Make your own free website on Tripod.com

Printable RSD News Page 6

Home
Site Map
Printable RSD News Page 1
Printable RSD News Page 2
Printable RSD News Page 3
Printable RSD News Page 4
Printable RSD News Page 5
Printable RSD News Page 6
RSDSA News Alerts Page 1
RSDSA News Alerts Page 2
RSD Hope News Alert Page 2
Medication News Page 1
RSD Hope News Alerts Page 1

Reflex sympathetic dystrophy: facts and hypotheses.


Kurvers HAJM

Complex Regional Pain Syndrome Type I (CRPS-I), formerly known as reflex sympathetic dystrophy, has long been recognized clinically. The purpose of this review was to outline the etiology, signs, and symptoms of CRPS, and examine the diagnostic tests and therapeutic options currently available. CRPS-I is associated with a wide variety of precipitating events, including injury to or disease of neural tissue, either centrally or peripherally. Usually, CRPS-II, formerly referred to as causalgia, is easily diagnosed because the precipitating event is an obvious trauma to a major nerve trunk, to tissues in close proximity to a major nerve trunk, or to regions rich in nerve endings. CRPS-II can also be caused by seemingly minor trauma. It has been reported that CRPS-I occurs most frequently in women > 50 y/o. Speculation exists on whether psychological factors may predispose particular individuals to the development of CRPS-I.

This review refrains from using the traditional separation between CRPS-I and CRPS-II for various reasons. First, although according to the traditional definition of CRPS-I, evidence of nerve damage is lacking, no specific clinical or electrodiagnostic criteria have been defined in order to rule out nerve injury. Secondly, clinical characteristics of CRPS-I patients do not differ from those of CRPS-II patients, which suggests that these two groups share similar pathophysiological mechanisms.

Signs and symptoms of CRPS can be categorized into autonomic, sensory, motor, and trophic disturbances. Abnormalities of color and temperature of the skin, sweating, and edema characterize the autonomic dysfunction. For most CRPS patients, stimulus-independent persistent pain is the most troublesome feature. In addition to stimulus-independent persistent pain, a wide range of stimulus-induced sensory abnormalities may be present, including hyperalgesia, allodynia, hyperpathia, and slow temporal summation of mechanical allodynia. Hyperalgesia and allodynia may result from thermal as well as mechanical stimuli. Hyperesthesia, hypesthesia, and paresthesia have also been reported. All of these sensory abnormalities may be exacerbated by stress, exercise, or cold. The motor disorder may consist of a limited range of active movement, weakness, easy fatigability, dystonia, paresis, and altered reflexes. Some patients develop muscle spasms or tremor of a limb. There may be alterations in growth rate of the hair and nails. The skin may become smooth and glossy, with a decrease or loss of normal wrinkles and creases. Rarely, skin pigment changes and/or ulcers are observed. Trophic changes of other tissues may also occur, including atrophic changes of subcutaneous tissues (pencil-point or tapered digits), and muscular wasting. At end-stages of the syndrome, contractures of tendons often occur and joints may become ankylosed.

The onset of symptoms of CRPS may vary from immediately to several weeks after injury. When the initiating event is non-traumatic, the onset may be slower and more insidious. The clinical course of CRPS has been divided into three stages: first (acute or hyperemic), second (dystrophic or ischemic), and third (atrophic). Various studies have demonstrated skin blood flow abnormalities, not only in the clinically affected, but also in the clinically unaffected extremity. The blood flow abnormalities are solely of microcirculatory origin. Laser Doppler flowmetry enable non-invasive evaluation of the skin microcirculation. Another means of studying skin blood flow non-invasively involves capillary (video) microscopy.

The ability to diagnose CRPS depends primarily on clinical assessment. There are no consistent routine laboratory findings in these patients. X-ray studies have been used. Sensitivity and specificity of x-ray in CRPS patients have been reported to be 69 and 71%, respectively. The percentage of CRPS patients demonstrating electromyography and nerve conduction velocity abnormalities usually ranges from 50-90%. Thermography and three-phase bone scanning may also be of help in establishing the diagnosis. Histopathological findings have also been reported.

Microcirculatory abnormalities similar to those observed in CRPS patients may occur in various other diseases. Angiography and Doppler ultrasonography are available in order to exclude the presence of major artery disease.

The most effective preventative measure is efficient control of pain and early mobilization. An effective treatment of CRPS is early recognition and treatment since patients with long-standing duration of disease are less likely to respond well. Physical therapy, corticosteroids, and transcutaneous nerve stimulation have been used with some success. The only therapy found to be effective for CRPS in large studies is aimed at interruption of the activity of the sympathetic nervous system (SNS). Methods include Bier block, paravertebral sympathetic ganglion blockade, and alpha-adrenergic blockade. The pathophysiological mechanisms underlying CRPS are felt to be due to altered (efferent) function of the SNS and neurogenic inflammation of sensory nerves. It is thought that neuropeptides released by excitation of sensory nerves may induce vasodilatation, increase vascular permeability, and excite surrounding sensory nerve fibers. At the level of the central nervous system, it has been suggested that the increased input from peripheral nociceptors alters the central processing mechanisms. Future therapeutic modalities for CRPS patients include continued research on blockade of adrenoceptors and capsaicin to decrease neurogenic inflammation. Neuropeptide-receptor blockers may reduce neurogenic inflammation.


Journal: Vasc Med, 3(3):207-214, 1998.
Reprint: 79 References Resident General Surgery, Dept of General Surgery, University Hospital Maastricht, P.O. Box 5800, 6202 AZ Maastricht, The Netherlands (Dr HAJM Kurvers) GM.02 JL9912/192 ©1999

------------------------------------------------------------------------------

Truths, errors, and lies around “reflex sympathetic dystrophy” and “complex regional pain syndrome”.


Ochoa JL

Many patients complain of chronic “neuropathic” pains, particularly following acute physical injury. These pains are often associated with positive or negative motor and sensory symptoms and related psychophysical signs which render the patients neurological. Experimental physical trauma to animals result in predictable motor, sensory, and vasomotor dysfunction, and even pain behavior, all of which tends to recover within weeks through natural repair.

Patients who display variations or permutations of such general clinical profile may harbor organic structural neurological damage or a somatoform pseudoneurological disorder, fraudulent malingering, the bizarre Munchausen’s condition, or a borderline personality with associated self-infliction of physical damage. Unfortunately, litigation and compensation issues tend to perpetuate both complaints and medical management, as the psychobiosocial scenario may become contaminated with secondary gain agendas from the patient and tertiary gain from health care providers or lawyers.

Various treatment modalities may dramatically relieve the subjective or psychophysical reflex sympathetic dystrophy (RSD) symptoms. Unfortunately, recurrence or “metastases” are almost the rule. Placebo response was never factored into the “diagnostic-therapeutic block” paradigm until the last decade. Iatrogenesis is inevitably part of the management outcome of RSD/complex regional pain syndrome (CRPS) patients. It is an error to assume that patients who display the clinical profile of RSD/CRPS have a discrete disease with one common etiology and definable pathophysiological mechanism leading to neurological manifestations. They merely harbor a nonspecific symptom complex with any possible variety of abnormal physiological or psychological backgrounds. It is a classic fallacy to assume that behind these patients’ pains and motor and sensory symptoms, there is a unique abnormal mechanism by which the sympathetic system causes not only the objective circulatory changes but also, indirectly, the painful neurological dysfunction. Errors include historical misinterpretation of vasomotor signs in symptomatic body parts and misconstruing symptomatic relief after “diagnostic” sympathetic blocks, due to lack of consideration of the placebo effect which explains the outcome. It is also not true that sympatholysis may specifically cure patients with unqualified “RSD.”

As extrapolated from observations in animals with gross experimental nerve injury, adducing hypothetical, untestable, secondary central neuron sensitization to explain psychophysical sensory-motor complaints displayed by patients with blatantly absent nerve fiber injury is not an error, but a lie. While conceptual errors are not only forgivable but natural to inexact medical science, lies, particularly when entrepreneurially inspired, are condemnable and call for peer intervention.


Journal: J Neurol, 246(10):875-9, 1999. 38 References
Reprint: Department of Neurology, Good Samaritan Hospital and Oregon Health Sciences University, 1040 NW 22nd Ave N-460, Portland, OR 97210 (JL Ochoa, MD)

Complex regional pain syndrome.
Rho RH

Complex regional pain syndrome (CRPS), formally known as reflex sympathetic dystrophy (RSD), is a regional, post-traumatic, neuropathic pain problem that most often affects one or more limbs. The nosology and terminology of post-traumatic limb pain have undergone a series of changes that have led to considerable confusion and controversy regarding the diagnosis and treatment of CRPS. The most common popular contemporary label is RSD, and this terminology is based on the notion that a pathologic sympathetically maintained reflex arc is involved in the generation and perpetuation of pain. Recent studies have shown that the sympathetic nervous system is not necessarily involved in every case and that a "reflex arc" has not been demonstrated. To bring some order and uniformity to this problem, CRPS has been subdivided into type 1 and type 2. The clinical features of the two types are identical, the distinguishing feature being the presence of a major peripheral nerve injury in patients with type 2.

Concerning diagnosis, no specific test is available for CRPS, and no pathognomonic clinical feature identifies this condition. Rather, identifying a constellation of history, clinical examination, and supporting laboratory findings make the diagnosis. Most patients with CRPS have an identifiable inciting or initiating injury, which may be trivial or severe. The key features are pain, allodynia and hyperalgesia, abnormal vasomotor activity, and abnormal sudomotor activity persisting beyond the period of normal healing. Pain usually spreads beyond the area of the initial injury and, in its most severe form, may involve the entire limb and, rarely, the contralateral limb.

Symptoms of sympathetic dysfunction may be present and may manifest as vasomotor and/or sudomotor instability. The symptoms typically come and go and, in later stages, may not be present at the time of the initial examination. The typical signs are color changes, temperature changes, and excessive sweating. Hyperhidrosis is a common finding early in the course of CRPS. If pain is relieved by sympathetic blockade, it is regarded as sympathetically maintained. Pain that is not relieved by sympathetic blockade is known as sympathetically independent pain. Sympathetically maintained pain can convert to sympathetically independent pain and, in the authors' experience, "pure" sympathetically maintained pain is rare. Patients who have had symptoms for months to years may have severe brawny edema, muscle atrophy and contractures, and marked cyanosis of the limb. Treatment at this late stage is often unsuccessful.

Although no specific diagnostic test is available for CRPS, several tests can be supportive in making the diagnosis. The most important role of testing is to help rule out other conditions. Some of the testing used includes vascular studies, electrodiagnostic studies, radiographic studies, and blood tests. Plain radiographs can show patchy osteoporosis as early as two weeks after the onset of CRPS.

At present, sympathetic blocks, once considered essential in the diagnosis, are not required to be positive for a diagnosis of CRPS. Since some patients do not have sympathetic dysfunction, it is important to identify them because of therapeutic implications. A pharmacological sympathetic block can be performed with an intravenous infusion of phentolamine; however, this technique has not gained widespread use. The more common and time-tested approach is to perform a local anesthetic sympathetic trunk block: a lumbar paravertebral sympathetic block for the lower extremity and a stellate ganglion block or upper thoracic sympathetic block for upper extremity symptoms. Although it is vital to obtain evidence of satisfactory sympathetic block and to demonstrate the absence of somatic nerve block for diagnosis, occasionally in treatment sympathetic and somatic block may be necessary for advanced disease.

Successful treatment of CRPS depends on an aggressive and multidisciplinary approach. Since pain and limb dysfunction are the major clinical problems, physical rehabilitation and pain control are the main treatment objectives. Comorbidities such as depression, sleep disturbance, anxiety, and generalized physical deconditioning should be treated. This means that a patient's pain and disability must be treated in a manner that allows rehabilitation to proceed. Drug therapy, including anti-depressant agents, gabapentin, corticosteroids, topical analgesics, opioids, and other drugs, has been used successfully. Regional anesthesia techniques, including sympathetic blocks and somatic blocks, are required in some cases. Neuromodulation, including spinal cord stimulation and intrathecal analgesia, have been used. Intrathecal baclofen has been shown to decrease the dystonia, improve functioning, and occasionally reduce pain levels.

Like most medical conditions, early diagnosis and treatment of CRPS increase the likelihood of a successful outcome. Accordingly, patients with clinical signs and symptoms of CRPS after an injury should be referred as soon as possible to a physician with expertise in evaluating and treating this condition. Mild cases respond to physical therapy and physical modalities. Mild to moderate cases may require adjuvant analgesia, such as gabapentin and/or an anti-depressant medication. An opioid should be added to the treatment regimen if these medications do not provide sufficient analgesia. Patients with moderate to severe pain and/or sympathetic dysfunction require regional anesthetic blocks to participate in physical therapy. Most patients improve with early treatment. A small percentage of patients develop refractory, chronic pain and require long-term multidisciplinary treatment, including physical therapy, psychological support, and pain relieving measures. A suggested treatment algorithm is given.


Journal: Mayo Clin Proc, 77(2):174-180, 2002. 10 References
Reprint: Div of Pain Medicine, Mayo Clinic, 200 First St SW, Rochester, MN 55905 (RH Rho, MD)

====================================================

SYMPATHETIC PAIN VERSUS RSD

 
There are many kinds of nerve fibers. Two that are easy to understand are the motor fibers, which let us move and the sensory fibers that let us feel. Another important group of fibers that is harder to understand includes the sympathetic nerves. These nerves arise from ganglia, which are collections of the fibers located outside of the spinal cord.
The ganglia function independently (automatically) from the rest of the nervous system.

The sympathetic nerves send branches to many places, including internal organs, coverings of the spinal cord (dura), intervertebral disks, muscles, tendons, ligamentous structures, and blood vessels. The job of the sympathetic nerve is to tell the brain and spinal cord when something goes wrong with any of the tissues that it innervates.

The injury may be major or minor in severity. When you sprain an ankle, first you feel a sharp electric pain, and then you feel a burning pain. The sharp pain comes from the fast pain fiber, and the second burning pain comes from the sympathetic nerve fiber. Usually, over time, this burning pain will stop. THIS TYPE OF SYMPATHETIC PAIN IS ENTIRELY NORMAL.

Sometimes the burning will not stop. When this happens, people often have a hard time describing where their pain begins or ends, but usually can tell you that the cold or shifts in the weather makes it worse. They may have noticed that since they hurt themselves the painful part always feels cold. As it becomes more severe their skin can become sweaty, and they won't want to move the painful part (stage 1).  When it is more severe still, they do not want anyone (or anything) to touch them where they hurt.

Unfortunately, most health care providers are not familiar with the proper diagnosis and treatment of sympathetic pain, however when they hear this kind of complaint, they should at least begin to think about it. If they do, often a diagnosis of Reflex Sympathetic Dystrophy (RSD) is made.

In true RSD, there is a decrease in the local blood flow of the injured part. If allowed to persist, then the cold, sweaty and swollen skin of stage 1 progressively gets worse until there is loss of range of motion or even loss of muscle mass (stage 2). In even more severe cases, the bones may thin as well (stage 3).

In RSD, the sympathetic nerve is felt to be overacting. Liken it to a car engine that is dieseling: the ignition is off, yet the engine is still on. In this case the sympathetic nerve stays on, even when the injury itself is old and no longer represents a new injury.

In the past, diagnostic studies were not that helpful for this disorder, so most doctors who knew anything about it at all felt that performing a sympathetic ganglion block could prove a diagnosis of RSD. This block is supposed to stop the ganglion from dieseling, and therefore decreased pain and increased blood flow should occur once the block is done.

If the desired response did not occur, then the patient was frequently said to have psychological factors affecting their perception of pain (this was also the case if no one thought of the diagnosis to begin with). This approach by in large has been a failure. Many people still complained of pain, and often were felt to have obvious physical signs of injury, even though they did not respond to blockade. Others had little or no signs of injury, but persisted with their complaints in a consistently reliable manner over time.

Fortunately, THERE IS NOW AWARENESS THAT NOT ALL SYMPATHETIC PAIN REPRESENTS RSD. There is also greater understanding of how to use diagnostic studies to categorize what type of sympathetic pain exists. The two tests that are used to objectify the presence of sympathetic pain syndromes are bone scans and thermography.

The bone scan is felt to be more specific, but the thermogram is far more sensitive. In order for a bone scan to be positive, there must be up to 30% bone loss. If the three-phase study is used, then there must be vasoconstriction (decreased blood flow) of large enough magnitude to allow for it to be seen on x-ray.

The thermogram shows skin temperature changes, but does not tell you the source of those changes. While skin temperature is felt to be under the control of the sympathetic nerve fibers, the study only tells you if it is present or not: there is no specificity as to the underlying generator (or injury site) causing the change. Further, up to one third show increased, not decreased blood flow.

Clearly waiting for a positive bone scan is far too late to treat patients with this disorder, and the characteristics of the thermogram require explanation in order to provide greater utility. With the classification of different types of sympathetic pain, the objective findings as well as the clinical presentation and response to treatment are now readily identifiable
===========================================

The Sympathetic Nervous System and RSD

 
This nervous system goes to all the body structures such as muscles, tendons, ligaments, etc. and organs. When one of these sites receives an injury it's the sympathetic nervous system's job to monitor the injury and tell the spinal cord and the brain about it. Sometimes it forgets to stop monitoring the injury. It keeps on running like a car engine that keeps running after being turned off

Symptoms of RSD
Stage 1
1. Cold Hyperalgesia- cold hurts. Patients feels excessive pain to cold
2. Mechanical Hyperalgesia-Excessive pain to movement, Movement
stimulates pain. Pressure from touch hurts.
3. Vasomotor changes- Color changes. Red or blue skin color.
4. Sudomotor changes - Sweating and / or swelling.
5. Scleratomally Mediated
6. Thermogaphic Change
7. Sympathetic fiber Hyperactivity

Stage 2
8. Contrature - Lost of range of motion, muscles atrophy (waste away)

Stage 3
9. Sudeks Atrophy - Bone loss or thinning
10. - Visceral somatic convergence - A coming together of the
symoathetic nerve supply to muscles, tendons, ligaments, etc. and the internal organs
11. Regional or sclerotomal thermographic vasoconstriction
 
The TRIPLE "C" SYNDROME
The Triple C Syndrome occurs when the C fiber, by reflex becomes super sensitive to an undrlying injury of the "A delta" nerve fiber. The "A delta" nerve is sensitive to vibration, and therefore people with this problem complain that driving or operating any machinery that vibrates makes them worse. Since the C fiber is trying to limit the effect of this injury, it intensely fires, causing vasoconstriction. People with this problem say that (1) cold is painful, (2) cold burns and (3) have cold skin. Thermographic examination shows localized or regional vasoconstriction. Sympathetic blockade is fruitless as once the block wears off, the C fiber will remain hyperactive in response to the underlying A delta injury. Treatment should instead be directed toward restoration of the A delta nerve to normal through "A delta" nerve block, electroceutical application (electrical treatments to restore normal nerve firing), vasodilation and nerve membrane stabilizing medicines ( Mexitil, Catapress, Tegretol, Dilantin, etc.) by mouth.

SYMPTOMS
1. Cold Hypesthesia - Patients don't feel the cold and cannot distinguish cold as cold. The patients feels it as something else.
2.Cold Hyperalgesia - Cold hurts but the patients cannot tell that it's the cold they are feeling.
3. Cold skin
4. Pain burns
5."A delta" Neuropathy - This is the nerve fiber that is best suited for feeling or experiencing vibration. It doesn't work anymore, the nerve is acturally damaged.
6. Denervation supersensitivity of sympathetic efferents - The sympathetic nerve that supplies the tissue goes wild or becomes super sensitive as a result. It causes all the blood vessels to constrict. The sympathetic nerve respond to a sympathetic nerve block because it's not the nerve that's injected.
7. Arteriolar smooth muscle - vasoconstriction - Tighten or closure of blood vessels.
8. Localized vasoconstrictive thermographic changes - Cold temperature change in local area around injury.
 
====================================================

 
 
©AWARE-RSD SUPPORT
Copyright 2005