HBOT & Reflex Sympathetic Dystrophy
Chapter 21 of the HBOT Manual


Reflex Sympathetic Dystrophy and Blood Flow

“References have shown that the 'reflex' aspect of RSD involves blood flow disturbances in mid brain structures. It would make sense therefore to use high dosages of oxygen in treatment.”

Philip James MD


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Effectiveness of hyperbaric oxygen therapy in the treatment of complex regional pain syndrome.

: J Int Med Res. 2004 May-Jun;32(3):258-62.

RSD

Kiralp MZ, Yildiz S, Vural D, Keskin I, Ay H, Dursun H.

Department of Physical Therapy and Rehabilitation, Gulhane Military Medical Academy, Haydarpasa Training Hospital, Istanbul, Turkey. mkiralp@hotmail.com

In this double-blind, randomized, placebo-controlled study we aimed to assess the effectiveness of hyperbaric oxygen (HBO) therapy for treating patients with complex regional pain syndrome (CRPS). Of the 71 patients, 37 were allocated to the HBO group and 34 to the control (normal air) group. Both groups received 15 therapy sessions in a hyperbaric chamber. Pain, oedema and range of motion (ROM) of the wrist were evaluated before treatment, after the 15th treatment session and on day 45. In the HBO group there was a significant decrease in pain and oedema and a significant increase in the ROM of the wrist. When we compared the two groups, the HBO group had significantly better results with the exception of wrist extension. In conclusion, HBO is an effective and well-tolerated method for decreasing pain and oedema and increasing the ROM in patients with CRPS.

PMID: 15174218 [PubMed - in process]
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Reflex Sympathetic Dystrophy

HYPERBARIC OXYGEN THERAPY
IN THE TREATMENT OF SUDECK'S SYNDROME
( RSD, Complex Pain Syndrome)

G. Lovisetti, L. Lovisetti , A.Favelli
Istituto di Terapia Iperbarica
via Oltrecolle 62, 22100 Como, Italy

SUMMARY:

The decrease in tissue hypoxia obtained with Hyperbaric Oxygenation (HBO2)counteracts the effects of reflex vasomotor disturbances caused by an injury in post-traumatic Sudeck's syndrome. In reflex sympathetic dystrophy, after an initial vasospasm, a loss of vascular tone with persistent vasodilatation. Causes increased osseous vascularity and rapid bone resorption. Chronic edema results from venous overload and passive capillary repletion:; local lack of oxygen and acidosis cause demineralization and bone protein, atabolism. The hypoxic static induces undifferentiated mesenchymal cells and younger fibroblast to a rapid maturation, with abnormal production of fibrous tissue, retraction, and adhesions and joint stiffness.

In our experience HBO2 proved to be very effective even after a few treatments resolve local swelling and to relieve pain 'in 13 of' 15 patients affected by Sudeck's Syndrome who had not positively reacted to other therapies. In 14 patients the sympathetic dystrophy affected the lower limb. Strict diagnostics criteria based on history, physical examination and radiological pictures have been respected. Technetium scintigraphy was performed and confirmed diagnosis in 7 cases. A second Te scintigraphy carried out after 20 sessions of HBO2 2.5ATA was available in 5 patients and demonstrated normalization of the vascular phase in 4 patients, and amelioration of the late (bone) phase in 3.

Post-traumatic Sudeck's Syndrome is a reflex sympathetic dystrophy which consists of pain and tenderness, usually in a distal extremity, associated with vasomotor instability. swelling and trophic skin changes arising after trauma. The severity of the syndrome is frequently unrelated to the severity of the injury and the dystrophy of often appears after minor trauma. The classic radiographic picture shows acute, patchy bone demineralization. Technetium scintigraphy displays augmented periarticular radionuclide activity. In its early manifestation as Sudeck's Syndrome is unrecognized or misdiagnosed and mistreated in many cases so the patient may have a prolonged and severe disability. No treatment, hitherto has proved to be very successful, once the disease has become established: various forms of physiotherapy, systemic administration of drugs ( anti-inflammatory agents, vasodilators, steroids, calcitonin ), peripheral chemical sympathectomy, infiltration of painful areas with local anesthetics, sympathectomy and sympathetic blocks, section of the sensory nerves or of the dorsal roots of the spinothalamic tract ( in intractable cases ) have been reported in the literature.

Despite any or all of these measures, many patients improve little or not at all, so that their symptoms persist for months or years. Some patients have attempted suicide because of all the psychological and economical problems related to the disease. The etiopathology of the condition is uncertain. The present pathogenic hypothesis is that after an injury to the limb there is an initial vasomotor reflex spasm and, in a second phase, a loss of vascular tone with persistent vasodilatation and rapid bone resorption.

The increased osseous vascularity appears on the radiogram as a mottled rarefaction caused by increased porosity and decrease in size, thickness and number of trabeculae. Chronic irritation of peripheral sensory nerve secondary to trauma and soft tissue damage determines increased afferent input, abnormal activity of internucial neuronal pool and continuous stimulation of sympathetic motor efferent fibers.

Accordingly to the "gate control theory", predominant small fibers input could result in the unchecked transmission of pain through an "open gate" and create the potential for summation, suppressing the influence of the substantia gelatinosa.

Capillary bed repletion, venous overload, opening of the arterovenous shunts provoke tissue hypoxia, catabolite formation, chronic edema and acidosis.

Acidosis, inactivity and vascular stasis determine bone resorption of the cortical haverslan system. Hypoxia and acidosis lead undifferentiated mesenchymal cells and younger fibroblast to proliferation and quicker maturation ( a state which requires lower oxygen consumption ) with abnormal fibrous tissue production, edema organization and joint stiffness. Reflex vasomotor disturbances, resulting in hypoxia, catabolite production and acidosis stimulate sensory nerve termination and close a vicious self sustaining cycle.

The use of HBO2 in the treatment of post-traumatic Sudeck's Syndrome is rational. In fact hyperbaric oxygenation induces vasoconstriction and reduce edema: this counteracts vascular stasis and venous repletion, increases depresses osteoblast activity and mineralization, reduces fibrous tissue formation. HBO2 therapy seems to break the vicious self sustaining cycle of reflex sympathetic dystrophy, because normalization of local tissue oxygen tension, pH and water interstitial content stops abnormal sensory nerve stimulation and efferent vasomotor phenomenon's.

MATERIAL AND METHOD:

Fifteen patients, (11 men and 4 women ) suffering for reflex post - traumatic dystrophy have been treated with HBO2 therapy. In 14 of the 15 cases the trauma affected the lower Limbs. The average age was 44.4 years. Initial injury was in 4 cases a calcaneus fracture ln 3 cases a malleolus fracture; in the remaining patients Sudeck's Syndrome followed tibial shaft fracture (2 cases), supracondylar femur fracture, multiple metatarsal bone fractures, multiple metacarpal bone fractures and in 3 cases only an history of minor trauma was collected. The disease involved foot | and ankle in 13 cases, the knee in one case and the- hand and the wrist in no case. 10 patients had immobilization ion in cast as the treatment of choice in 3 cases ( supracondylar femur fracture, multiple metacarpal bone fractures, malleolus fracture) the patient underwent surgical treatment. Time elapsed between trauma and diagnosis was 2- 8 months.

Strict diagnostic criteria for inclusion in the study hen been based on history of injury to an extremity, basic examination and radiological picture. Technetium scintigraphy was performed in 7 cases to confirm diagnosis and in 6 cases assessed the evolution of the disease. Clinical diagnosis was based on the presence of pain, tenderness, swelling, vasomotor instability and joint stiffness long lasting after a trauma. Radiographic criteria included patchy. bone demineralization, osteoporosis and cortical cavitation. All the patients were in the acute phase of the syndrome. No case of treatment of the initial or of the atrophic stage has been included in the present study. HBO2 protocol consisted in 20 sessions at 2.5 ATA ((5 sessions A week). A further series of 10 sessions was performed in patients (3 cases ) present partial clinical recurrence during the week ensuing the termination of the 20 session protocol. A previous calcitonin regimen, although of very limited efficacy, was maintained during HBO2 therapy in 5 subjects. No patient used analgesic drugs during HBO2 treatment.

Avoidance from weight bearing, functional limb rest and use of an elastic stocking were strongly counseled in patients with lower limb involvement. Te scintigraphy was performed at the end of the 20 HBO2 sessions in 6 cases. Radiographic controls were scheduled at 2 and 4 months.

ILLUSTRATIVE CASE REPORTS

  1. A 50 year old bricklayer sustained a sprain to his left ankle which remained untreated. After two months ankle pain. quite slight at the beginning, get increasing with paroxysmal exacerbations ,extending to the forefoot and forcing the patient to suspend his work. The radiogram showed the classical picture of reflex sympathetic dystrophy. Pharmacological agents and physiotherapy remained for months ineffective. Presenting to our observation,6 months after the injury, the patient was unable to walk without crutches, suffered of intense and unduly pain and was severely depressed, lacking of confidence in any form of treatment. Clinical examination revealed minimal swelling of the ankle, cutaneous hypersensitvity and a 50% decrease in movement of the subtalar and tibiotalar. After the first week of HBO2 therapy the patient referred significant decrease in pain which after the second week almost disappeared. A progressive and complete recovery of the movements of the joints involved was recorded. After 20 sessions of HBO2 patient was free of any symptom and walked normally. Te scintigraphy demonstrate normalization of the vascular phase and clear reduction of hypercapration in the late phase. Resolution of radiographic picture was slow.
  2. 58 year old man. pensioner after an untreated left fore foot distortion the patient complained persistent refractory pain swelling, limitation of motion in the extremity and marked disability to walk. On the basis of clinical radiologic and To scintigraphic findings diagnosis of reflex algodystrophy was formulated 5 months after trauma. After only four HBO2 treatments pain and swelling disappeared at the completion of the schedule the patient walked correctly without crutches and was very satisfied. Te scintigraphy at the end of the therapy demonstrated significant reduction in the hypercaptation of the forefoot. At the 2 month control discrete amelioration in the radiologic pattern was observed.

RESULTS:

After the first week of HBO2 a marked reduction of pain and tenderness in the extremity was observed in 9 patients: discrete clinical improvement has been recorded in 3 cases. Reduction of swelling and restoring of movements in the affected extremity has been progressive during the course of HBO2 therapy. At the completion of the first HBO2 cycle complete recovery ( no pain complete restoration of movements in the affected joints, no swelling) has been observed in 4 cases. Marked clinical improvement (occasional light pain minimal swelling at the evening, almost normal movements in the affected joints) was present in 5 cases. Moderate clinical improvement (reduction of pain and swelling partial restoration of movements ) has been present in 4 cases. In 2 patients despite some reduction of swelling significant pain persisted, in one of these patients, however, pain was present only during weight bearing on the affected extremity and in part could be referred to progressive subtalar degenerative changes after a calcaneus fracture. In 4 cases partial relapse of the symptoms in the weeks ensuing the completion of the first 20 HBO2 sessions lead to a second 10 session HBO2 cycle with complete recovery. In the 6 cases controlled at the Te scintigraphy after the 20 HBO2 sessions normalization of the vascular phase was observed in 4 patients, and reduction in the hypercaptation in the late (bony) scintigram was present in 3 cases. No case of worsening of the scintigraphic picture has been recorded. Resolution of the classic radiologic pattern has been generally slow: In a few patients significant improvement at the 2 month control has been observed.

REFERENCES

  1. Atkins RM. Duckworth . Kanis JA. Features of algodystrophy after Colles' fracture. J Bone Joint Surg 72B:105-10,1990.
  2. Benning R. Steinert . Diagnostic criteria of Sudeck Syndrome. Rontgenblatter 41: 239 45,1988
  3. Katz MM. Hungerford DS. Reflex sympathetic dystrophy affecting the knee. J Bone Joint Surg 69B:797-803,1987.
  4. Kozin F. Ryan LM,Carrera GF, Soin JS. Am J Med 70:23-30,1981.
  5. Melzack R. Wall PD Pain mechanisms: a new theory. Sience 150:971-9,1965.
  6. Oriani G. Malerba . Ossigenoterapia iperbarica.applicazoni cliniche : sindromi neuro algodistrofiche. Ed. 510,1989.
  7. Paleari CL. Brondolo W. La sindrome di Sudeck Post-traumatica.Ed. Minerva Mediva, 1960.
  8. Poplawski ZJ' Wiley AM, Murray JF. Post-traumatic dystrophy of the extre-mities. J Bone Joint Surg 65A:642-55.1983.
  9. Schurawitzki H. Wickenhauser J. Fozouldis I. Sadil V, Flalka V. Sudeck syndrome a combined clinico-roentgenologic-nuclear medicine study. Unfall urgie 14:238-46 1988.
  10. Schutzer SF, Gossling HR. The treatment of reflex sympathetic dystrophy syndrome. J Bone Joint Surg 66A: 625-29, 1984
  11. Von Rothkirch T Blauth W. Helbig S. Sudeck syndrome of the hand. Historical review, treatment concept and results. Handchir-Mikrochir Plast-Chir 21:115-26,1989.
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Undersea & Hyperbaric Medicine, Vol. 22, No. 4, 1995
Hyperbaric oxygen and the reflex sympathetic
dystrophy syndrome: a case report
G. PEACH

Hyperbaric Medicine Department, Shock Trauma Center, University of Baltimore Medical Center, Baltimore, Maryland

Peach G. Hyperbaric oxygen and the reflex sympathetic dystrophy syndrome: a case report. Undersea Hyperbaric Med 1995; 22(4):407-408. --A patient suffering from acute smoke inhalation also had a long medical history that included reflex sympathetic dystrophy syndrome of the left foot and ankle. The entire foot and ankle were tender and cool to palpation; range of motion was severely reduced She was referred for hyperbaric oxygen therapy, and 15 min into the first treatment (46 min at 60 fsw) she reported a lessening of the pain in her foot; moreover, the foot was less cyanotic and warmer to the touch. Subsequent treatments continued to improve her conditions and for longer periods of time.

reflex sympathetic dystrophy syndrome, hyperbaric oxygen therapy, foot, ankle
A 44-yr-old woman was referred to our department suffering from acute smoke inhalation. The patient had an extensive medical history, including reflex sympathetic dystrophy syndrome (RSDS) of the left foot and ankle. A physical examination revealed a mottled and cyanotic foot and ankle. The entire foot and ankle were tender and cool to palpation; range of motion was severely reduced for both plantar and dorsiflexion. The patient's test results indicated a carboxyhemoglobin of 6.9%. She was unable to perform the psychometric test due to a severe headache.

Because of the symptom (headache) she was given hyperbaric oxygen (HBO) therapy. The protocol in this institution for CO poisoning is 46 min of HBO at 60 feet of sea water (fsw). No complications developed during the compression and the patient tolerated the treatment well. Fifteen minutes into the treatment she reported relief of pain in the foot, and the foot was less cyanotic and warmer to the touch. The patient stated that her foot was "pinker than it's been in years" and that she was completely free of pain.

She was asked to keep track of the duration of "pinkness" and pain relief: the foot stayed warm and pink for 8 h after treatment and painless for 18 h. She was next offered treatment at 33 fsw during the next scheduled 90-min session to take place the following day. Her foot was warm and pink for l h after this treatment and painless for 2 h. She was treated the following week at 45 fsw for 30 min, and after this session the patient reported that her foot remained warm, pink, and painless for 30 h.

DISCUSSION

Reflex sympathetic dystrophy syndrome is a chronic condition of severe burning pain, extreme sensitivity to touch, swelling, excessive sweating, and changes in bone and skin tissue. Researchers (1) now believe that the symptoms occur because an injured nerve or nerves send mixed signals to the brain. In effect, these inappropriate signals short-circuit and interfere with normal blood flow and sensory signals, thus generating the symptoms of RSDS. The unremitting pain has caused many patients much physical and emotional misery.

This particular patient had few options for relief of the chronic pain associated with RSDS. She is allergic to steroids, non-steroidal anti-inflammation agents, and all narcotics; vasodilators were also ineffective. It is significant that her pain was relieved after initiation of HBO therapy.

Manuscript received May 1995; accepted June 1995.

REFERENCE

1. Lankford R, Thompson J. RSDS upper and lower extremity: diagnosis and management:
operative hand surgery, vol 26. St. Louis, MO: Mosby, 1977:163-178.

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Reflex Sympathetic Dystrophy And HBOT

Title

The synergistic effect of sympathectomy and hyperbaric oxygen exposure on transcutaneous PO2 in healthy volunteers.

Author

Thomas PS; Hakim TS; Trang LQ; Hosain SI; Camporesi EM

Address

Department of Anesthesiology, State University of New York Health Science Center, Syracuse 13210, USA. hschosp.umag.thomasp.

Source

Anesth Analg, 88(1):67-71 1999 Jan

Abstract

The benefit of hyperbaric oxygen (HBO2) exposure is dependent on the oxygen delivery. Such benefit may be limited by the fact that hyperoxia causes vasoconstriction and decreases blood flow. The aim of this study was to determine whether regional sympathectomy attenuates this vasoconstriction response and thus improves oxygen delivery. In a double-blinded manner, healthy volunteers were subjected to HBO2 in a monoplace chamber on two occasions separated by at least 1 wk.

Transcutaneous oxygen (tcPO2) and carbon dioxide (tcPCO2) on the forearm were monitored continuously, and blood flow in the axillary artery was measured using angiodynography before and after exposure to HBO2. During one visit, each volunteer received a sympathetic block to the upper extremity by an injection of lidocaine into the brachial plexus at the axilla. During a second visit, the volunteer received a placebo injection of isotonic sodium chloride solution into the brachial plexus of the same side. Skin temperature was recorded on the back of the hand.

All subjects exhibited a small but significant increase in skin temperature (2.5%) and in upper limb blood flow (23%) (P < 0.05%) after sympathectomy, but not after isotonic sodium chloride solution injection. Sympathectomy increased tcPO2 marginally while in room air.

However, during HBO2, tcPO2 was substantially and significantly higher (409.8+/-98.8 mm Hg) after sympathectomy compared with that after isotonic sodium chloride solution injection (171.3+/-38.1 mm Hg). tcPCO2 did not change significantly after sympathectomy or during HBO2. Thus, sympathectomy presumably improved oxygen delivery by preventing vasoconstriction during hyperoxia. The results suggest that sympathectomy may be a useful adjunct to HBO2 therapy in patients in whom vascular resistance is increased because of sympathetic tone or hyperoxia.

IMPLICATIONS: Sympathetic nerve block of the extremities markedly enhances tissue oxygen delivery during hyperbaric oxygen treatment.

Sympathectomy may be a beneficial adjunct treatment to hyperbaric oxygen in peripheral vascular insufficiency.

Adult ; Blood Gas Monitoring, Transcutaneous * ; Brachial Plexus DE/PH ; Double-Blind Method ; Female ; Human ; Hyperbaric Oxygenation * ; Male ; Nerve Block MT ; Oxygen *AD/ME ; Skin ME ; Skin Temperature DE/PH ; Sympathectomy, Chemical * ; Vasoconstriction PH

Publication Type
CLINICAL TRIAL; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL

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Will Hyperbaric Oxygen Therapy Become a Viable Treatment Modality for Fibromyalgia Syndrome?
RSD
Pavel I. Yutsis, M.D.

In the present era of scientifically oriented medicine it has become increasingly difficult to design and conduct scientific research to prove or disprove efficacy of a given therapeutic modality. Often times, however, we learn how new modalities can help sufferers of different health conditions only by accident.

Many fibromyalgia patients can easily appreciate how much pain and swelling in the extremities can effect their well being and quality of life.

There is a condition, symptoms of which remind me of symptoms of fibromyalgia. The condition that I am referring to is called Reflex Sympathetic Dystrophy Syndrome (RSDS)

Reflex Sympathetic Dystrophy Syndrome (RSDS) is a painful condition that in addition to “burning” pain, tenderness and swelling of extremities can include swelling, sweating, warmth and/or coolness, flushing, discoloration and shiny skin. RSDS is also known as “the shoulder-hand syndrome,” “causalgia” and “Sudeck’s atrophy.” There are many theories why RSDS can take place. Some of them suggest that irritation of nervous tissue can cause abnormal impulses along nerves that subsequently effect blood vessels and skin.

The onset of RSDS symptoms can come unexpectedly and sometimes it can come in several stages.

Stage I Acute (3-6 months) - during this stage, pain, swelling, burning, flushing, sweating and tenderness can develop. Also during this stage, physician can notice patchy bone thinning on the X-ray.

Stage II Dystrophic (3-6 months) - during this stage, swelling and flushing usually diminish, but changes in skin when it becomes shiny, thickened coupled with development of contracture and persistent pain can occur.

Stage III Atrophic - during this stage, loss of motion and function in the involved extremities, thinning of the fatty layers under the skin and significant osteoporosis will take place.

Usual treatment for RSDS includes:

   * Cool, moist applications
   * Gradual exercising
   * Non – steroid anti-inflammatory drugs
   * High doses of Pregnasone
   * In severe cases a nerve block with anaesthetic is injected into the specialized area
   * A few reports reflecting efficacy of hyperbaric oxygen therapy (HBOT) attracted my attention. One of them tells how a patient who was suffering from acute smoke inhalation also had a long medical history that included Reflex Sympathetic Dystrophy Syndrome of the left foot and ankle. The entire foot and ankle were tender and cool to palpation and range of motion was severely reduced. Patient was referred for hyperbaric oxygen therapy to ward off symptoms of smoke inhalation. She underwent a number of HBOT sessions. Fifteen minutes inside the hyperbaric chamber during her first session patient enthusiastically reported lessening of pain in her foot. She also was extremely happy to tell the whole world that her foot is much warmer to the touch and is not as blue as it used to be. Subsequent treatment improved her condition.

Pain, inflammation, tenderness and swelling are the terms too familiar to fybromyalgia sufferers and I am sure that many of them have been wondering if hyperbaric oxygen therapy (HBOT) could be their savior.

Case in Point: BD, a 55 year old nutritionist from Costa Rica, has been suffering from fibromyalgia syndrome for a period of ten years prior to coming into my office and requesting hyperbaric oxygen therapy (HBOT). She also recently suffered a ruptured appendicitis with leftover necrotic tissues in her lower abdominal region. BD has the whole “bouquet,” Epstein-Barr virus, cytomegalo virus (CMV), yeast overgrowth, allergies, asthma, you mention it, she had it. I saw BD following twenty hyperbaric oxygen treatments (HBOT) and guess what? Her fibromyalgia pains disappeared completely and took along the whole myriad of concurrent symptoms!

A number of patients who suffer from fibromyalgia and have been treated with hyperbaric oxygen therapy have reported the same improvement in their pain severity, anxiety levels and fatigue. Certainly, they were ecstatic to learn that their energy level has risen to the sky and finally libido showed up for a change and their outlook moved to the other side.

Pavel I. Yutsis, M.D.
Permission to Print

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RSD Alert       http://www.rsdalert.co.uk/treatments/HBOT.htm
SKIP (Supporting Kids in Pain)  http://shsskip.swan.ac.uk/Information/HBOT.htm
From Dr. Kenneth Stoller on RSD http://hbotnm.com/rsd.html



Hello all,

My name is Ken Carson and I completed 18 HBOT session last Friday, May 10, 2002, for RSD, now known as CRPS.  I had RSD starting in my right knee after a torn meniscus at work over a year ago.  After 9 doctors, tests, pills, gadgets, PT and nerve blocks that did nothing or made my situation worse.  The RSD had spread to about 75% of my body.  When I asked my 1st Pain Clinic doctor about HBOT he laughed at me an claimed to never have heard of it for treating RSD, and I would be throwing my money away.  I researched the net for more info on HBOT and how it may help treat my RSD.  Not much information was out there about HBOT and treating RSD but what I found was promising. After finding lots of information on the benefits of oxygen and the effects of pressure on the nerve systems I felt it might just help.  The local hospital has an HBOT chamber but I "did not meet criteria" and the cost was about $2,000 for 1 treatment.  We made arrangements to go to the Ocean Hyperbaric Neuro center for HBOT.

Prior to treatment I had to stop and rest twice trying to walk the 1 block from the hotel to the clinic.  After the first treatment I was pain free in all but my lower back, I walked 3 miles without stopping and up 2 flights of stairs.  After the second treatment the pain in my back was gone.  After the 4th treatment I walked for 13 miles, pain free.  The 13 miles was a little much, I had not been able to walk in a year and the RSD had reduced muscle and developed Osteoporosis in my bones.  After that I kept my walks to 3-5 miles at a time.  All the symptoms of RSD are gone, the stabbing, burning, pins&needles and aches are gone.  My body temp is stable, appetite and digestion have returned, skin color went from gray with black circle under my eyes to normal, the gash on my shin healed (happened over a year ago), rashes from the RSD went away, brain is working sharp again.

Feel free to use my story as a testimonial for others.  I will keep you updated, I know I've only been free of the RSD symptoms for a few weeks now.  It's great to have a chance at life again WITH OUT a wheel chair.  The staff at OHNC was the best!  I was treated like a person.  Seeing first hand others at the clinic, I felt my RSD was minor.  I'll never be able to forget the amazing results I witnessed there.  Keep up the good work and again thanks for my life back.  My only regret is not to have done it sooner, it would have saved a lot of hardships not to mention muscle and bone loss I now need to recover.
Sincerely,
Ken Carson
Effectiveness of HBOT 
regional pain syndrome
SUDECK'S SYNDROME
HBOT & RSD
a case report
Reflex Sympathetic Dystrophy & HBOT
HBOT
& Fibro. Syndrome?
LINKS