therapy. Studies have shown that there is inadequate evidence to unequivocally report the benefit of sympathetic blockades on pain levels and motor function. It was reported that approximately 85% of CRPS patients report a positive acute effect following sympathetic blocks.3 In contrast, others have reported that sympathetic blockade or sympathectomy had minimal effect with only 7% reporting lasting success.5

More recently, there has been a shift towards restored functional abilities instead of pain control as the primary goal of treatment. Exercise therapy is considered one of the key elements of this process.7 Physical therapy is an important component to treatment although aggressive therapy can be detrimental in early stages when pain levels are high. Although one functional goal is to improve joint motion and strength, passive movements are frequently too painful and should be avoided in acute patients.4 Passive therapy, followed by active isometric and then active isotonic training can be pursued when pain levels diminish.3

A multidisciplinary approach to treatment should be pursued with these patients. Various modes of therapy may be considered. The primary goal of pharmacological intervention is pain relief.7 In the early onset, under the assumption that neurogenic inflammation is the pathological mechanism, NSAIDs and steroids may be administered as a form of pain control. Even so, Vacariu reported that few clinical trials have shown benefits.7 There are no long-term studies on the use of opioids in treating CRPS or other neuropathic pain although this is thought to be an effective initial course of therapy in order to manage pain levels. Tri-cyclic antidepressants have been shown to have an analgesic effect and are used in doses smaller than those needed to produce anti-depressant effects (75–150mg/day).3 The use of TCAs may be related to interrupting the pain cycle by improving sleep, mood, and anxiety. Physical therapy, and to a lesser degree occupational therapy, has been effective in reducing pain and improving active mobility in patients with CRPS I of less than a one year duration.9

For evidence-based practitioners, chiropractic practice has progressed to being more than simple joint manipulation. The current case represents the increased awareness that many conditions require some physical therapy component, including specific exercise regimes. The patient had multidisciplinary management and was treated with spinal manipulative therapy, soft tissue therapy, acupuncture, and home exercises by the chiropractor. There have been limited studies published regarding the chiropractic treatment of CRPS and similar conditions. Besides the current case, only one published case report regarding chiropractic management of CRPS was found. This study reported drastic upper limb symptom improvement in one patient following a total of three cervical manipulations and home exercise therapy.10 The current case had a similar level of improvement in upper limb symptomatology and functional ability following first rib, clavicle, and cervicothoracic manipulation.

These two CRPS cases are encouraging with respect to the results obtained using a non-pharmacological multi-disciplinary approach to care. CRPS can be a severe, debilitating condition of which the effects may be long lasting. A key factor in the prognosis and recovery of CRPS patients is early intervention focusing on restoration of functional abilities. Manipulative therapy serves to restore joint function and may be effective in improving somatic dysfunction associated with CRPS and other similar conditions.4 Home exercises and a return to activities of daily living may limit the overall disability and shorten recovery time.

Although the diagnostic criteria of CRPS were met in the current case, the true pathophysiology of the disease is yet to be completely understood. Due to the varied symptom presentation and extent of affliction, it may be unclear which conservative therapies will be most beneficial in the treatment of CRPS. In order for clinicians to make truly accurate diagnoses and treatment protocols for this group of patients, more investigation of therapies such as chiropractic care, acupuncture, massage, and exercise as they relate to the pathophysiology are needed.

Click Here For The Original Article Online.



r. Harris Joins Medical Staff at Central Mississippi Medical Center

r. Harris Joins Medical Staff at Central Mississippi Medical Center

Central Mississippi Medical Center recently announced that Carol D. Harris, M.D., has joined its medical staff and is affiliated with Advanced Diagnostic Pain Center in Jackson, MS. Dr. Harris is board certified in Pain Management and Anesthesiology.

She received her medical degree from the University of Mississippi Medical Center in Jackson, MS. After receiving her medical degree, Dr. Harris completed an internship as well as a residency in anesthesiology at Loyola University in Maywood, IL. Dr. Harris completed a pain fellowship at Texas Tech University Health Sciences at Lubbock, TX.

Dr. Harris treats acute, chronic cancer and post-operative pain patients. Pain disorders treated at Advanced Diagnostic Pain Center include: acute chronic low back and neck pain; post-surgical failed back syndrome; spinal disc, facet and nerve root-pain; “whiplash” – cervical neck pain’ complex regional pain syndrome (CRPS); reflex sympathetic dystrophy (RSD); headache; diabetic neuropathy; pelvic pain; post-herpetic neuralgia and other pain conditions resulting from disease and injury.

She has been in practice since 1995, serving most recently as an Associate Anesthesiologist of Joliet at St. Joseph Provena Hospital in Joliet, IL.

Click Here For The Original Article Online.


Faulty wiring mystifies mechanics and doctors alike

<!– Faulty wiring mystifies mechanics and doctors alike Boston Globe I was confident at the inspection station. My trusty ’96 Mazda Protege was driving fine. But I got a shock that day: a black rejection sticker for emissions. “Get a tune up,” I was urged. Anne Louise Oaklander December 17, 2007 –>
My perspective

Faulty wiring mystifies mechanics and doctors alike

By Anne Louise Oaklander December 17, 2007

I was confident at the inspection station. My trusty ’96 Mazda Protege was driving fine. But I got a shock that day: a black rejection sticker for emissions. “Get a tune up,” I was urged

When that didn’t work, the repairs began. A new battery, a new alternator, a second battery – still I failed. I began to realize that my problem was not actually emissions, which were pristine, but electrical problems that prevented storage of my auto’s emissions data.

Somewhere during the garage visits, bills, and phone calls, it occurred to me that my car had the same problem as my patients with neuralgia, a type of chronic pain caused by nerve damage. They are laid low by pain in various locations, but medical exams and tests often show no cause.

Their problem is not actually where their pain is felt, but in the nerves that carry pain messages to the brain. Normally, pain neurons only fire briefly during injury or illness to signal a problem, but short-circuits can make them fire continually, just like my engine warning light that stayed lit for months.

Some neuralgia patients, whose symptoms are often triggered by common conditions such as shingles, diabetes, and osteoarthritis of the spine, are prescribed effective medications and may get pain relief. More often their “mystery pain” goes untreated as doctors fail to recognize and treat its neurological causes. And physicians, no matter how caring, must also weigh the chances of federal scrutiny when prescribing strong pain medicines for patients without sufficient explanation for their pain.

Many neuralgia patients undergo unnecessary repairs just like my Protege. These include local-anesthetic injections that help only briefly while the area is numbed. I remember the woman whose dentist tried to treat her neurological jaw pain by doggedly extracting one innocent molar after another, leaving her toothless and impoverished, and no better.

Most surgeries do not help neuralgia, and surgery causes or worsens many cases.

In addition to living with chronic pain, my patients have to cope with an unforgiving medical and disability system with little tolerance for elusive problems. My fruitless phone calls to the Registry of Motor Vehicles pale next to my patients’ efforts to seek insurance coverage, disability benefits, worker’s compensation, or simply to get a doctor to listen and help.

Medical tests aren’t sensitive enough to detect subtle electrical problems, just as my mechanic’s tests couldn’t find the fault that was causing loss of my car’s emission’s data. Lack of evidence is interpreted as evidence of lack of a problem, and my patient’s symptoms are attributed to psychological causes, character flaws, or to just plain lying to con a doctor into writing a narcotics prescription.

With each new agency, each new doctor, my patients need to retell their complicated histories to convince yet another skeptical listener. Most feel vaguely guilty for having such a difficult problem, and many wonder at some point if indeed they might be crazy. Some cry with relief when I tell them that I have seen their kind of problem before and it is caused by neurological damage, not neurosis.

Some eventually give up, traumatized twice – once by their illness and once by our system. I am haunted by the memory of a woman who killed herself last year, believing this the only way to end her suffering.

Last month, my story took a turn for the better: On a whim, Eddie, the mechanic who has worked doggedly to fix my Protege’s problem, plugged it into the inspection computer. By some miracle, at that moment it held enough data for me to PASS! We shared a giddy moment.

But my lawfulness is temporary. My car’s nerves are still fickle and my check engine light still goes on and off at will. I must expect rejection at my next emissions test. I’ve heard that Motor Vehicles is ending tailpipe-emissions testing altogether, which will leave no option for cars like mine to pass. Will we have to junk otherwise well-running cars that can’t meet the new rules?

Given the complexity of our own neurological wiring, perhaps physicians, medical insurers, and disability boards should also make provisions, so that patients with chronic pain from wiring problems can still get the care and compassion they need.

CNN Video: Support Groups

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Support Groups


Experimental Surgery Saves Woman’s Life

Experimental Surgery Saves Woman’s Life

A Montgomery County woman is home after an experimental and controversial treatment that restored her life.

23-year-old Lindsay Spengler has battled Reflex Sympathetic Dystrophy (RSD) for a decade now. For the past five years, she’s been confined to a bed, unable to walk or eat.

The strange neurological condition made her feel like her body was on fire.

“There were days when it was like, ‘Lord, I can’t do this any more,'” Lindsay said.

The disease first surfaced when she was 13-year-old. She suffered a broken thumb while playing softball, but her nervous system essentially thought her body never repaired the wound.

Doctors in the United States treated her, but they said only an experimental treatment in Mexico could relieve her pain.

Friends and strangers helped her raise $200,000 to make the trip. She was in Mexico for three months, and doctors put her in a medically-induced coma to reset her nervous system.

“And I remember as soon as I could wake up, and I could say something, I said, ‘Mom, there is something different. Something is different,” Lindsay said.

Most of her pain is now gone, and she is learning to walk. She is recovering in her Montgomery County home as she continues physical therapy.

“For everything you guys did, letters of encouragement, money, whatever, I am just so so thankful,” she said.

Lindsay wants to help other people suffering with RSD and would like to answer any questions you may have. You can contact her through her website:

By John Atwater

Click Here For The Original Article Online.


Battling to beat the odds

AMBUSH: The Spirit of Juno, which was attacked by pirates in the Indian Ocean

DOING WHAT SHE LOVES: Kirsten sailing in the Millennium Round the World Yacht Race.

ROYAL VISIT: The Princess Royal presents Kirsten with her trophy for coming second in the UK National Challenger ­Championships at Oxford in 2002.

Battling to beat the odds

09 January 2008

KIRSTEN Pollock was the youngest member of the crew on Spirit of Juno, one of four boats in the Millennium Round the World Yacht Race.

It was a hair-raising adventure. Kirsten, then 19, joined the race in Sydney, Australia, and was on board for 10 months.

She remembers with a kind of ironic relish piloting the boat through a seven-hour storm and even being attacked by pirates.

Sadly, the attackers were nothing like Johnny Depp and nowhere near as charming as Captain Jack Sparrow.

But the well-equipped £4million boat made an attractive target.

Kirsten, 27, says: “We were attacked by pirates in the Indian Ocean. We were four days out of Darwin and sailing towards Christmas Island.

“It was a dark night, quite windy. I was on watch and I had five crew above deck with me. I saw a ship coming towards us and I thought they would pass us on the left.

“But as it came next to us, it turned and tried to ram us. Then the gunfire started. We had done a pirate drill. We knew what we would do in the event of an attack.

“These are modern day pirates, they come on the boat and take your passports, money, jewellery and sometimes even kill people – that’s why sometimes boats and people just disappear.

“We turned all our lights off. I was on the helm and, when I realised what was happening. I stamped on the floor to let the skipper know – his berth was just below where I was standing. We all carried knives at all times and different people were given different jobs.”

How did they escape? “We outran them. It was a windy night and we were already going at 19-20 knots so our sails could outrun their engine – they were trying to shoot our sails.

“To try to avoid their gunfire, I was just weaving backwards and forwards so that we were not giving them an easy target.

“We managed to lose them but they were on our radar for 24 hours.

“We had a most experienced crew but it was strange. The people you thought would stay calm panicked and the people you thought would panic stayed calm.”

Alarming in a quite different way was having to spend four hours up a mast in a force-nine gale.

“There had been damage to one of the halyards that hold the sail up. The electrics had blown and a wire had become damaged and had to be replaced.

“The mast was 100ft high and it was bloody windy. I was always the idiot who did that sort of thing. I do like the adrenalin rush but it was quite scary at the time.”

The Spirit of Juno was second out of the four boats in the race and when she came home Kirsten successfully applied for a job on board a yacht.

“We would have been sailing in the Caribbean in winter and the Mediterranean in summer. It was May 2001 and I was due to fly out two weeks later. I was 21.”

Kirsten never got to take the job: “I slipped on the stairs and fell from the top to the bottom.

“I hurt my back but at first the only damage seemed to be to my knee – there was damage to tendons and ligaments. I thought in a few weeks it would be OK.

“But instead of getting better, it got worse. I was in absolute agony. I couldn’t bend my knee and I couldn’t take any weight on my leg even with crutches.

“I went back to the hospital, My knee was examined from the inside with a camera and the consultant said there was nothing wrong with it.”

After further investigation, Kirsten was diagnosed with Reflex Sympathetic Dystrophy or Complex Regional Pain Syndrome, a condition where messages fail to get through from the brain to the limbs but the limbs suffer extreme pain.

This was now affecting both her legs and is understood to have been triggered by trauma to her body.

Kirsten said: “I looked on the internet and terrified myself. I thought my sailing career was over for good. I had worked so hard to get my sailing qualifications and it was going to be over just like that.

“It was devastating. I had always played sport – I took up sailing for my Duke of Edinburgh’s Award as a schoolgirl because it was one of the few sports I hadn’t tried.

“Then, in 2002, I heard about the Sailability clubs. I had never heard of the Challenger boats (specially adapted craft for disabled people). I went along to the club and there were people in wheelchairs and on sticks piloting boats.

“I met Judy Figgures (a disabled sailor from St Ives) and she said she had a spare boat in her front garden and asked if I would I like to borrow it for the weekend.”

Kirsten started taking part in regattas and getting placed. “In the end, I was crying because I was back doing what I thought I could never do again. I was back sailing again, doing what I love doing.”

Since then, Kirsten has won the Scottish Open Challenger Championships two years running and was second overall in the UK National Challenger Championships in 2002.

This year also, she was part of a crew of seven on a 51ft boat in the Fastnet Race.

“It was an unadapted boat but I managed to bum-shuffle around it. If there is any chance of getting on a boat, that will be me off, whether it is adapted or not.”

Kirsten’s disability also brought romance into her life … although not for her.

After she joined the Sailability Club at Grafham, her mother, Lesley, met Robin Gumbrell who was honoured last month by the Royal Yachting Association for his services to the club. Robin and Lesley live in Hartford and Kirsten is hoping to move nearby to a suitably-adapted flat.

Kirsten’s ambition is to join the Paralympics sailing team but so far her condition is not recognised as a disability for that purpose.

“It is incredibly frustrating. An able-bodied person born without thumbs would qualify as disabled but I am in a wheelchair and I don’t.

“Apparently, my disability can’t be measured. All the other sailors are very supportive and can’t believe it either.

“After everything I’ve been through it’s hard to have to jump through even more hoops.”

INFORMATION: Contact Sailability on 01480 810521.

Click Here For The Original Article Online.


Pain Relief for Some, With an Odd Tradeoff

Pain Relief for Some, With an Odd Tradeoff

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For people with chronic pain, relief comes with a tradeoff. Bed rest means missing out on life. Drugs take the edge off, but they also dull the senses and the mind.

But there’s another potential option: implantable stimulators that blunt pain with electrical impulses. In this case, the tradeoff is living with a low-grade buzzing sensation in place of the pain.

The devices, which are implanted near the spine, are not widely used. They are expensive, don’t work for everyone and rarely offer complete relief. Industry officials estimate that fewer than 10 percent of eligible patients opt for the treatment.

But when they do work, they can be life-changing. Carolyn Stewart, 45, of Clifton, N.J., has lived with chronic back pain since she was 18, when she had surgery after a car accident. Then four years ago, a procedure for a collapsed lung accidentally resulted in nerve damage that caused excruciating pain. “I just want to sleep normally and not have pain that wakes me up every 20 minutes,” she said.

Ms. Stewart has been using pain drugs to cope, but side effects, including fatigue and constipation, only add to her discomfort. A few years ago she did a “test drive” of a spinal cord stimulator and experienced a significant drop in her pain. Insurance troubles delayed a permanent implant, but this month she is finally undergoing surgery to attach the device to her spinal cord. “It’s not going to be 100 percent,” she said. “But I will be happy with a 50 percent change.”

Not every patient feels that way. Ms. Stewart’s physician, Dr. Andrew G. Kaufman, director of interventional pain management at Overlook Hospital in Summit, N.J., described a patient who tested a stimulator and experienced “unbelievable” pain relief, yet simply couldn’t adjust to the sensation created by the device and decided not to keep it. “She couldn’t get over the background buzzing,” Dr. Kaufman said.

Still, most patients accept this vibrating version of white noise, says Dr. Richard North, a retired neurosurgery professor at Johns Hopkins who developed several patents related to the technology, although he no longer receives royalties.

“When they first feel the sensation they say, ‘That’s weird,’” said Dr. North, who treats patients at the LifeBridge Health Brain and Spine Institute in Baltimore. “It quickly becomes clear that ‘weird’ is going to be just fine if it replaces the pain.”

Chronic pain is a particularly difficult problem to understand and solve. Pain is normal after an injury or because of a health problem. But sometimes the nerves misfire and continue sending intense pain signals to the brain even after the injury heals. Dr. Vijay B. Vad, a sports medicine specialist at the Hospital for Special Surgery in Manhattan, compares the problem to a thermostat in a cool room. “If it’s 65 degrees in the house, but the thermostat thinks it’s 50 degrees, the heat keeps running,” Dr. Vad said.

The condition, complex regional pain syndrome, or C.R.P.S., typically develops after a medical procedure or an accident. But even minor injuries, like a sprain from a fall, can cause it. The syndrome may follow 5 percent of all injuries, according to the Reflex Sympathetic Dystrophy Association, an advocacy group for people with chronic pain.

Spinal cord stimulation works by implanting an electrode near the spinal cord, inserted through the same place where epidural pain relief is injected for women in labor. Electrical pulses scramble or block the pain signals traveling through the nervous system, preventing them from reaching the brain.

But spinal cord stimulators offer significant relief to only about half the patients who try them. In September, the journal Pain published the largest-ever clinical trial of spinal cord stimulators, comparing their use with conventional pain therapies, including drugs, nerve blocks and physical therapy. The study, which was financed by the implant maker Medtronic, followed 100 patients who had undergone spinal surgery and had developed chronic pain in one or both legs.

Every patient received conventional pain treatment, but half were also given a spinal cord implant. Pain fell by half for 48 percent of the implant patients but only 9 percent of the others.

The implants cost about $20,000, and the procedure, hospital care and follow-up can bring the total bill to about $40,000. In August, the medical journal Neurosurgery showed that spinal cord implants were far cheaper than additional operations to treat pain.

Another concern is that patients who require high doses of stimulation drain the battery quickly, requiring surgery to replace the device. New rechargeable versions of the stimulators have helped resolve that concern.

For some patients, relief is only temporary, and the pain returns. Doctors say simple adjustments to the device may solve that problem.

“Sometimes efficacy wanes over time, but I still believe in them,” said Dr. Kaufman, also an assistant professor of anesthesiology at the New Jersey Medical School. “When drugs don’t work, what else is there?”