ACUTE AND CHRONIC PAIN SYNDROMES (CPS) OF PRIMARILY NEUROPATHIC ORIGIN... (article)

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ACUTE AND CHRONIC PAIN SYNDROMES (CPS) OF PRIMARILY NEUROPATHIC ORIGIN CAUSALGIA AND OTHER REFLEX SYMPATHETIC DYSTROPHIES: B. REFLEX SYMPATHETIC DYSTROPHY (I-5)

Reflex sympathetic dystrophy (RSD) is an all-inclusive term applied to a great variety of seemingly unrelated disorders that in the past were described separately under the names of minor causalgia, post-traumatic pain syndrome, post-traumatic spreading neuralgia, post-traumatic vasomotor disorders, post-traumatic painful arthrosis, Sudeck's atrophy, sympathalgia, shoulder- hand syndrome, chronic traumatic edema, post-traumatic edema, and reflex dystrophy (among others). Indeed, Ascherl and Blümel (75) have pointed out that there are 9 other terms in English for this syndrome, as well as 26 terms in German and 9 in French. The precipitating factor may be accidental or surgical trauma or one of a variety of disease states, but all are characterized by varying degrees of pain, vasomotor and other autonomic disturbances, delayed recovery of function, and trophic changes. If applied early, sympathetic interruption produces prompt relief of pain and disappearance of the pathophysiology. As previously mentioned, these similarities prompted me in 1953 to suggest that all of them be considered under the generic term "reflex sympathetic dystrophy."

Although a post-traumatic painful disorder associated with vasomotor disturbance was first described by Wolff in 1877 and again by Kummell in 1895 (see 1), Sudeck (76) published the first classical description of this syndrome in 1900. Subsequently, additional reports were published by many others, most notably in 1933 by Fontaine and Herrmann (77), who called it "post-traumatic painful osteoporosis." Five years later Livingston (78) reported cases manifested by severe aching pain and mild signs of reflex sympathetic dystrophy under the term "post-traumatic pain syndromes." In 1940 Homans (79) first used the term "minor causalgia" to designate post-traumatic syndromes manifested primarily by burning pain, hyperesthesia, and allodynia not due to major nerve injury. Subsequently the term was used by Livingston (25), who noted the similarity between minor causalgia and post-traumatic pain syndrome and came to the conclusion that they represented lesser degrees of the same pathophysiologic process as causalgia. In 1946 Evans (80) used the term "reflex sympathetic dystrophy" for some but not all of the conditions I have included. Although these various conditions have similar symptoms and respond to sympathetic interruption, the degree of one particular sign or symptom may be so prominent as to almost obscure the others—a factor responsible for the different terms used.

Reflex sympathetic dystrophies are clinically much more important than causalgia because they are frequent causes of pain and disability, especially in orthopedic and industrial practices, and also because prompt recognition and effective treatment result in rapid remission of symptoms and complete recovery. For many years they were frequently misdiagnosed and improperly treated, or both, and in patients sustained prolonged or permanent disability. Fortunately, in recent years there has been an increased awareness of these disorders, and effective therapy is being carried out in more and more patients.

Etiology

Reflex sympathetic dystrophy can be produced by: accidental injury, surgical or other iatrogenic injury, and micro- or macrotrauma associated with certain occupations; it is also associated with certain diseases such as myocardial infarction and necrologic disorders.

Trauma

Trauma secondary to accidental injury is the most common cause of reflex sympathetic dystrophy (77-84). Injuries include sprain; dislocation; fracture, usually of the hand, feet or wrists; traumatic amputation of fingers; crush injury of fingers, hands or wrists; contusions and even minor cuts; or pricks of the fingers, hands, toes, or feet. I have encountered a number of cases that followed laceration of the wrist, hand, or foot, such as occur when the hand is accidentally thrust through a window, or more frequently with industrial accidents. There is no correlation between the severity of the injury and the incidence, severity, and the course of these symptoms. Indeed, most of these cases often follow minor injuries to those regions particularly rich in nerve endings such as the skin and pulp of the fingertips, the skin of the hand, and the periarticular structures of the interphalangeal wrist and ankle joints. Reflex sympathetic dystrophy can also occur as a result of minor injury to a peripheral nerve even though significant neurologic signs do not develop promptly after the injury. Stein (85) has drawn attention to the role of trauma to the median nerve as it passes through the carpal tunnel consequent to Colles' fracture in causing reflex sympathetic dystrophy, relieved by nerve decompression. Similar cases have been reported by Horowitz (57).

Iatrogenic Injury

A number of cases of RSD have developed from iatrogenic complication of surgical or medical therapy including amputation of the hand or fingers, excision of small ganglia or tumors of the wrist, forceful manipulation, tight casts, and myelography (57, 86). A significant number of cases of reflex sympathetic dystrophy have been reported that developed after accidental insertion of needles into the median nerve in the course of starting an infusion or into the sciatic nerve in the course of giving an intramuscular injection of analgesics (57, 87, 88). The syndrome can also develop after injection into or near major nerves of such irritating agents as thiopental sodium and alcohol.

Although reflex sympathetic dystrophy is most frequently seen in adults, I have seen the syndrome in a number of children, and several reports on RSD in children have been published by others. The case of a 5-year-old girl I managed is cited in the first edition of this book (1, p. 936). Carron and colleagues (87) reported this syndrome in 3 children ranging from 3 to 10 years of age. Ruggeri et al. (88) reviewed the literature up to 1980 and reported on 6 cases of their own. Therapy is discussed in a later section, and more detailed consideration of RSD in children is presented in Chapter 29.

DISEASE

In recent years it has become apparent that although injury is the most common cause of reflex sympathetic dystrophy, various visceral, neurologic, and musculoskeletal diseases or disorders can also produce this syndrome. The most common of these is the "shoulder-hand syndrome," characterized by pain and disability of the shoulder and pain and swelling of the ipsilateral hand. Although these symptoms consequent to myocardial infarction had been mentioned by Weir Mitchell and later by Osler during the 19th century and by several writers during the first four decades of the present century (see 1 for refs.), it was Steinbrocker (89) who coined the term and classified the stages of this syndrome, which has been reported to occur in as high as 22% of patients who have had myocardial infarction (see 1 for refs.). The course of this condition is similar to that which will be described for the syndrome.

Reflex sympathetic dystrophy has also been reported to develop in a very small number of patients with diabetic neuropathy (57), herniated disk disease (90), degenerative joint diseases of the cervical spine, and such neurologic disorders as cerebrovascular accident, tumors of the neuraxis, poliomyelitis, multiple sclerosis, traumatic lesion of the brain stem, and related conditions (91). These patients have the essential characteristics of reflex sympathetic dystrophy including burning pain, allodynia, hyperpathia, and pain on movement in the affected extremity. Loh et al. (91) have reported several patients whose symptoms were relieved by sympathetic interruption.

I have managed a number of patients with signs and symptoms of reflex sympathetic dystrophy consequent to infiltration of the brachial plexus in the supraclavicular region or in the axilla or in the lumbosacral plexus in the pelvis by extension or metastases of carcinoma (1). These patients manifested the characteristic burning, aching pain, edema, and vasomotor disturbances of the extremities, which were relieved by sympathetic blockade. Subsequently, similar cases of reflex sympathetic dystrophy associated with cancer and relieved by sympathetic blockade were reported by others (see Chapter 24).

Clinical Manifestations

Reflex sympathetic dystrophy, like causalgia, is manifested by pain, allodynia, hyperalgesia, and hyperesthesia and frequently by vasomotor and sudomotor disturbances and skeletal muscle hypotonia. Later features are weakness, atrophy, and trophic changes of the skin and its appendages and of the muscle, bones, and joints. The symptoms may be severe (grade 1), moderate (grade 2), or mild (grade 3).

Grade 1 Reflex Sympathetic Dystrophy

Grade 1 reflex sympathetic dystrophy is characterized by clinical features that are similar to classic causalgia. The pain is severe, burning, knife-like or lancinating, unrelieved by rest, subject to exacerbation by the slightest emotional or physical stimulation, and often associated with severe vasomotor and sudomotor disturbances. In Tahmoush's study of four patients with causalgia due to peripheral nerve injuries and four patients with similar symptoms caused by various injuries not involving major nerves, he noted that the symptoms were similar in character and degree (3). The McGill Pain Questionnaire revealed that the present Pain Intensity (PI), the pain descriptors, and the Pain Rating Index (PRI) were similar in the two groups, who had had the syndrome for an average of 17 months. As previously mentioned, these data and other factors led Tahmoush (3) to believe that there is no difference between classic causalgia and reflex sympathetic dystrophy. There are some differences, however. For example, in many patients with RSD due to non-nerve injuries, the pain usually develops after several weeks or months and becomes severe with time. This pattern is in con trast to that observed with causalgia, in which the onset of pain is immediate or within the first several days.

Grades 2 and 3 of RDS

Grade 2 reflex sympathetic dystrophy is usually characterized by dull, throbbing, aching, burning diffuse pain and moderate or mild vasomotor and sudomotor disturbances. Grade 3 is the mildest and perhaps the most common form, representing the border zone between the normal response of an extremity to trauma or disease and the more severe disorders previously described. Because of the mildness of the symptoms and the paucity of physical signs, many patients in this cat egory never receive the benefit of correct diagnosis and appropriate therapy.

Comment

One of the most striking features of this syndrome is that although all cases show the aforementioned pathology of reflex sympathetic dystrophy, one sign or symptom is frequently out of proportion to the others. In some there is severe pain with little or no vasomotor disturbances: in others there is little pain but intense vasomotor hyperactivity such as coldness, cyanosis, and hyperhidrosis. In others there is marked edema with varying degrees of vasomotor disturbances and pain, and in still others, pain and vasomotor phenomena are present without any evidence of swelling. Almost invariably, trophic changes occur later in the disease if appropriate therapy is not carried out; spontaneous remission is rare. In spite of differences in signs and symptoms, certain features are common to all cases of the syndrome. The most notable is that the pain and physical signs usually do not conform to known patterns of segmental or peripheral nerve distribution. Moreover, they have a tendency to spread proximally so as to involve the entire limb and occasionally the ipsilateral quadrant of the body. This remarkable tendency for constant long- established pain and associated phenomena to spread is a characteristic and one of the most impor tant features of this syndrome.

Course of the Syndrome

The course of reflex sympathetic dystrophy also varies depending on the severity of the disorder and whether proper treatment is instituted or not. Without treatment, the disorder passes through three stages:

FIRST(ACUTE) STAGE. In the first (acute) stage, which usually begins days or weeks and sometimes months after the injury, the patient experiences constant burning or aching pain, allodynia, hyperalgesia, hyperesthesia, hyperpathia, localized edema, muscle spasm, and tenderness of the affected part of the limb (Fig. 11-5). The pain is usually aggravated by movement, emotional stress, and auditory and visual stimuli. All of these factors are conducive to limitation of motion of the affected limb. During the early part of this stage the pain is usually localized in the distal part of the limb and the skin is usually warm, dry, and red. Toward the end of the stage, the pain spreads and the skin becomes cyanotic, cold, and sweaty. Subsequently there is accelerated growth of the hair and the nails, and skin changes begin to appear. During the early and middle part of this stage, roentgenograms reveal no bony changes, but bone scans with technetium (99mTc) fluorophosphate show increased uptake by the small joints (90). In patients with grade 3 and some patients with grade 2, the first stage lasts 6 to 8 weeks and then subsides spontaneously or responds rapidly to treatment. In most of grade 2 and all of grade 1 cases that remain untreated, the symptoms become progressively worse. The first stage can last as long as 6 months.

SECOND (DYSTROPHIC) STAGE. The second stage which develops about 3 to 6 months after onset of the syndrome in untreated patients, is characterized by continuous burning, aching or throbbing pain, marked allodynia, hyperalgesia, and hyperpathia, and the skin is cool, pale gray, and frequently cyanotic. The edema changes from a soft to a brawny type of glaze overlying the skin, there is decreased hair growth which then becomes scant, and the nails become brittle, cracked, and heavily grooved, and there is increased thickness of the joints and muscle wasting so that movement becomes even more limited (Fig. 11-6). Early in the second stage roentgenograms show spotty osteoporosis, but later these bony changes spread and eventually become indistinguishable from severe diffuse osteoporosis, especially in the epiphyseal region.

THIRD (ATROPHIC) STAGE. The third stage is characterized by marked atrophic tissue changes that have become irreversible. The burning pain, allodynia, and hyperpathia may be less severe. The skin becomes smooth, glossy, drawn, and pale or cyanotic, and the skin temperature is decreased. The nails become increasingly brittle and ridged with lateral arching. Subcutaneous tissue is very atrophic with marked decrease in fat pads, and the digits are thin and pointed. Atrophy of the muscles, particularly the interossei of the hand or foot, is marked. The interphalangeal and other joints of the foot or hand are extremely weak, have limited motion, and finally become ankylosed. Contraction of the flexbor tendons often occurs at this stage (Fig. 11-7), and occasionally subluxations are produced. Bone atrophy becomes diffuse and marked (Fig. 11-8).

Many of the patients in stages 2 and 3 of the disease develop psychologic and emotional disturbances including anxiety, followed by depression and other characteristics discussed in Chapter 8. In a retrospective study of 125 patients with reflex sympathetic dystrophy seen at the Mayo Clinic, Subbarao and Stillwell (92) administered the Minnesota Multiphasic Personality Inventory (MMPI) to 45 patients and noted that 14 (31%) had abnormal HS (hysteria), D (depression), and HY (hypochondriasis) scores, and in 18 (42%) the HS and HY scores were both abnormal. On the basis of the descriptions of the symptoms, all of these patients were in stage 2 or stage 3 of the disease. Although some patients have predisposing psychologic problems, in some 90% of patients these are the result rather than the cause of prolonged pain and disability. Psychiatric studies by de Takats (63) and Schumacker and Abramson (81) clearly demonstrated this relationship. Among the 142 male military patients managed by the latter authors, virtually all of the patients had assumed the attitude and behavior of the chronic invalid: they were weary from prolonged disability and hospitalization and usually had a relatively hopeless viewpoint toward the possibility of eventual recovery. Only in 11 patients, however, was a neuropsychiatric disorder diagnosed by psychiatric consultants.

The ABC Syndrome

Recently Ochoa (58) described a newly recognized painful syndrome in a small group of patients. He believes this syndrome represents a subset of causalgia/RSD, and he calls it the ABC (Angry Backfiring C nociceptor) syndrome. This syndrome has been found in patients with major sciatic nerve injury, diabetic neuropathy, and other neuropathic disorders. The following are the characteristics of the syndrome: (a) stimulus-induced pain in response to low-intensity skin stimulation (hyperalgesia, allodynia) and often spontaneous burning pain; (b) induced pain is characteristically elicited by both mechanical and thermal stimuli—he named this polymodal hyperalgesia (PH); © in most patients decreasing the skin temperature abolishes both spontaneous and mechanically induced pain, whereas increasing the temperature aggravates both symptoms. Less often this thermal dependence is reversed (i.e., cold aggravates and heat relieves the pain), and in still other more unfortunate patients, the thermal dependence is bipolar, expressing aggravation by either increasing or decreasing the temperature. He termed such influence of one stimulus energy on the perception threshold of another cross-modality threshold modulation (XTM); (d) vasodilation with warming of symptomatic skin as best revealed by thermography is a key sign of the syndrome; and (e) symptoms that are up-modulated by increased temperature may worsen during sympathetic blocks. As discussed in some detail in the section C, Ochoa believes this syndrome is due to sensitization of polymodal nociceptors (CPNs) and that the most rational therapeutic strategy is drug- induced desensitization of CPNs.

Diagnosis

A diagnosis of reflex sympathetic dystrophy is based on the following criteria: ( 1) history of recent or remote accidental or iatrogenic trauma or disease; (2) presence of persistent pain that is burning, aching, and/or throbbing in character; (3) one or more of the following: (a) vasomotor and/or sudomotor disturbances; (b) trophic changes, edema of the limb, sensitivity to cold, muscle weakness or atrophy, or trophic changes; and (4) relief of pain and modification of signs after regional sympathetic blockade. As previously mentioned in connection with causalgia, the fourth criterion is considered by most writers on the subject as one of the most important diagnostic features of reflex sympathetic dystrophy. While the "typical" case of reflex sympathetic dystrophy can be diagnosed without difficulty, many subtle cases of grade 3 RSD present only one or two of the symptoms and signs, thus simulating other diseases—or the entire symptomatology may be vague and confusing, making a differential diagnosis difficult. In such cases it is particularly important to carry out a detailed history, thorough physical examination, quantitative sensory and sympathetic testing, and to use thermography and advanced radiologic techniques.

Sensory/Sympathetic Testing

The value of testing the cutaneous mechanical and thermal nociceptive thresholds (cold and heat) has already been mentioned in relation to causalgia and is also a useful tool in patients with reflex sympathetic dystrophy. Procacci and associates (see 5) studied the cutaneous pain threshold and the galvanic skin reflex in patients with RSD and found them abnormal. Regional sympathetic blocks restored these parameters to normal, suggesting that these techniques might be useful in the diagnosis of RSD and in evaluating the efficacy of sympathetic blockade.

Thermography

The bases and clinical application of thermography in helping diagnose patients with chronic pain is discussed in detail by LeRoy in Chapter 34. Here I will briefly discuss its use to help in making the diagnosis or to settle confusing cases of RSD. Hendler and associates (93) used this tool to evaluate 224 consecutive patients complaining of chronic pain without positive radiologic, neurologic, orthopedic, or laboratory evidence and who had been referred to them for psychiatric evaluation. Abnormal thermographic results in the affected limb (a reduction in temperature of 1 C or more) were found in 43 (19%) of the patients. Of this group, 32 (74%) patients had evidence of reflex sympathetic dystrophy. The diagnosis was confirmed by sympathetic block, which in some patients was followed by sympathectomy, resulting in permanent pain relief. Figure 11-4 shows the diagnostic value of thermograms in one of the patients examined by LeRoy. Ochoa (58) has found thermography valuable in investigating and defining the characteristics of the ABC syndrome and indeed in helping in diagnosis of reflex sympathetic dystrophy.

Radiologic Techniques

Since the mid 1970s an increasing number of publications have appeared on the use of fine- detail radiography, photon absorptiometry, and bone and joint scintigraphy. In a study of nine patients with RSD syndrome, Genant et al. (94) found diffuse and periarticular soft tissue swelling, osteopenia, and endosteal and intracortical bone resorption in 75 to 100% of the extremities studied. Carlson and associates (90) reported that in patients with RSD, roentgenograms of the affected limb were normal, but bone scan with technetium (99mTc) pyrophosphate showed increased uptake in the affected limb, particularly the distal joints of the foot. More recently, Holder and MacKinnon (95) reported on 145 consecutive patients with RSD who underwent three-phase radionuclide bone scanning (TPBS), which revealed specific patterns for positive radionuclide angiograms, blood pooling, and delayed images. They found the delayed images to be very sensitive (96%) and specific (97%) and to have highly significant negative predictive value (99%). They concluded that TPBS provides an objective marker for RSD and can be used to exclude a diagnosis of the syndrome in patients who have subtle or vague symptoms. Scintigraphy is also useful in following the response of patients to treatment (90, 94, 96).

Prognosis

Some mild, early cases subside spontaneously in a few weeks, and some moderately severe cases have a self-limited course and heal spontaneously within a year, but in most instances RSD without proper treatment progresses through the various phases. This is particularly true of the more severe and chronic forms that show widespread signs and symptoms. Unless adequately treated, patients develop irreversible trophic changes and psychologic/emotional disturbances, so that there is mental as well as physical invalidism. In this stage functional, economic, and social rehabilitation of such patients is hardly ever obtained, and they may end up having their extremities amputated, requiring sanitarium care, or even committing suicide (57). Such severe prognosis emphasizes the great importance of prevention and early proper treatment of this syndrome.

Treatment

No correlation has been established between the type and severity of injury and the incidence of reflex dystrophy or its course, but clinical evidence strongly suggests that this disorder can be prevented in a certain number of cases (see 1 for refs.). The preventive measures include treatment at the site of injury, early and adequate relief of pain with analgesic block, and psychologic support of the patient. Proper care of the local injury requires debridement, removal of foreign bodies, adequate reduction of fractures, surgical correction of torn muscles, tendons, and ligaments, and active treatment of infection. Although it is important to utilize immobilization and bed rest when the degree of injury requires such measures, in many cases of simple sprains or fracture early active motion may help to prevent the development of reflex mechanisms that lead to dystrophy. In addition to providing pain relief, regional analgesia that includes sympathetic blockade improves the circulation of the injured part and thus enhances healing and reduces edema. There is also evidence that it helps to prevent reflex sympathetic dystrophy (see 1 for refs.).

Patients who develop reflex sympathetic dystrophy should receive specific and aggressive treatment, which consists initially of a series of regional sympathetic blockades, and if these provide only transient relief of pain, sympathectomy. Other therapies that have been reported as effective include transcutaneous nerve stimulation and systemic corticosteroids. Regardless of the form of therapy, patients presenting with stage 2 or stage 3 of the disease should also have a vigorous physical therapy and exercise program and, if appropriate, psychotherapy. Although some patients with mild reflex sympathetic dystrophy recover spontaneously or with the aid of conservative measures, many, unfortunately, do not. Bonica (1, 6, 7), Kiger (97) and many others (10, 27, 63, 78- 85) have emphatically warned against excessive delay in applying specific therapy. This consideration is especially important when the pain and the other symptoms are moderate and there is a natural tendency to continue with more conservative measures.

Regional Sympathetic Blockade

During the early stages of reflex sympathetic dystrophy, regional sympathetic blockade achieved a local anesthetic or with intravenous regional sympathetic block constitutes the primary and most effective treatment of this disorder. The efficacy of regional sympathetic blockade in the management of reflex sympathetic dystrophy is attested by the results achieved by those who have had extensive experience with this disorder. De Takats (63) reported that 87% of the patients treated with sympathetic blocks alone obtained complete recovery, and Evans (80) reported arrest of symp toms or considerable improvement in all 12 patients treated only with this method. Many other reports attesting to the efficacy of sympathetic blockade can be found in the first edition of this book (1, p. 930).

Provided it is properly executed, response to regional sympathetic blockade is invariably prompt and dramatic, with prompt relief of pain, allodynia, and hyperpathia; if the patient has evidence of vasoconstriction, the block results in increase in the temperature of the limb, disappearance of cyanosis, and decrease in swelling over the next several hours and improved func tion in a few days. The duration of the response produced by local sympathetic block varies from a few hours to several days, whereas with intravenous regional sympathetic blockade with guanethidine the duration is considerably longer. Personal experience and the results reported by many others (25, 78, 80-85, 87, 91, 98) suggest that, properly used early in the course of the disease, sympathetic blockade combined with vigorous physical therapy cures some 80% of the patients with reflex sympathetic dystrophy. Proper use requires correct diagnosis, early treatment, and complete sympathetic interruption of the limb, promptly followed by physical therapy.

When local anesthetic block of the regional sympathetic supply is used, the initial injection can serve as a diagnostic and prognostic procedure and can be done with any of the local anesthetic solutions. If the initial block produces partial or no relief, the block is incomplete, the diagnosis is incorrect, or both. In such instances the technique should be repeated several times and the completeness of sympathetic interruption ascertained before a final decision is made. If the block produces relief, thus confirming the diagnosis, it should be repeated with a long-lasting agent such as 0.2% tetracaine (Pontocaine) or 0.25% bupivacaine (Marcaine) solution as often as necessary to maintain continuous pain relief. Blocks are continued until the patient is completely cured or reaches a plateau with this form of therapy.

Wang and his associates (98) compared the long-term effects of sympathetic blockade with those of conservative treatment in 51 patients with reflex sympathetic dystrophy after soft-tissue injury or associated with peripheral nerve lesion caused by accidental injury or surgery to the hand. Although the clinical condition of the patients who received conservative treatment was less severe initially, at a 3-year follow-up, only 5% had complete pain relief and another 40% had good or partial improvement, for a total of 45%. Among the patients treated with sympathetic blockade, 75% had complete pain relief or good response—a significantly higher rate than that for patients who were treated conservatively. Further analysis revealed that, at 3-year follow-up, improvement with sympathetic blockade had occurred in 80% of the patients who had received treatment within 1 month of the onset of RSD, 75% in those treated within 1 to 6 months, and 71% in those treated within 6 to 12 months. Of those patients who suffered from "painful neuropathy," 53% showed improvement at 3-year follow-up, whereas of those with RSD due to fracture or soft-tissue injuries, 94% reported improvement. These data emphasize the importance of early treatment and the fact that in patients who develop RSD following nerve injury sympathetic blockade is effective but to a lesser extent than those in whom RSD is due to non-nerve injuries.

The use of intravenous regional sympathetic block (IRSB) with guanethidine every 2 days minimizes the need for repeated insertion of needles and provides a prolonged effect. In a study intended to compare IRSB and stellate (cervicothoracic) sympathetic block with a local anesthetic in 19 patients with reflex sympathetic dystrophy, Bonelli and associates (99) noted that both techniques provided good pain relief, but the duration of analgesia and sympathetic blockade was significantly longer in the guanethidine group. At 1-month and 3-month follow-up it was noted that the IV guanethidine block carried out every 4 days up to a total of 4 blocks was comparable with the cervicothoracic sympathetic block every other day for a total of 8 blocks. Similar results have been reported by Loh, Nathan, and their associates (62, 65, 68, 92) and by Hannington-Kiff (100).

Engkvist and associates (101) reported on 24 patients who had sustained amputation of the fingers with damage to the digital nerves 6 months to 5 years earlier and who developed cold allodynia. Patients had a feeling of chilling discomfort that increased to pain on exposure to cold temperature. All of the patients had reduced thresholds for cold pain (in the injured hand cold pain was provoked at a temperature that was 5.5°C higher than the corresponding area in the uninjured hand, and exposure to cold caused the hand to become white or bluish-white). Moreover, 16 of the patients had vibration allodynia (application of 130 Hz, which could be tolerated in the uninjured hand, caused pain in the injured hand). Intravenous guanethidine (20 ml diluted to 40 ml injected into the arm) eliminated the cold allodynia; the hand became warm and the vibration allodynia was eliminated in 7 of the 16 patients who had it. In 11 patients the benefit disappeared after 1 week, but 9 patients had relief that lasted 2 to 12 weeks. Seven of the latter group were given repeated blocks every second or third month during the cold period of the year, with benefit. In view of the long interval between the injury and the sympathetic blockade, these results can be considered impressive.

As already mentioned in connection with causalgia, on the basis of its advantages over repeated sympathetic block, intravenous guanethidine is likely to be considered the primary form of therapy for reflex sympathetic dystrophy in the future.

Other Nonsurgical Therapies

Transcutaneous Electrical Nerve Stimulation

Ruggeri and his associates (88) have reported that transcutaneous electrical nerve stimulation (TENS) is also highly effective for reflex sympathetic dystrophy. On the basis of treatment of several patients, they claim that this technique, like sympathetic block, produces cure in over 90% of the patients treated. Others who have used TENS have found that although there is significant pain relief during the initial phase, there is a drop off after several weeks of therapy. In view of these results and in view of the availability of intravenous guanethidine, it is likely that TENS used alone will not become an established therapy for this syndrome except as an adjunct to physical therapy (see below).

Systemic Drugs

In the section on causalgia, it has already been mentioned that propranolol has been found effective for treatment of reflex sympathetic dystrophy by Tahmoush (3) and others (70). On the basis of the highly favorable results achieved with phenoxybenzamine in the treatment of causalgia reported by Ghostine and his associates (52), it can be predicted that this drug will also be effective in the treatment of reflex sympathetic dystrophy. The dosages of these two drugs have already been mentioned.

Kozin and associates (96) have reported impressive results with systemic oral corticosteroid therapy in 17 patients with reflex sympathetic dystrophy. In most instances they prescribed 60 to 80 mg of prednisone for 2 to 4 days and then decreased the dosage by 10 to 20 mg every 2 to 4 days, and later tapered the dose rapidly from 40 mg to 5 mg; the dosage remained at this level for several additional weeks.

Cryotherapy

Patients with burning pain, hyperalgesia, and allodynia that is made worse by heat or is unaffected and/or aggravated by sympathetic block may be relieved by immersing the limb in a bucket of ice water (54).

Sympathectomy

In patients in whom a series of sympathetic blocks produces complete but only temporary relief, sympathectomy should be considered (1, 5-7, 81-85). Whether this should be achieved chemically or surgically depends on the particular patient's physical condition, the severity of the disease, and the patient's attitude toward both techniques. Chemical sympathectomy with 6% aqueous phenol or 50% alcohol produces sympathetic interruption for several weeks to several months and is especially useful in older or poor-risk patients. In patients who are younger and in good physical condition, surgical sympathectomy is preferable.

Adjunctive Therapy

Physical Therapy

In managing patients with reflex sympathetic dystrophy, sympathetic blockade should be combined with progressively more vigorous physical therapy. Temporary pain modulation is first accomplished with radiant heat, whirlpool, and perhaps TENS, and edema is minimized with elevation, pressure pump, and pressure dressings (1, 5-7, 83, 84, 98). Range-of-motion and stretching exercises are then used to counteract the tendency toward contractures. Motor re-education, relaxation, and strengthening exercise are added as the condition allows. Prior to dismissal from formal therapy, the patient should always be instructed in a home exercise program to maintain gains.

When pathologic changes, such as shortening of tendons, are present in advanced cases, orthopedic care is necessary for recovery of function after sympathectomy. In any case, it is important to consider and muster all possible therapeutic methods and neglect no useful adjuvant in treatment.

Psychotherapy

As previously mentioned, many patients with longstanding, chronic reflex sympathetic dystrophy undergo psychologic and emotional disturbances as a result of long suffering and disability. Intense psychologic support and encouragement to undertake a vigorous program of physical therapy and exercise of the limb and to use it as much as possible should be part of all treatment. Specific aids to allay fear, anxiety, and apprehension are essential, and depression should be treated with tricyclic antidepressants. If severe psychopathology is deemed to be present, psychiatric consultation and a course of psychotherapy should be implemented.

C. MECHANISMS OF CAUSALGIA AND REFLEX SYMPATHETIC DYSTROPHY

In 1872 Weir Mitchell (12) proposed that the pain of causalgia was due to two mechanisms: a peripheral mechanism was responsible for the pain in the field of the injured nerve, and a central mechanism was responsible for the extension of pain beyond the territory served by the injured nerve. A somewhat similar though more sophisticated hypothesis was proposed a year later by Létiévant (13), who stated that three anatomic sites were fundamental to the mechanisms: the peripheral nerve and its point of irritation, the spinal centers, and the sensorium. He believed that local irritation due to the injury produced impulses that were transmitted to the spinal centers, where an abnormal neural activity developed and spread to adjacent centers if the impulses were strong and sustained.

In the ll½ decades that have elapsed, many other hypotheses have been suggested to explain causalgia and other reflex sympathetic dystrophies. In virtually every case the proposed hypothesis was intended to explain the character of the burning pain, allodynia, hyperalgesia, and hyperpathia, and other symptoms. Those proposed during the past half-century have also tried to explain the relief of pain by sympathetic interruption within the context of the neurophysiologic evidence available at the time. Although most writers have acknowledged that the pathophysiology involves peripheral nerves and the central nervous system, some writers have insisted that the primary site or critical dysfunction is in peripheral tissues; others have believed it to be in peripheral nerves; and still others insisted that it is primarily or wholly in the spinal cord or higher parts of the neuraxis. A comprehensive summary of the hypotheses proposed prior to 1952 is contained in the first edition of this book (1, pp. 966-973), and more recent reviews can be found in one of my publications (7) and in those of Sunderland (102), Jänig (103), Devor (104), Ochoa and associates (58, 105) and Schott (106).

After reviewing various hypotheses and data available at the present time, I am convinced now as I was 35 years ago that causalgia involves abnormal neural activity in every part of the nervous system. This disorder, like many others, is a dynamic, ever-changing process affecting all parts of the nervous system and affected by inhibitory and excitatory events in the periphery, spinal cord, and other parts of the neuraxis, and by supraspinal descending influences. Therefore causalgia can be considered to be initiated and maintained by peripheral and/or peripheral-central mechanisms. This hypothesis is in conformance with the classification of chronic pain mechanisms discussed in Chapter 8. I will first discuss the evidence about the peripheral mechanisms and then consider peripheral-central mechanisms. Comments are limited to the most important recent findings relevant to both mechanisms. Other details are presented in Chapter 8.

Peripheral Mechanisms

Sympathetic Dysfunction

In many patients the peripheral part of the mechanism involves the sympathetic nervous system, which undoubtedly plays a critical role because sympathetic interruption relieves the spontaneous pain, allodynia, and hyperpathia. Moreover, there is evidence that sympathetic fibers supply large myelinated mechanoreceptors (107). A rich sympathetic nerve supply is found in dorsal root ganglia, some of the sympathetic fibers supplying the blood vessels of these structures and others supplying the afferent neurons (108). It has also been calculated that there are about 330,000 varicosities in a noradrenergic nerve per cubic millimeter, so that peripheral nerves accompanied by sympathetic nerves are bathed in a solution of norepinephrine whenever there is sympathetic activity (109). It has been found that intra-arterial injection of adrenalin increases the alpha-beta spike of the action potential of the sciatic nerve about 100% and occasionally as much as 300% (107, 109). Moreover, although the slowly-adapting I receptors are silent in the absence of mechanical stimu lation, they develop a resting discharge due to sympathetic stimulation (3). In contrast, sympathetic stimulation has no persistent effect on A-delta or C-polymodal nociceptive afferents in the absence of tissue damage (3). However, tissue damage causes damage to the nerve membrane, which then becomes extremely sensitive to norepinephrine liberated locally. The hypersensitivity involves terminals that may be anatomically intact but physiologically and pharmacologically act abnormal. In patients with causalgia that had been relieved by sympathectomy, Wallin and associates (110) found that intracutaneous injection of norepinephrine in the previously causalgic skin reproduced the pain and allodynia. Through microneurographic studies they concluded that the nociceptive information was carried by A-delta nociceptors.

Studies from experimentally induced neuromas have shown that some myelinated afferent fibers develop an increased resting discharge originating in the neuroma or dorsal root ganglia (104, 111). These studies have shown that during the first day or two after injury, almost all fibers are silent, but during the period of 3 to 16 days an intense spontaneous barrage occurs in all myelinated neuroma fibers (105). Thereafter there is a decrease in neural activity to relatively low but stable levels. Sympathetic stimulation or topical application of norepinephrine or slight mechanical distortion greatly excites many of the fine terminals in the sprouts and causes increase in the ongoing activity and firing in previously silent units. In this regard it is important to note that Devor and associates (see 105) have discovered an important genetic determinant in the intensity of the ectopic neuroma barrage. This finding might help explain why causalgia and reflex sympathetic dystrophy do not develop in all patients who are injured. Devor (104) has reported that he and his associates have estimated that 65% of all myelinated sciatic nerve fibers are sensory and that the incidence of spontaneous activity in neuroma afferents 3 to 16 days after operation is 25% ± 11.6%. In contrast, during this phase no more than 2% of unmyelinated axons in rat neuroma have detectable ongoing discharges, suggesting that C-polymodal nociceptors are not the primary cause of spontaneous pain.

In connection with damage of sympathetic fibers, one must consider the older theory that discharges in sympathetic efferents directly activate adjacent "pain afferents" by electrical (ephaptic) cross talk through closely opposed axon membranes in regions of injury (27). After a period of doubt of the existence of artificial synapses that began in the mid 1970s, recent studies in animal models of chronic demyelination, of regeneration, and of neuroma formation have confirmed the existence of ephapse in long-term injured nerves (104, 112). Such cross talk tends to be a late consequence of nerve injury, however, and does not involve the appropriate axon population (104). Furthermore, in experimental preparations, afferent discharges conducted centrally from zones of nerve injury have characteristics of endogenous pacemakers rather than duplication of sympathetic outflow patterns (104). Moreover, the ephapse hypothesis does not explain the complete relief of spontaneous pain, allodynia, and hyperpathia achieved with nerve block distal to the nerve injury nor that achieved with intravenous guanethidine regional block or with other adrenergic agents that block sympathetic function at the terminals of postganglionic sympathetic fibers.

These and other data showing the persistence of adrenergic chemosensitivity in the neuroma have prompted Devor (104) to suggest that chemical rather than electrical (ephaptic) cross talk is the mechanism responsible for activation of high-threshold afferents by sympathetic efferents in the region of nerve injury in causalgia. More specifically, he has proposed (a) that sympathetic efferent activity releases catecholamines (including noradrenalin) into the extra-cellular space within the neuroma; (b) that these molecules bind to ectopic alpha adrenergic receptors on nearby demyelinated afferents and/or afferent sprouts, producing a local depolarization (generator potential); and (c) that this sets off (or changes) repetitive discharge in axons whose membrane properties have been changed locally as a result of the lesion, transforming the axons from spike propagators to spike generators. Because of the abnormal electrogenic properties of these fibers, an abnormal afferent discharge is generated. Although these changes might be operative in causalgia associated with peripheral nerve injuries, they are not relevant to those cases of RSD in which the nerve is not injured, and they cannot explain the efficacy of nerve blocks distal to the site of nerve injury or of intravenous guanethidine regional block. Moreover, because neuroma formation takes days, this hypothesis cannot explain the immediate onset of the pain and allodynia after nerve injury in many patients.

Sensitization of Polymodal Nociceptors

In his recent report of patients with the ABC syndrome, which Ochoa (58) considers a small subset of causalgia or RSD, the predominant mechanism in these patients is sensitization of polymodal nociceptors. Ochoa's elegant and meticulous clinical studies entailed the combined use of intraneural microrecording, thermography, modality-specific quantitative sensory tests, monitoring of the function of the sympathetic nervous system, and differential nerve blocks. That sensitization of polymodal nociceptors is involved is suggested by the presence in these patients of polymodal hyperalgesia (PH) and proven in one patient by microrecording of single C-fiber polymodal nociceptors. Further evidence was provided by the failure of differential A-fiber block to abolish PH and cross-modality threshold modulation (XTM) at least for the cold-dependent relief of symptoms suggesting that this is not due to gating in the central nervous system by specific thermoreceptor afferents. That C fibers are involved is further suggested by the fact that whereas PH and XTM resisted A-fiber block it disappeared with sustained block of C fibers. In patients in whom reduction of skin temperature abolished the pain it could be shown that at the stage when cold sensation was suppressed by selective A-fiber block, cooling completely abolished existing spontaneous pain and the warmth-induced hyperalgesia. Ochoa also noted that the skin warming from vasodilation can occur in the absence of sympathetic vasoconstrictive failure. He believes that this is due to antidromically triggered release of CPN endings of transmitters known to be vasoactive and able to sensitize the nociceptor endings that are the target of the primary noxious agent rather than the nerve fiber.

After a comprehensive review of his findings and those of others, Ochoa (58) concluded that in these patients the pathophysiology is not excitation of cold-specific afferents, but inhibition of warmth-sensitive membrane transducers. He believes that reducing the skin temperature shuts off specific warmth-sensitive transducers within the excitable membrane of normally multisensitive and now hypersensitive polymodal nociceptors. He suggested that in patients with XTM in reverse ( in whom spontaneous pain and mechanical hyperalgesia improve by increasing the skin temperature), it is the specific cold-sensitive transducers within the polymodal nociceptive membranes that are sensitized. Finally, he presented evidence in these patients that sympathetic block does not produce relief and suggested that an actively functioning sympathetic nervous system may even contribute to symptomatic relief through reflexively sustained cooling by vasoconstriction. I hope that these types of comprehensive clinical investigations in patients with causalgia, RSD, and other painful neuropathic conditions will be done more widely in order to elucidate their basic mechanisms.

Peripheral-Central Mechanisms

Hypotheses of central mechanisms of causalgia and reflex sympathetic dystrophy suggest that the primary site or critical dysfunction in the central nervous system includes the "vicious circle" hypothesis of Livingston and the "central biasing mechanism" of Melzack, which have been summarized in Chapter 8, and Sunderland's "turbulence" hypotheses (102). Sunderland suggested that causalgia is the functional expression of the intensity of the retrograde neuronal reaction in which pools of dorsal horn neurons become converted into foci of abnormal activity.

In a brilliant interpretation of recent experimental data and review of the literature on human clinical material. Roberts (4) has proposed an important hypothesis that helps to explain many phenomena of causalgia and RSD. This hypothesis (see Figure 11-9) suggests that trauma in some peripheral tissue first activates unmyelinated C nociceptors, which in turn activate and sensitize wide-dynamic-range (WDR) neurons in the dorsal horn whose axons ascend to higher centers. This sensitization persists, so that the WDR neurons now respond to activity in large-diameter A mechanoreceptive afferents, which are activated by brushing or light touch. This state produces allodynia. Moreover, these sensitized WDR neurons respond to mechanoreceptive activity initiated by sympathetic efferent action on sensory receptors in the absence of cutaneous stimulation and thus produce spontaneous pain or what he calls "sympathetically maintained pain" (SMP).

Roberts (4) marshaled experimental evidence to support his hypothesis that in most patients with SMP the allodynia provoked by gentle mechanical stimulation of the skin results from activity in low-threshold mechanoreceptors and not in nociceptive afferents. This concept that activity in low-threshold mechanoreceptors is responsible for the pain and allodynia of RSD was first suggested by Loh and Nathan (65) and later by Tahmoush (3); it is at variance with the data reported by Ochoa (58), which invokes the involvement of C fibers, and with the data reported by Wallin and associates (110), who demonstrated involvement of A-delta nociceptive afferents.

Roberts ( 4) also has provided evidence that sympathetic efferent activity causes repetitive mechanoreceptor discharge and that, except for high-threshold mechanoreceptors in injured tissue, sympathetic efferent activity does not activate nociceptors because their mechanical thresholds are too high to subserve allodynia. Thus this hypothesis comfortably explains spontaneous pain, allodynia, and perhaps hyperpathia through similar mechanisms. The normal low-threshold mechanoreceptors are excited naturally by sympathetic outflow and of course by natural mild mechanical stimuli. The afferent activity of such normal peripheral apparatus would find a disturbed physiology of the WDR neurons in dorsal horn, and which, when excited, would send nociceptive impulses toward the brain to be perceived as painful.

Nathan (62, 109) has used the abnormal state within the dorsal horn of the neuraxis as an explanation for reflex sympathetic dystrophy caused not only by injury or disease of limbs, but also by central nervous system pathology. These concepts are illustrated in Figure 11-10. As can be noted in Figure 11-l0A, a lesion involving a peripheral nerve causes disturbed physiology not only at the point of entrance, but also in the adjacent segments of the dorsal horn, and these in turn affect additional adjacent segments. Similarly, lesions of the neuraxis cause dysfunction of dorsal horn neurons, and this spreads to contiguous neurons and out along the afferent nerves that enter and end in the affected dorsal horn segments. Both types of lesion are effectively relieved by sympathetic blockade.

The role of the morphologic and pathophysiologic alteration of central nervous system neurons in causing neuropathic pain and other sensory and motor disturbances has been further strengthened by recent animal studies carried out by Wall, Woolf, and associates, cited in Chapter 7 (p. 176) and in Chapter 8 (pp. 186,187) and in Chapters 72 and 94. The role of pathophysiologic changes in the nerve following injury has been reviewed recently by Jänig (113), and the central changes mediating neuropathic pain have been re viewed by Devor (114). Wall (115) has also recently provided an update on his concept of the three different types of central control systems (rapid, slow sensitivity control and prolonged connectivity control) to explain the stability and instability of central pain mechanisms. The information provided by these reviews makes it obvious that the mechanism by which complex peripheral and central changes following peripheral nerve injury leads to various forms of pain, hyperalgesia, hyperpathia, and associated somatomotor and sympathetic motor abnormalities that are only marginally understood. This makes it difficult to assess the importance of individual pathophysiologic processes in the generation of clinically relevant pain and strongly suggests that much more research is needed to elucidate the mechanisms of pain of causalgia and reflex sympathetic dystrophy.

see: http://neuro.vetmed.ufl.edu/neuro/Jo...es/CPS_Art.htm

InHisHands · 06-29-2007, 06:48 PM

It was too long to put the summary and references in the above post so here they are:

Quote:

SUMMARY

Causalgia is an unusual and most fascinating painful disorder that follows partial injury to nerves. It is usually seen during wartime, but it is also seen in civilian patients subjected to high- velocity injury to peripheral nerves. It has so many peculiar characteristics specific to it that it deserves to have the name causalgia exclusively. One of the most important features of the condition is that sympathetic interruption promptly relieves the burning pain, allodynia, and hyperpathia. If sympathetic interruption is done early, it cures the condition.

A number of other conditions that I have included under the generic name of reflex sympathetic dystrophy have symptoms that are similar to those of causalgia, though less severe, and on the basis of their responses to sympathetic blockade it is probable that the underlying mechanisms are also the same. Reflex sympathetic dystrophy is clinically more important than causalgia because it occurs more frequently and can be cured if recognized and properly treated.

Careful review and assessment of various hypotheses that have been proposed about the mechanisms of causalgia and RSD reveal that, notwithstanding the vast amount of neurophysiologic and neuropathologic evidence acquired since Mitchell and Létiévant, we are still far from thoroughly understanding the mechanisms of these disorders. Moreover, we have not advanced much conceptually, because most authorities believe that causalgia is due to mechanisms that involve dysfunction of various parts of the peripheral and central nervous system as originally proposed by Mitchell and Létiévant. The available data suggest that: (a) the sympathetic nervous system plays a critical role in producing spontaneous pain; (b) persistent sensitization of WDR neurons in the dorsal horn of the neuraxis occurs as a result of the initial massive input from nociceptive afferents that occurs at the time of injury; © low-threshold mechanoreceptive afferents activated by light tactile stimulation can provoke increased excitation of the WDR neurons and thus produce allodynia; (d) the large-diameter low-threshold mechanoreceptor afferents can be activated by sympathetic efferent activity; and (e) in some cases the endings of polymodal nociceptors are sensitized.

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111. Wall, P.D., and Gutnick, M.: Ongoing activity in peripheral nerves: The physiology and pharmacology of impulses originating from a neuroma. Exp. Neurol. 43:580, 1974.

112. Seltzer, Z., and Devor, M.: Ectopic transmission in chronically damaged peripheral nerves. Neurology 29:1061,1979.

113. Jänig, W: Pathophysiology of nerve following mechanical injury. In Pain Research and Clinical Management. Vol. 3. Proceedings of the Vth World Congress on Pain. Edited by R. Dubner, G.F. Gebhart, and M.R. Bond. Amsterdam, Elsevier, 1988, pp. 89-108.

114. Devor, M.: Central changes mediating neuropathic pain. In Pain Research and Clinical Management. Vol. 3. Proceedings of the Vth World Congress on Pain. Edited by R. Dubner, G.F. Gebhart, and M.R. Bond. Amsterdam, Elsevier, 1988, pp. 114-128.

115. Wall, P.D.: The John J. Bonica Distinguished Lecture: Stability and instability of central pain mechanisms. In Pain Research and Clinical Management. Vol. 3. Proceedings of the Vth World Congress on Pain. Edited by R. Dubner G F. Gebhart, and M.R. Bond. Amsterdam, Elsevier, 1988 pp. 114-128, pp. 13-24.

FIG. 11-5. Hands of a patient in the acute phase of reflex sympathetic dystrophy that developed 10 days after accidental injury that produced linear fracture of the scaphoid and lunate bones of the wrist. The left hand was edematous and red. The patient experienced moderately severe burning aching pain, which was promptly relieved with cervicothoracic sympathetic block. A series of four such treatments, done every other day, eliminated the edema and the skin changes as well as the pain.

FIG. 11-6. Hands of a patient with stage 2 reflex sympathetic dystrophy that developed after severe laceration of the volar surface of the left wrist caused by a swing saw. Within a few hours of the accident the wound was cleansed, cut tendons and nerves were repaired, and the wound was closed. Several days later the patient began to experience a diffuse burning pain and increased sensitivity of the thenar eminence in the palm, which became progressively worse. A. Two months after injury. Note trophic changes similar to those of the patient in Figure 11-3. Treatment consisted of a series of cervicothoracic sympathetic blocks and physical therapy. B. More than a year after injury. Treatment produced relief of burning pain, but some trophic changes remained.

FIG. 11-7. Photographs of the hands of a patient (MB) who developed reflex sympathetic dystrophy following pressure necrosis of the left forearm. This patient accidentally took an overdose of a muscle relaxant for spasticity of the lower extremities that was due to spinal cord injury. Soon after taking the relaxant she fell to the floor with her left arm underneath her body and a cigarette lighter beneath the arm. She remained in this position for 24 hours, when she was discovered by a relative. Soon afterwards she began to experience a diffuse burning pain and weakness of the hand and forearm, which were treated conservatively with analgesics and physical therapy for several months. A. Photograph taken some three months after the accident. Although the lesion gradually healed, the pain, weakness and trophic changes became progressively worse. When seen in consultation nearly 6 months after the accident she presented with grade 3 RSD. A series of diagnostic cervicothoracic sympathetic blocks was carried out with partial pain relief, after which sympathectomy was advised, but because of severe congenital malformation of the cervicothoracic portion of the spinal column and because of her poor physical condition it was decided to carry out chemical sympathectomy. After this procedure the pain gradually, albeit slowly, became less but never disappeared, and the contractions and osteoporosis remained (B, C) despite intensive therapy (see Fig. 11-8).

Fig. 11-8. Roentgenograms of the hands of MB. A. Moderate degree of osteoporosis in the left hand 3 months after injury. B. More severe and more diffuse osteoporosis of the left hand and a normal right hand, 15 months after injury.

Fig. 11-9. Diagram of the physiologic model developed by Roberts. A. Immediate response to trauma. Action potentials in C nociceptors propagate through the dorsal root ganglia (DRG) to the spinal cord, where they activate and sensitize wide-dynamic-range (WDR) neurons whose axons are sent to higher centers. B. The WDR neurons remain sensitized and now respond to activity in large- diameter A-mechanoreceptors, which are activated by light touch. This state produces allodynia. C.The same sensitized WDR neurons respond again to A-mechanoreceptor activity, but this activity is initiated by sympathetic efferent actions on the sensory receptors in absence of cutaneous stimulation. This phase represents sympathetically maintained pain. Modified from Roberts, W.J.: An hypothesis on the physiological basis for causalgia and related pain. Pain, 24:297, 1986.

Fig. 11-10. Model proposed by Nathan. A. Lesion of a peripheral nerve produces an abnormal state in the dorsal horn, first in the segments of entrance of the damaged nerve and subsequently in adjacent segments, making the peripheral nerves adjacent to the one that was injured also develop an abnormal state. B. Spread of abnormal state from a lesion in the dorsal horn or other parts of the neuraxis to neighboring regions and out along afferent nerves that end in the affected posterior horn. Compare with Figure 8-4. From Nathan, P.W.: Involvement of the sympathetic nervous system and pain. In Pain and Society. Edited by H.W. Kosterlitz and L.Y. Terenius. Weinheim, Verlag Chemie, 1980.

InHisHands · 06-30-2007, 06:29 AM

I am not sure that I 100% agree with this article- using ice and a sympathectomy both are agreed for the most part to be bad for RSD.

Abbie · 06-30-2007, 09:10 AM

Quote:

Originally Posted by InHisHands

I am not sure that I 100% agree with this article- using ice and a sympathectomy both are agreed for the most part to be bad for RSD.

I agree with you on the not agreeing with this article...
The newest information according to the summary was from 1988. 19 yrs ago!!!!!!!!!!

Too much has changed since then....
Thank you for taking the time to look this up and for sharing it with us...it is a very interesting read!!!

Abbie

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