RSD

Reflex Sympathetic Dystrophy

On rare occasions in the treatment of trauma and acquired diseases of the extremity, expected end results may not be forthcoming; instead it is alarming to find that the patient has a great deal more pain, swelling, stiffness, and dysfunction than was anticipated. Although it is well known that patients who have Dupuytren's contracture, hypertrophic arthritis (osteoarthritis), or a predisposition to fibrosis will have increased swelling and stiffness after injury or surgery, it is disheartening to see a patient develop an extreme amount of discomfort and disability for no obvious reason. The eventual outcome of such cases may well be determined by the early discovery of the true nature of this condition; although it is relatively rare, reflex sympathetic dystrophy (RSD) must always be kept in mind.

CLASSIFICATION

When the various clinical forms of reflex sympathetic dystrophy are considered in terms of their severity, they may be listed in increasing order, as follows:

1) Minor causalgia

2) Minor traumatic dystrophy

3) Shoulder-Hand syndrome

4) Major traumatic dystrophy

5) Major causalgia

CLINICAL MANIFESTATIONS

One of the most prominent characteristics of RSD certainly is pain. In the nerve injury types of causalgia, the pain is most often described as burning in nature. In the non-nerve injury types of RSD the pain also may be burning but will be described more commonly as aching, boring, stinging, cutting or searing. In most cases the pain is severe and constant. Another distinguishing feature is the patient's intolerance to motion of the joints of the involved extremity because of the severity of pain. Almost universally present are marked tenderness and dysesthesia. Another constant finding is swelling, which is often fusiform in nature. Stiffness, at times profound, is due not only to the fact that motion is exquisitely painful but also to increased fibrosis about the joint structures. Vasomotor changes may be present in the form of constriction of the arteriole which produces pallor; vasoconstriction of the veins, which produces a dusky cyanosis; or at times vasoconstriction of both the arteries and veins, causing a bluish-gray tint. Other manifestations, such as sudomotor, temperature, and atrophic changes and osteoporosis, are also present.

DIAGNOSTIC CRITERIA25

It is of utmost importance to make an early diagnosis in cases of reflex sympathetic dystrophy because early treatment is much more effective than treatment at a later stage. This, at times, becomes somewhat difficult because of the varied symptoms in each of the three clinical stages and the variation of the symptoms in the five clinical types of RSD. It is also of utmost importance to rule out other conditions that are characteristically known to produce pain, swelling, stiffness and dysfunction but do not come under the classification of reflex sympathetic dystrophy. Traumas or disease occurring in patients who have a tendency toward increased fibrosis (such as patients with Dupuytren's, arthritis, long-standing diabetes, the primary type of carpal tunnel syndrome, and other collagen disorders) will often produce a stiff-hand syndrome. Although it is not uncommon to see a "flare reaction" in these types of patients after injury or disease, it is very important not to confuse them with reflex sympathetic dystrophy.

The dominant characteristic of RSD is that the symptoms and signs are much more profound than ordinarily would be expected from a trauma or disease occurring in an otherwise normal individual. In a normal individual the signs and symptoms will improve with time, but in the patient with RSD they get progressively worse. The four cardinal symptoms and signs are as follows:

1) Pain

2) Swelling

3) Stiffness

4) Discoloration

The secondary signs and symptoms which are most often present but not necessarily inevitable, are as follows:

1) Osseous demineralization

2) Sudomotor changes

3) Temperature changes

4) Trophic changes

5) Vasomotor instability

6) Palmar fibromatosis

If all of the cardinal symptoms and signs are present and at least several of the secondary symptoms and signs exist to a degree much greater than normally expected, a presumptive diagnosis of reflex sympathetic dystrophy can be made. Actual confirmation of this diagnosis, however, comes after interruption of the sympathetic nerve reflex has produced some amelioration of the patient's condition. One cannot, however, rule out RSD upon a single attempt to interrupt the sympathetic reflex arc. At least three or more blocks with completely negative effects should be used so that RSD may be conclusively ruled out. It is also important to make sure that the attempted interruption in the sympathetic arc has been technically successful as evidenced by warmth and dryness of the extremity.

CAUSES

For RSD to occur in a patient, the following three factors must be present at the same time:

1) A painful lesion

2) Diathesis, or susceptibility, of the patient

3) An abnormal autonomic reflex

When the painful stimuli persist in a patient with the diathesis for the disease (a susceptible individual) and the abnormal autonomic reflex is not interrupted, the patient is on the way toward developing RSD.

Painful Lesion There is an infinite variety of kinds and severity of painful lesions. Trauma, of course, is the most common form of painful lesion and may be nerve injury, as in causalgia, or crush injury, as in major traumatic dystrophy. However, it may be minor, such as a mashed end of finger or a minor fracture or sprain. Any painful condition, such as a vascular lesion or even an acute episode of arthritis, may be severe enough to precipitate RSD.

Diathesis Two different types of diathesis are recognized. The first diathesis is tendency of the patient to be a "hypersympathetic reactor." These patients have increased sympathetic nerve activity.(50) When a history is being taken, the patient is always asked if he has sweaty palms (hyperhidrosis) or other evidence of increased sympathetic nerve activity, such as a history of pallor or excessive coolness of fingers and toes when they are exposed to colder temperatures. On physical examination one often finds evidence of peripheral vasoconstriction and poor capillary refill on the uninvolved extremity. Also, other historical evidence of vasomotor dysfunctions such as fainting, excessive blushing, or even migraine headaches is often obtained in patients with RSD.

The second diathesis has to do with psychological makeup of the patient. This type of diathesis is more difficult to determine than the hypersympathetic reactor. However, in most patients with reflex sympathetic dystrophy it is possible to recognize that they have certain psychological traits that are often described by psychiatrists as "fearful, suspicious, emotionally labile, inadequate personality, chronic complainer, dependent personality, insecure and unstable personality." One almost never discovers a psychological trait in a patient with RSD who is stoic or a "Spartan." Patients who develop reflex sympathetic dystrophy also have the tendency to have a very low pain threshold. This type of patient will usually not be very cooperative in carrying out the doctor's orders, will think up many excuses for not doing what he is told, and will try to control his own treatment and seek to place the blame for his condition on others.

Abnormal Autonomic Reflex The exact mechanism by which the normal sympathetic reflex persists and becomes an abnormal one is certainly not known. In the normal state, when an injury has been sustained, a sympathetic reflex is a part of the body's response to injury; this at first produces vasoconstriction, and then vasodilation takes over to facilitate the repair process (32). However,if the sympathetic reflex continues or is more pronounced than normal because of an abnormal feedback mechanism, an atypical sympathetic reflex ensues. In 1943, Livingston (34) suggested that when afferent pain fiber stimulation persists, an abnormal activity results in the "internuncial pool" of the spinal cord, which produces increased sympathetic function. Melzack and Wall (39), in 1965, helped to shed some light on this abnormal reflex by their gate control theory of pain. They propose that there are special cells in the substantia gelatinosa of the dorsal horn of the spinal cord that have the duty of modulating the transmission of afferent stimulation from the sensory nerves. They report that these special cells interpret the sensory impulses and relay to the brain a message of pain. They suggest that the large, myelinated afferent fibers "close the gate" but impulses transmitted along the small C fibers "open the gate," allowing a little bit of stimulus to be perceived as a great deal of pain. This may well be the explanation of the well-known fact that in RSD the patient's complaint of pain is out of proportion to the injury.

In most series of cases, the most common cause of this form of RSD is Colles' fracture, and we found a high proportion of these to have a carpal tunnel syndrome as a complication. We believe that the traumatic carpal tunnel syndrome is most likely to be the noxious stimulus that incites the RSD.

Doupe (15) et al., in 1944, reported that the partial nerve injury caused a pathologic "artificial synapse" at its site because of loss of the integrity of the normal myelin sheath, allowing "cross-stimulation" between the efferent sympathetic fibers and the afferent sensory fibers.(32) This type of "fiber interaction" allows occurrence of an abnormal reflex that possibly accounts for the marked burning pain and the increased sympathetic stimulation of the distal portion of the extremity.

DIAGNOSIS

To achieve early recognition of RSD, one must be suspicious when a patient's complaint of pain is out of proportion to the degree of trauma. Of course, many injuries and acquired diseases produce pain, swelling, stiffness and deformity, but the diagnosis of RSD can be made when there is a great deal more pain, swelling, stiffness, deformity, osteoporosis, and vasomotor, sudomotor, and trophic changes than one would ordinarily expect for that degree of trauma or disease.

THERMOGRAPHY

A newer technique of objectively diagnosing, quantifying and substantiating significant positive response to treatment is thermography.

Thermography is a non-invasive (painless and harmless) study of heat changes of skin dermatomes throughout the body. Thermography can be done either electronically or by liquid crystal. With the liquid crystal type, one utilizes a unique elastomeric thermally sensitive film that can be readily contoured to display the thermovascular patterns of the body.

During the procedure the technologist will change "cassettes" for different body parts. The reason for this is that each cassette is a precalibrated representation of temperature difference between each color. The temperature difference with liquid crystal will vary from cassette to cassette. These cassettes are a highly sophisticated, new, innovative and precisely calibrated piece of equipment that are extremely sensitive to heat changes.

The patient should be thoroughly informed about what will transpire during the thermographic exam and how to prepare for this painless, noninvasive procedure. Although the patient may continue any medication, he should NOT smoke for at least 8 hours prior to the exam and should be advised to bathe well before the procedure as dirt and oil will affect the exam.

After completing medical forms, the patient, attired in a gown especially designed for the exam, waits in the exam room for about 15 minutes while his body temperature stabilizes and adjusts to room temperature.

Then three sets of Polaroid color photographs record the thermographic findings along the dermatome paths of both extremities. Repeating the photographic sequence at 15 minute intervals, the technician will take approximately 40-50 pictures during the exam which lasts about 1 1/2 to 2 hours. The time interval rules out "artifacts" and allows comparison of persistent abnormalities. A follow-up thermographic exam may be necessary to evaluate a suspected abnormality or to check on progressive improvement.

Thermography is also a very valuable tool for monitoring the treatment of RSD, since it will reveal a return to normalcy, after the problem has been successfully eliminated.

LOWER EXTREMITY INVOLVEMENT

The clinical manifestations of RSD involving the lower extremity are similar to those involving the upper one. There is pain, either burning or otherwise and constant or intermittent; vasospasm, as manifested by a cold, cyanotic extremity, pallor and increased sweating; edema; atrophy of the soft tissues if the syndrome has been present for any length of time; osteoporosis and limitation of movement of the ankle joint, foot, and occasionally even the knee. At times one sees vasodilation, but most often vasoconstriction or vasospasm is manifest. However, not all pain is causalgia, and naturally one has to rule out various complications, such as thrombophlebitis, arterial occlusions, tight casts or dressings, infections, arthritis, post-herpetic neuralgia, and the acute compression syndromes of the lower extremity. If these can be ruled out, one may be seeing the onset of RSD. As previously emphasized, the patient's complaint of pain is usually out of proportion to the severity of the injury.

SPECIFIC TREATMENT

The basis for proper treatment of RSD is early recognition. The best way to achieve this is to keep in mind the possibility of major and minor causalgia and mimo-causalgia* in all cases of trauma to the extremity.

The old axiom that early diagnosis and early treatment produce the best results has never been more correct than in the case of reflex sympathetic dystrophy. Delay in starting the treatment because of difficulty of diagnosis is certain to produce a greater residual in the form of pain, stiffness and dysfunction. It is therefore important to rule out other forms of dystrophies that produce similar but not so severe symptoms so that the appropriate treatment for RSD may be given without delay.

It has already been stated that there are three etiologic factors (persistent painful lesion, diathesis, and abnormal sympathetic reflex) that must be present at the same time before reflex sympathetic dystrophy can occur. The treatment is therefore to remove one or more of these factors, and one would hope the vicious cycle can be broken. Although this may stop the forward progress of the disease, it cannot return the patient to normalcy. It would follow therefore that treatment should include attempts to eliminate the initiating painful state, modify the patient's diathesis if possible, and interrupt the abnormal sympathetic reflex.

Of these three approaches to the treatment, the elimination of the abnormal sympathetic reflex is usually the easiest to perform and by all odds the most direct and successful approach. Depending on the severity and the duration of RSD, this may be accomplished with the use of one or more of the following regimens; use of sympatholytic drugs, local anesthetic blocks on somatic

* Hereinafter used to designate all the nonnerve injury forms of RSD.

nerves or "trigger points," pharmacologic or chemical blocks of the stellate ganglion and the upper thoracic chain, or use of an upper thoracic sympathectomy.*

The rationale for sympathetic block or sympathectomy is the interruption of the abnormal reflexes being mediated by the sympathetic nervous system.(64) Regardless of the basic pathogenesis of the syndrome, interruption of the sympathetic nerve with disruption of the sympathetic reflexes is nearly always curative of pain. Sympathetic blocks are both diagnostic and therapeutic. In early cases, the relief of pain may well last beyond the duration of the block and even be curative. Repeated blocks should be performed until pain is controlled. Ordinarily three or four are the maximum. If relief from repeated sympathetic blocks becomes less effective or static and the initial response is dramatic but of short duration, surgical sympathectomy should be considered.

There are several ways to effect a sympathetic block: Bier- reserpine, Bier-Methylprednisolone, TENS, and Stellate-ganglion or lumbar blocks.

BIER-RESERPINE BLOCKS are done if simpler methods have failed,

or if the patient is unable or unwilling to participate in the extensive therapy needed to effect treatment. All the blocks are repeated as needed so long as they seem to be helping, every few days, weeks or even months. This type of block entails utilizing a tourniquet on the involved extremity, and instilling a local anesthetic, usually 1/2% lidocaine, (50 cc for the upper extremity and 100 cc for the lower extremity), and reserpine, a sympathetic blocking agent (1 mg for the upper extremity, and 2 mg for the lower extremity) intravenously (as you would to give therapeutic fluids) until the extremity is completely anesthetized, then manipulate all stiffened joints until normal, or as close to normal as possible passive motion is obtained. After the tourniquet is released, the patient is immediately started on intensive therapy to desensitize the painful areas and maintain the motion.

BIER-METHYLPREDNISOLONE BLOCKS are often used, and are done in a similar fashion as Bier-Reserpine Block, but with the addition or substitution of methylprednisolone, a corticosteroid, which may break the pain-stiffness-pain cycle.

For the upper extremity, STELLATE GANGLION BLOCKS are employed by the use of 1% lidocaine or 0.25% bupivacaine (Marcaine), bathing the stellate ganglion which lies at the level of C7, D1. With the patient's head extended and turned away from the operator, the needle is inserted at a point 4 cm lateral to the midline and 4 cm up from the clavicle to a depth of 4 cm in the neck, with the needle directed medially and somewhat inferiorly toward the lateral bony mass of C7, D1. An injection of 10 ml of local anesthetic is customary. Profound Horner's syndrome, with warming and drying of the hand and relief of pain, follows immediately on satisfactory block of the stellate ganglion.

LUMBAR BLOCK is somewhat more difficult than stellate block. One commonly used technique is one involving three needles placed 5 cm laterally to the midline opposite the transverse processes of L1, L2, and L3, or L2, L3, and L4. Ten ml of 1% lidocaine is then injected into each needle. Within a few moments a sympathetic effect is apparent, with warming and drying of the foot and relief of pain.

* See references 3, 6, 27, 39, 62, 64, and 74.

SYMPATHECTOMY25

If stellate ganglion blocks have not been started early enough in the course of reflex sympathetic dystrophy, it may not be possible to break up adequately the abnormal sympathetic reflex with blocks alone. This is especially true in the very severe cases of major traumatic dystrophy and causalgia. If definite benefit has accrued from at least one to three blocks and yet the duration of benefit is not long enough or the relief of pain is less than complete, and especially if the duration of this disease has been at least 4 to 5 months, in all likelihood a surgical sympathectomy will be required in order to give the patient the desired relief. In many cases, one can reach a decision to do surgery after the second block, but at other times one may need to use four to six blocks before determining whether the intermittent blockade will be sufficient or a surgical sympathectomy will be necessary. One should expect, however, that the patient with reflex sympathetic dystrophy has a diathesis that may make him more likely to complain of pain around the sympathectomy operative site. Fortunately, this post- surgical neuritis seldom lasts more than a few weeks.

ADJUNCTIVE TREATMENT32

Although interrupting the abnormal sympathetic reflex by a block or surgical sympathectomy is certainly the most important means of treatment, other modalities may be helpful by interrupting this vicious cycle at other points. Since a persistently painful lesion is one of the ingredients for the production of RSD, one must attempt to relieve the pain if possible. If a carpal tunnel syndrome is present, a surgical release of the median nerve compression must be considered.

In the case of a well-localized painful lesion, such as an injured nerve, it is possible to perform a somatic nerve block with a local anesthetic at some point proximal to the noxious stimulus. This, of course, not only relieves the pain and prevents the possibility of abnormal feedback but also prevents sympathetic efferent stimuli from traveling distal to the nerve block. This is effective for neuromas over the dorsal sensory branch of the radial nerve around the radial styloid area. This may be blocked every other day with a few milliliters of a local anesthetic at a slightly different point each time. In 1971 Omer and Thomas (48) described a periodic perineural infusion of a local anesthetic around a "trigger point."

Certainly, there is no way to change the diathesis of the patient, but one may attempt to minimize its effect by using tranquilizers, such as diazepam (Valium), or the ordinary analgesics. Relieving the patient's pain and anxiety helps to decelerate the vicious cycle somewhat.(32) Several anti-inflammatory agents have been suggested, but we believe that they do not treat the underlying cause (abnormal autonomic reflex); however, they may be helpful in diminishing pain and swelling and possibly in preventing excessive fibrous tissue proliferation in the ligamentous structures about the joint. Of all the anti-inflammatory agents, steroids seem to be more efficacious. We do not suggest, however, that these be given in lieu of a sympathetic block or sympathectomy.

If there is vasospasm, vasodilators may be used either by mouth or at times by intraarterial injection. These include tolazoline (Priscoline) a mixture of dihydroergocornine, didhydroergocristine, and didhydroergokryptine (Hydergine), nylidren (Arlidin), papaverine (Pavabid), cyclandelate (Cyclospasmol), phenoxybenzamine (Dibenzyline), Vasodilan, and intraarterial reserpine. Because there usually is a vasoconstriction, the patient should be advised to stop smoking. We have not been able to confirm the successful treatment of RSD with propranolol.(63)

THERAPY is an important part of the ancillary treatment of RSD. It must be used properly, however, or it becomes detrimental, rather than helpful. As soon as possible, the hand should be returned to the "balanced hand" or "resting hand" position, so that fewer deforming forces will be exerted on the hand. Dynamic splints may be used to obtain wrist extension, metacarpophalangeal joint flexion and proximal interphalangeal joint extension. The wrist is the keystone of the balanced hand position. With dynamic splinting, great care must be taken to prevent the splint from becoming tight enough to produce pain. This is especially true in such dynamic splints as the "flexion glove." Active motion should be started early and employed throughout the treatment. For effective results the hand must be actively exercised for a few minutes out of each half hour. We use sustained effort exercises for 10 seconds in each direction - flexion and extension. Passive exercises should be employed only when the patient has been sufficiently cautioned not to exert any force on the hand that is painful. It is advisable that no one manipulate the hand except the patient, who is the only one to know when the point of pain is being approached. Forceful active or passive exercise will increase the patient's pain, swelling, and stiffness, since these patients are hypersensitive to pain, which will accelerate the vicious cycle. It is useful for the patient to massage the hand frequently. This has long been known to be helpful, but only recently Melzack and Wall,(39) with their gate control theory of pain, give a possible explanation of its benefit. Massaging the hand floods the sensorium with normal sensory impulses and "drowns out" the atypical sensory impulses of the abnormal sympathetic reflex -- the large diameter fibers "close the gate" to the small pain fibers. Another way of blocking out the pain is through the use of the transcutaneous electric nerve stimulator, which may be worn on the extremity while the patient exercises the hand and attempts to function with the hand or leg. This may be used for several hours each day.

ADJUNCTIVE SURGERY on the patient with RSD other than that to relieve the source of pain, such as nerve entrapment to remove a painful neuroma, or to revise a troublesome amputation stump should be avoided whenever possible. It is recommended that no surgery be done on the involved extremity until the abnormal autonomic reflex has been eliminated either by repeated sympathetic nerve blocks or with a sympathectomy. On rare occasions a capsulotomy or tenolysis procedure to restore motion is indicated, but this should be done only after RSD has been completely relieved.

Certainly, the most important treatment for reflex sympathetic dystrophy is the interruption of the abnormal sympathetic reflex arc,(74) and this should be done as soon as possible by one of the above-mentioned methods, whether it be a sympathetic nerve block or a surgical sympathectomy. There are, however, other forms of treatment that are helpful and are based on the three etiologic factors. It should be emphasized that these methods of treatment should not be used to the exclusion of the blockade of the sympathetic reflex arc.

Elimination of swelling should be one of the first goals, since it is well known that swelling causes pain and ischemia. Both of these conditions will aggravate the "vicious cycle." Patients should be given specific instructions on how to elevate the hand at all times so that the hand is the highest part of the body. If a traumatic carpal tunnel syndrome has occurred secondary to the swelling, this may well need to be treated by elimination of a severely flexed position of the wrist. In many cases, it can be helped by the injection of a long-acting steroid around the flexor tendons going through the carpal tunnel (but not near the ulnar or median nerves). A surgical release of the carpal tunnel may occasionally be necessary but should not be done except under the protection of sympathetic blockade.

TRANSCUTANEOUS NERVE STIMULATION,(72) if used early in the course of the disease, may well help to reduce pain. The electrical stimulation is directed toward the large-diameter myelinated afferent nerve fibers of light touch and proprioceptive sensation. It is believed that this constant stimulation of these large-diameter fibers will "close the gate" on the small non- myelinated slow-conducting C fibers of pain. This is usually accomplished with a small battery-operated stimulator that is connected to the patient with electrodes and can be worn for many hours at a time.(35, 40, 46) During these periods of reduced pain, it may well be possible for the patient to do his hand exercises or participate in functional activities without aggravating his condition. Unless the transcutaneous electrical stimulator is utilized very early in the course of RSD, it has little chance of diminishing the pain to a significant degree.

SYSTEMIC STEROIDS

Steroids of a sufficiently high dosage do provide a sense of well-being to the patient and relieve pain to some degree if for no other reason than by reduction of the swelling. Also, it is quite likely that steroids over a long enough period of time may diminish the intense fibrotic reaction that occurs with reflex sympathetic dystrophy. It is therefore true that steroids are of some benefit to patients with RSD, but they are not capable of interrupting the abnormal sympathetic reflex, which is the dominant factor in the pathogenicity of RSD.

If one uses steroids, he must recognize their limited application, and they should not be used to the exclusion of blockade of the sympathetic nervous system. The use of steroids is certainly not without some risk of producing steroidism, activating gastric ulcers, and producing hypertension and severe osteoporosis. Steroids, however, can be useful for the treatment of the "flare reactions" commonly seen after injury or surgery in patients who have Dupuytren's contracture, hypertrophic or psoriatic arthritis, long-standing diabetes, or other collagen diseases such as primary carpal tunnel syndrome. It is probably because of the benefit to this group (not to be confused with RSD) that some workers(21) have reported good results with the use of steroids for the treatment of reflex sympathetic dystrophy. It is much more expedient and effective to produce sympathetic- activity blockade rather than to expose the patient to the complications of high doses of steroids.

TREATMENT OF THE DIATHESIS

Since the diathesis for reflex sympathetic dystrophy is an inherent trait of the patient, there is little possibility of changing this in any way that will help to break up the vicious cycle present in RSD. Mood-modifying drugs have been suggested for the treatment of RSD(28) such as diazepam (Valium), trifluoperazine (Stelazine), chlorpromazine hydrochloride (Thorazine), chlordiazepoxide hydrochloride (Librium), amitriptyline hydrochloride (Elavil) and fluphenazine dihydrochloride (Prolixin). Although it is doubtful that the diathesis can be significantly changed with the use of drugs, it might well enable a patient to tolerate his condition a little better and make him more receptive to the real treatment of RSD, which is the interruption of the reflex sympathetic arc. Pak (52) has suggested that consultation with a psychiatrist is indicated because he believed that a large number of patients had a psychiatric problem. In general, we have not found that psychiatric consultation offers the patient a great deal more than simply enabling him to understand his condition and become more cooperative in the treatment.

HAND THERAPY

An overzealous therapist who gives passive manipulation of the hand to the point of pain without the patient's abnormal sympathetic reflex having been blockaded or eliminated is very likely to cause a worsening of the patient's condition rather than an improvement of it. The old saying that "pain is gain" is certainly not true in reflex sympathetic dystrophy. The patient with RSD is hypersensitive to pain and any painful manipulation will promptly accelerate the vicious cycle and will cause the already painful, swollen, and stiff joint to become even more reactive. It is first necessary to blockade the efferent sympathetic impulses (the "protective umbrella") before it is possible to carry out a vigorous exercise program.

The basis of any exercise program should be gentle active exercises without coming to the point of pain. It is much better to exercise the hand frequently and for short periods rather than a few longer periods of more strenuous exercises. More improvement in motion is accomplished by 3 minutes of gentle active exercises every 30 minutes (while awake) than a longer exercise period three or four times a day. It is not until after the sympathetic blockade has decelerated the vicious cycle that it is safe for the patient to be taught gentle passive exercises. The hand therapist should be a teacher and a cheerleader but not a manipulator and should encourage the patient to do the exercise himself without causing pain, so that motion will improve rather than produce greater reaction in the tissues from overzealous stretching.

EXERCISES

A program called the "three flexion and extension exercises" has been developed which simply applies the principle of the "Bunnell Block" in the flexion exercises without the use of the block itself by the patient. The first exercise is in flexion; all three joints of all fingers are very gently flexed passively as far as possible without coming to the point of pain, and then an active assist in flexion is provided (while the fingers are still held passively in flexion). This exercise is sustained for 10 seconds, with the use of as much power as possible, just short of pain. Next, the fingers are extended as far as possible without pain, for 10 seconds. In the second exercise, the patient holds each individual finger (or in some cases all four fingers at the same time) with his uninvolved hand so that the metacarpophalangeal joint is held in as much extension as possible (without pain). While the metacarpophalangeal joint is therefore blocked in extension, the patient makes an active effort to flex the fingers as far as possible just short of pain. This flexion exercise is sustained for 10 seconds, followed by 10 seconds of extension. The third exercise is done the same way, except that this time the patient blocks not only the metacarpophalangeal joints but also the proximal interphalangeal joints in as much extension as possible without pain and then uses as much active power to flex the distal interphalangeal joint as he can just short of pain. This is also sustained for 10 seconds and again followed by 10 seconds of sustained-effort extension. The "three flexion and extension exercises" are then followed by 10 seconds of light massage of the digits,hand, and wrist. This entire procedure is continued until it has been done for 3 minutes, and the exercise period should be repeated once every 30 minutes. This, of course, requires a great deal of the patient's time, but it must be done frequently to become effective. The patient therefore must become his own primary therapist, because the exercises needed could not be supplied by the hand therapist in the therapy department more often than twice daily. Similar 10-second sustained effort exercises are done for the wrist in all planes of motion (extension, flexion, radial and ulnar deviation, and supination and pronation). If shoulder and elbow joints have also stiffened, they too are exercised.

HEAT

In many cases, gentle heat can be used effectively to reduce muscle spasm and to allow the patient to do his exercises with less pain and a greater gain of motion. Heat is helpful, however, only if it is used with elevation. Heat with the extremity in dependence should not be used because this will cause stagnation in the lymphatic and venous system, which will result in greater swelling. This would then eliminate the use of the whirlpool bath in the treatment of RSD for fear of causing increased swelling and reaction. Hot, wet towels, the paraffin bath, and a heating pad all can be used with elevation, however, and can easily be applied at home by the patient after sufficient instructions have been given by the therapist. Swelling can also be reduced with the use of the thermoelastic glove, which will provide warmth and a gentle compression to help control swelling and reduce pain. Patients should be warned that they should avoid cold temperature because this will increase vasoconstriction, they should therefore always wear warm gloves when going outside in cold weather. Since it has also been shown that smoking of tobacco produces tissue ischemia by increasing vasoconstriction (l0), they should be advised to stop smoking so that at least this factor can be removed from the many causes of tissue ischemia in the patient with RSD.

SPLINTING

The purpose of splinting at first is to rest the hand, to relieve pain on motion and to relieve muscle spasm. The splints should be light and should be made of thermoplastic material so that they can be frequently reheated and changed in position. The ultimate goal is to return the position of the hand to the "resting-hand" or "balanced-hand" position, which is approximately 45 degrees of wrist extension, slight ulnar deviation of the wrist, 70 degrees of flexion in the metacarpophalangeal joint and 30 degrees of flexion in the proximal interphalangeal joint. The reason we call this the resting-hand or balanced-hand position is that it is the result of all forces exerted by the extrinsic muscle pull, the intrinsic muscle forces, and the static forces. This position would then be in a balanced state or a resting state. This is the position where there are fewer deforming forces being exerted on the joints. There are also fewer pathologic forces present when the hand is in this position.

As time goes on, the splint is periodically reheated and the wrist extension is increased. After reducing the wrist flexion contracture and getting the wrist up into at least mild extension, one can then become more vigorous in reducing extension contractures of the metacarpophalangeal joints and flexion contractures of the proximal interphalangeal joints. This reduction is accomplished with a dorsal thermoplastic splint with an outrigger and rubber-band slings to produce a gentle extension force on the interphalangeal joints.

These dynamic splints, of course, exert passive motion on the joint, and our rule about never allowing a passive force to become painful certainly applies to splinting. Pain produced by an ill-fitting splint or splint adjusted too tightly can be just as detrimental to the patient's stiff hand as painful passive manipulation. The splints should be worn most of the time but should be removed every 30 minutes for the prescribed program.

FUNCTIONAL ACTIVITIES

In the beginning, activity may be as simple as placing wooden rings over round pegs or stacking blocks, but as better motion is accomplished and the patient has more confidence, the therapist will be able to teach him to do more sophisticated functional activities. The therapist needs to be very observant so that she can pick up any new degree of motion or power developed by the patient, which can then be put to work in doing a different and more advanced type of functional activity. The therapist should be one step ahead of the patient in setting goals for physical accomplishments. Eventually, the hand therapist should have the patient doing functional activities that simulate the type of work he will be doing when he returns to his employment, as with the work simulator.

REHABILITATIVE SURGERY

At some point in the recovery of the patient, evaluation must be made according to the needs of the patient as to what degree of motion is required and to what extent a contracture can be acceptable for the required degree of function necessary for the patient's well being. One should have a very limited expectation of regaining a considerable degree of motion after rehabilitative surgery, but at times it may be deemed necessary to gain even a few degrees of motion so that the patient is provided with his required extent of function. There are therefore some very restricted indications for rehabilitative surgery to regain motion in the patient with reflex sympathetic dystrophy though this, in general, should be discouraged.

Also, the surgery should be delayed until the patient's pain has disappeared or until the reactivity and the excessive fibrosis in the joints have diminished as much as possible and the tissues around the joints have returned to a state of homeostasis to the greatest degree possible. Rehabilitative surgery also should not be done so long as the patient shows progressive improvement with exercise and splinting and functional activity regimens.

The types of surgical procedures most likely to provide the patient with improved motion are as follows:

1)Capsulotomies of metacarpophalangeal joints

2)Capsulotomies of the proximal interphalangeal joint (with or without resection of the volar plate)

3) Capsulotomy of the volar wrist joint to relieve flexion contracture; tenolysis of the flexor tendon(s) with release of transverse carpal ligament

4) Resection of the tenodesed flexor digitorum superficialis tendon(s) at the level of the proximal interphalangeal joint.

SUMMARY

1)"Reflex sympathetic dystrophy" should be the name used for all of the vasomotor trophic disturbances, which have been given various names in the past.

2) These three etiological conditions must be present at the same time for reflex sympathetic dystrophy to develop:

a. Persistent painful lesion

b. Diathesis (patient's susceptibility)

c. Abnormal sympathetic reflex

3)These are the five clinical types of reflex sympathetic dystrophy (listed in ascending order of severity);

a. Minor causalgia

b. Minor traumatic dystrophy

c. Shoulder-hand syndrome

d. Major traumatic dystrophy

e. Major causalgia

4)In order for one to make a presumptive diagnosis of reflex sympathetic dystrophy, these four cardinal symptoms and signs should be present:

a. Pain

b. Swelling

c. Stiffness

d. Discoloration

5) At least several of the following secondary symptoms and signs must also be present before a presumptive diagnosis of reflex sympathetic dystrophy can be made.

a. Osteoporosis

b. Sudomotor changes

c. Temperature changes

d. Trophic changes

e. Vasomotor instability

f. Palmar fasciitis

6)The dominant distinguishing feature of reflex sympathetic dystrophy is the fact that all the symptoms and signs are very much more severe than would ordinarily be expected for a similar type of inciting painful trauma or disease in an otherwise normal individual.

7)The most important treatment of reflex sympathetic dystrophy is some type of interruption of the sympathetic reflex arc so that the abnormal sympathetic reflex is eliminated.

8)The earlier the sympathetic reflex arc is eliminated, the better the result.

9)A confirmed diagnosis of reflex sympathetic dystrophy can only be made when the interruption of the sympathetic reflex arc has been shown to produce at least a definite measure of improvement.

10)There is a high incidence of traumatic carpal tunnel syndrome occurring in the major traumatic dystrophy type of reflex sympathetic dystrophy; when this condition is found to be present, the compression of the nerve should be relieved surgically.

11)No surgery should be performed without having the "protective umbrella" of some type of sympathetic blockade.

12)The hand therapist should use great care to avoid any painful active or passive exercise on the part of the patient and should be equally as cautious to make sure that no pain is created by the splinting program. The therapist should be only a teacher and not a manipulator.

13)Indications for reconstructive surgery to regain motion should be very restrictive, and the expectations should be limited.

CONCLUSION

RSD is an important entity because of its devastating pain and disability. Hopefully in the future it will be more readily recognized in most disciplines of medicine, especially by physicians and surgeons dealing with trauma. A better understanding of the various clinical forms of RSD will foster the early recognition of this condition, so that appropriate treatment may be instituted promptly. Suspect RSD when pain, swelling, and stiffness are out of proportion to the severity of injury or disease. Watch for color, temperature, and sudomotor changes, atrophy, and osteoporosis. Although no one etiologic concept is entirely satisfactory, it is well established that the condition is perpetuated by overactivity of the sympathetic nervous system. Sympathetic blocks are important both diagnostically and therapeutically. About half the patients will be relieved of pain by the use of blocks alone, whereas the remaining half will require sympathectomy for prolonged relief.

Although pain may be relieved, the distressingly high incidence of disability and treatment failures occurs because treatment has been instituted too late in the course of the disease. Patients with RSD are often misunderstood and discredited, mismanaged, or neglected long enough to preclude successful functional rehabilitation.

REFERENCES

Adson, A.W., and Brown, G.E.: Raynaud's disease of upper extremities; successful treatment by resection of sympathetic cervicothoracic and second thoracic ganglions and intervening trunk, J.A.M.A. 92:444-449, 1929.

Atkins, H.J.B.: Sympathectomy by axillary approach, Lancet 1:538-539, 1954.

Barnes, R.: The role of sympathectomy in the treatment of causalgia, J.Bone Joint Surg. 35B:172-180, 1953.

Betcher, A.M., Bean, G., and Casten, D.F.: Continuous procaine block of paravertebral sympathetic ganglions, J.A.M.A. 151:288-292, 1953.

Bonica, J.J.: The management of pain, with special emphasis on the use of analgesic block in diagnosis, prognosis and therapy, Philadelphia, 1953, Lea & Febiger.

Bonica, J.J.: Causalgia and other reflex sympathetic dystrophies, Postgrad Med. 53:143-148, 1973.

Carron, H., and Weller, R.M.: Treatment of post-traumatic sympathetic dystrophy, Adv. Neurol. 4:485-490, 1974.

Casey, K.L.: The neurophysiologic basis of pain, Postgrad Med. 53:58-75, 1973.

Chapman, L.F., Ramos, A.O., Goodell, H., and Wolff, H.G.: Neurohumoral features of afferent fibers in man, Arch. Neurol. 4:617-650, 1961.

Coffman, J.D., and Davies, W.T.: Vasospastic disease: a review, Progr. Cardiovasc. Dis. 18:123-146, 1975.

Denmark, A.: An example of symptoms resembling tic douleureux produced by a wound in the radial nerve, Royal Med. Chir. Trans. 4:48-52, 1813.

DeSaussure, R.L.: Causalgia, Clin. Neurosurg. 25:626-636, 1978.

de Takats, G.: Reflex dystrophy of extremities, Arch. Surg. 34:939-956, 1937.

de Takats, G.: Causalgic states in peace and war, J.A.M.A. 128:699-704, 1945.

Doupe, J., Cullen, C. H., and Chance G.Q.: Post-traumatic pain and causalgia syndrome, J. Neurol Neurosurg. Psychiatry 7:33-48, 1944.

Eaton, R.G.: Correspondence Newsletter 1985-24.

Edmundson, A.S., and Calandruccio, R.A.: Drug therapy for causalgia, Mississippi Doctor 34: 239-241, 1957.

Evans, J.A.: Reflex sympathetic dystrophy: report on 57 cases, Ann. Intern. Med. 26:417-426, 1947.

Forster, R.S. and Fu, F.H.: Reflex Sympathetic Dystrophy in Children. A Case Report and Review of Literature. Orthopaedics 8:4, 475-477.

Fowler, F.D., and Moser, M.: Use of hexamethonium and Dibenzyline in diagnosis and treatment of causalgia, J.A.M.A. 161:1051-1053, 1956.

Genant, H.K., Kozin, F., Bakerman, C., McCarty, D.J., and Sims, J.: The reflex sympathetic dystrophy syndrome, Radiology 117:21-32, 1975.

Gerard, R.W.: The physiology of pain: Abnormal neuron states in causalgia and related phenomena, Anesthesiology 12:1-13, 1951.

Glick, E.M.: Reflex dystrophy (algoneurodystrophy): results of treatment by corticosteroids, Rheumatol. Rehabil. 12:84-88, 1973.

Granit, R., Leskell, L., and Skoglund, C.R.: Fiber interaction in injured or compressed region of nerve, Brain 67:125-140, 1944.

Hamilton, J.: On some effects resulting from wounds of nerves, Dublin J. Med. Sci. 13:38-55, 1838.

Homans, J.: Minor causalgia: a hyperesthetic neurovascular syndrome, N. Engl J. Med. 222:870-874, 1940.

Hunter, J.M., Schneider, L.H., Mackin, E.J., and Callahan, A.D.: Rehabilitation of the hand, ed. 2, St. Louis, 1984, The C.V. Mosby Co.

Kennard, M.A.: Sensitization of spinal cord of cat to pain-inducing stimuli, J. Neurosurg. 10:169-177, 1953.

Kirklin, J.W., Chenoweth, A.I., and Murphey F.: Causalgia: a review of its characteristics, diagnosis, and treatment. Surgery 2l:321-342, 1947.

Kleinert, H.E., Cole, N.M., Wayne, L., and others: Post-traumatic sympathetic dystrophy, Orthop. Clin. North Am. 4: 917-927, 1973.

Kux, M.: Thoracic endoscopic sympathectomy in palmar and axillary hyperhidrosis, Arch. Surg. 113:264-266, 1978.

Kwan, S.T.: The treatment of causalgia by thoracic sympathetic ganglionectomy, Ann. Surg. 101:222-227, 1935.

Lankford, L.L.: Reflex sympathetic dystrophy. Omer, G.E., Jr., and Spinner, M., editors: Management of peripheral nerve problems, Philadelphia, 1980, W.B. Saunders Co.

Lankford, L.L., and Thompson, J.E.: Reflex sympathetic dystrophy, upper and lower extremity: diagnosis and management. In American Academy of Orthopaedic Surgeons: Instructional course lectures, vol.26, St. Louis, 1977, The C.V. Mosby Co.

Leriche, R.: The surgery of pain (translated and edited by A. Young), London, 1939, Bailliere, Tindall & Cox.

Livingston, W.K.: Pain mechanisms: a physiological interpretation of causalgia and its related states, New York, 1943, The MacMillan Co.

Long, D.M.: Electrical stimulation for relief of pain from chronic nerve injury, J. Neurosurg. 39:718-722, 1973.

Lorente de No, R.: Analysis of the activity of the chains of internuncial neurons, J. Neurophysiol. 1:207-244, 1938.

McGrath, M.A., and Penny, R.: The mechanisms of Raynaud's phenomenon, Part I, Med. J. Aust. 2:328-333, 1974.

Mayfield, F.H., and Devine, J.W.: Causalgia, Surg. Gynecol. Obstet. 80:631-635, 1945.

Melzack, R., and Wall, P.D.: Pain mechanisms: a new theory, Science 150:971-979, 1965.

Meyer, G.A., and Fields, H.L.: Causalgia treated by selective large fibre stimulation of peripheral nerve, Brain 95:163-168, 1972.

Mitchell, J.K.: Remote consequences of injuries of nerves and their treatment, Philadelphia, 1895, Lea Brothers.

Mitchell, S. W., Morehouse, G.R., and Keen, W.W.: Gunshot wounds and other injuries of nerves, Philadelphia, 1864, J. B. Lippincott Co.

Mitchell, S.W.: On the diseases of nerves resulting from injuries in contributions relating to the causation and prevention of disease, and to camp disease. In Flint, A., editor: United States Sanitary Commission Memoirs, New York, 1867.

Mitchell, S.W.: Injuries of nerves and their consequences, Philadelphia, 1872, J.B. Lippincott Co.

Moore, D.C.: Regional block, Springfield, Ill., 1967, Charles C. Thomas, Publisher.

Nashold, B.S., Jr., and Friedman, H.: Dorsal column stimulation for control of pain, J. Neurosurg. 36:590-597, 1972.

Nathan, P.W.: On the pathogenesis of causalgia and peripheral nerve injuries, Brain 70:145-170, 1947.

Omer, G.E., Jr., and Thomas, S.R.: Treatment of causalgia: review of cases at Brooke General Hospital, Tex. Med. 67:93-96, 1971.

Omer, G.E., Jr., and Thomas, S.R.: The management of chronic pain syndromes in the upper extremity, Clin. Orthop. Rel. Res. 104:37-45, 1974.

Owens, J.C.: Causalgia, Am. Surg. 23:636-643, 1957.

Paget, J.: Clinical lecture on some cases of local paralysis, Med. Times 1:331-332, 1864.

Pak, T.J., Martin, G.M., Magness, J.L. and Kavanaugh, G.J.: Reflex sympathetic dystrophy, review of 140 cases, Minn. Med. 53:507-512, 1970.

Palumbo, L.T.: Upper dorsal sympathectomy without Horner's syndrome, Arch. Surg. 27:743-751, 1955.

Pare, A.: Les Oeuvres d'Ambroise Pare (historic de defunct), Roy Charles IX, Tenth Book 4l:401, Paris, 1598, Gabriel Buon.

Patman, R.D., Thompson, J.E., and Persson, A.V.: Management of post-traumatic pain syndromes, Ann. Surg. 177:780, 1973.

Pool, J.L., and Brabson, J.A.: Pain on stimulating the distal segment of divided peripheral nerves, J. Neurosurg.

3:468-473, 1946.

Porter, J.M., Lindell, T.D., Leung, B.S., and Reiney, C.G.: Effect of intra-arterial injection of reserpine on vascular wall catecholamine content. Surg. Forum 22:183-185, 1972.

Procacci, P., Francini, F., Maresca, M., and Zoppi, M.: Skin potentials and EMG changes induced by cutaneous electrical stimulation. II. Subjects with reflex sympathetic dystrophies. Appl. Neurophysiol. 42:125-134, 1979.

Richards, R.L.: Causalgia -- a centennial review, Arch. Neurol. 16:339, 1967.

Rosen, P.S., and Graham, W.: The shoulder-hand syndrome: historical review with observations on 73 patients, Can. Med. Assoc. J. 77:86-91, l957.

Ross, J.P.: Causalgia, St. Barthol. Hosp. Rep. 65:103-188, 1932.

Shumaker, H.B., Speigel, I.J., and Upjohn, R.H.: Causalgia: the role of sympathetic interruption in treatment, Surg. Gynecol. Obstet. 86:76-86, 1948.

Simson, G.: Propranolol for causalgia and Sudeck's atrophy, J.A.M.A. 227:327, 1974.

Smithwick, R.H.: The rationale and technique of sympathectomy for the relief of vascular spasm of the extremity, N. Engl. J. Med. 222:699, 1940.

Snider, R.L., and Porter, J.M.: Treatment of experimental frostbite with intra-arterial sympathetic blocking drugs, Surgery 77:557-561, 1975.

Spurling, R.G.: Causalgia of the upper extremity: treatment by dorsal sympathetic ganglionectomy, Arch. Neurol. Psychiatry 23:784-788, 1930.

Steinbrocker, O.: The shoulder-hand syndrome: associated painful homolateral disability of the shoulder and hand with swelling and atrophy of the hand, Am. J. Med. 3:402-407, 1947.

Steinbrocker, O.: The shoulder-hand syndrome: present perspective, Arch. Phys. Med. Rehabil. 49:388-395, 1968.

Sudeck, P.H.M.: Ueber die acute entzundliche Knockenatrophie, Arch. Klin. Chir. 62:147-156, 1900.

Sunderland, S.: Pain mechanisms in causalgia, J. Neurol. Neurosurg. Psychiatry 39:471-480, 1976.

Walker, A.E., and Nulson, F.: Electrical stimulation of the upper thoracic portion of the sympathetic chain in man, Arch. Neurol. Psychiatry 59:559-560, 1948.

Wall, P.D., and Sweet, W.H.: Temporary abolition of pain in man, Science 155:108-109, 1967.

White, J.C., Smithwick, R.H., and Simeone, F.A.: The autonomic nervous system, ed. 3, New York, 1952, MacMillan, Inc.

White, J.C.: Sympathectomy for relief of pain. In Bonica, J.J., editor: Advances in neurology, International Symposium on Pain, vol. 4, New York, 1974, Raven Press.

Zhu, S., Lu, S., et. al.: Intrafascicular decompression in the treatment of causalgia with special reference to the mechanism. Annals of Plastic Surgery 15:460-464, 1985.

Ecker, A.: Contact Thermography in Diagnosis of Reflex Sympathetic Dystrophy: A new look at Pathogenesis. Thermology 1:106-109, 1985.

Combined Sympathectomy and Guanethidine Failure in Causalgia (worsening with each intervention) Neurothermoj and Electromyog 1:2, 1984.

Umetasu, S.: Telethermography in the Differential Diagnosis of Reflex Sympathetic Dystrophy and chronic pain syndrome. Pain Therapy 63-72, 1983.

Ecker, A.: Reflex Sympathetic Dystrophy Thermography in Diagnosis: Psychiatric Considerations. Psychiatric Annals 14:787-793, 1984.

Prough, D., McLeskey, C., Poehlng, G., et al: Efficacy of Oral Nifedipine in the Treatment of Reflex Sympathetic Dystrophy. Clinical Reports 62:796-799, 1985.

Pochaczevsky, R: Thermographyin Post-TraumaticPain. Thermology 1:253, 1986.

Burg, H.E.: Verification of Traumatic Reflex Sympathetic Dystrophy by Liquid Crystal Thermography. Thermology 1:245, 1986.

Roberts, W.J, Fogleson, B.A.: Neuronal Basis for Sympathetically Maintained Pain. Thermology 1:244-253, 1986.

Foley, K.M.: The Treatment of Pain in The Patient with Cancer. Cancer Journal for Clinicians 36:194-215, 1986.

Chamberlain, D.P., & Chamberlai, B.D.L.: Changes in the Skin Temperature of the Trunk and Their Relationship to Sympathetic Blockade during Spinal Anethesia. Anesthesiology 65:139-143, 1986.

Ignacio, D., Gilbert, G., Shibuya, J., Pavot, A.P.: Infrared Imaging and Bone Scan in the Diagnosis of Reflex Sympathetic Dystrophy. Thermology 1:245, 1986.

Kenzora, J.E.: Sensory Nerve Neuromas -- Leading to Failed Foot Surgery. Foot & Ankle 7:110-117, 1986.

Uricchio, J.V.: Thermography in the Evaluation of Causalgia. Medical Thermology 134-137, 1986.

Aldea, P.A., Shaw, W. W.: Management of Acute Lower Extremity Nerve Injuries. Foot & Ankle 7:82-94, 1986.

LeRoy, P.L., Brunner, W. M., Christian, C. R., Filasky, R., Leroy, S.: Neurosurgical Thermography. Discussion of Selected Preoperative, Intraoperative and Postoperative Applications. Medical Thermology, pp302-307, 1986.

Tietjen, R.: Reflex Sympathetic Dystrophy of the Knee. Clinical Orthopaedics and Related Research 209:234-243, 1986.

Ingall, J.F.: Abstract: Reflex Sympathetic Dystrophy: A Common Problem. Initial Special Edition, p 11, December 1986.

Uricchio, J.V.: Electronic Thermography in Orthopaedic Practice: Its Use in Soft Tissue Injuries of the Neck and Back. Medical Thermology 62-72, 1986.

Greene, N.M.: A New Look of Sympathetic Denervation during Spinal Anesthesia 65:137-138, 1986.

Outline - Thermography for Selected Neurological and Musculoskeletal Conditions. AMA DATTA REPORT, 1986.

Hobbins, W.B.: Basic Concepts of Thermology and Its Application in the Study of The Sympathetic Nervous System. Presented Second Albert Memorial Symposium, Washington, D.C., September 17, 1986.

Rothschild, B.M.: Thermogrphic Assessment of Bone and Joint Disease. Orthopaedic Review 12:33-48, 1986.

Cailliet, R.: Neurologic Disorders of the Foot. Foot and Ankle Pain Edition 2, F.A. Davis Company, 1986, pp. 159-179.

Ignacio, D., Azer, R.N., Shibuya, J., Pavot, A. P.: Thermographic Monitoring of Sympathetic Nerve Block. Thermology 2:21-24, 1986.

Omer, G.E.: Management Techniques for The Painful Upper Extremity. Microreconstruction of Nerve Injuries. W. B. Saunders Company, 1987, pp 145-159.

Dirksen, R., Rutgers, M.J., Coolen, J.M.W.: Cervical Epidural Steroids in Reflex Sympathetic Dystrophy. Anesthesiology 66:7-73, 1987.

Perelman, R.B., Adler, D.B., Humphreys, M: Reflex Sympathetic Dystrophy A Thermographic Evaluation. The Journal of Neurological & Orthopaedic Medicine and Surgery 8:47-49, 1987.

Fields, H. L.: On the Mechanisms and Management of Pain. Practitioner's Consult, pp 2-12.

Kanner, R.: Pain Management. JAMA 256:2112-2113, 1986.

Escobar, P.L.: Reflex Sympathetic Dystrophy. Orthopaedic Review 20:41-46, 1986.

Newman, D., Durand, J., Munez, S, et. al: Efficacy of Pentoxifyline in Raynaud's Syndrome. Thermology 1:245, 1986.

Meulen, D.C., Massoud M.: Bone Scintigraphy in the Evaluation of Children with Obscure Skeletal Pain. Pediatrics 79:587-592, 1987.