Reflex sympathetic dystrophy syndrome Case report with a review of the literature

Michael Markof, D.M.D.,* and Anthony Farole, D.M.D.,** Philadelphia, Pa.

THOMAS JEFFERSON UNIVERSITY HOSPITAL

A case of reflex sympathetic dystrophy syndrome (RSDS) is presented in which the condition was exacerbated after the excision of impacted teeth. A review of the English language literature describes manifestations, distribution, etiology, pathogenesis, histology, and diagnosis of RSDS. Treatment modalities are reviewed, and recommendations for the management of the patient with a history of RSDS are detailed. (ORAL SURG. ORAL MED. ORAL PATHOL. 61:23-28, 1986)

R eflex sympathetic dystrophy syndrome (RSDS) is primarily a neurovascular pain dysfunction com- plex affecting the limbs. It has been known by many names and in various forms for at least 120 years. In well over half the patients reported, an antecedent event such as trauma, systemic disease, or unrelated surgery was implicated in the initiation or exacerba- tion of signs and symptoms. Psychogenic input by way of the “pain gate” of Melzack and Wall’ may greatly influence onset, progression, and resolution of this condition.

Pain and edema, disproportionately severe for the stimulus, lead to protective immobility, which, if allowed to continue, results in trophic skin changes, patchy osteoporosis, and permanent limb contrac- tures. There are no consistent laboratory findings that confirm the diagnosis; rather, such values serve to eliminate other diseases within the differential diagnosis. Steroids, sympathetic blockade, and phys- ical therapy are among the more popular modes of treatment at this time; all methods are claimed by their advocates to have superior rates of successful clinical resolution. However, there are no dependably curative treatments, and more than half the patients in a large study had residual symptoms after treat- ment.2 The childhood-adolescent form of RSDS, though comparatively rare, is much less severe and

*Chief Resident, Division of Oral and Maxillofacial Surgery. **Assistant Professor and Assistant Director, Oral and Maxillo- facial Surgery Residency Program.

has a much better prognosis, with few if any residual symptoms.

A case of RSDS is reported in which an acute exacerbation followed simple excision of impacted teeth under general anesthesia.

CASE REPORT

On Oct. 11, 1983, a 20-year-old white woman came to our institution’s Division of Oral and Maxillofacial Sur- gery complaining of soreness of maxillary and mandibular third molar areas during the past week. Her medical history was remarkable for a 3-year history of RSDS (followed up by our hospital’s Neurology Department), thoracic outlet syndrome (under care of the Orthopedic Department), anemia (followed by our hematologist), and hemoptysis of unknown cause (evaluated by our otolaryn- gology service). In addition, the patient had childhood asthma, which had been inactive without medication for the last 7 years, and mitral valve prolapse. She was taking diazepam, 4 to 10 mg, four times a day for spasms of the left neck and shoulder, and an oral iron supplement. She reported being allergic to cefazolin sodium (Ancef) and myelogram dye.

Physical examination revealed Horner’s syndrome on the left side (secondary to earlier cervical sympathectomy) and healthy oral tissues, except for pharyngeal edema, minor pericoronitis around the mandibular left impacted third molar, bilateral malpositioned maxillary third molars, and an impacted mandibular right third molar. Panoramic x-ray film demonstrated normal bony architec- ture with bilateral maxillary, completely impacted fourth molars.

Because of the patient’s mitral valve prolapse, elimina-

23

24 Markoff and Farole Oral Surg. January, 1986

tion of any source of infection and potential bacteremia was deemed necessary, and in light of the extensive medical history the patient was scheduled for admission for the excision of ail third and fourth molars. Penicillin was prescribed and the patient was instructed to use saline oral rinses in the time interval before admission.

On admission Oct. 18, 1983, a standard history was taken and a physical examination was given. Additional history was significant for several episodes of fever of unknown origin and exacerbation of RSDS in the left arm and leg. Surgical history revealed a scalenectomy, appen- dectomy, removal of the left first rib (to treat thoracic outlet syndrome), cervical sympathectomy, laparoscopy, arthroscopy of the left knee, fasciotomy, and lumbar sympathectomy between March 1981 and July 1983.

Her past medical history revealed that the patient suffered frequent, severe headaches with accompanying nausea and vomiting, which she claimed her neurologist related to her RSDS. The patient said she had chronic anemia during the previous 6 months, a left scapular bursa injury secondary to sympathectomy surgery, and numb- ness of the left shoulder, with swelling of the left arm, pain of the occiput and neck, and associated muscle spasms. A family history was noncontributory, and she neither drank alcohol nor smoked.

Physical examination was remarkable for the Horner’s syndrome of the left side and a II/VI systolic murmur. The following laboratory tests were performed: complete blood count with differential, prothrombin time, partial throm- boplastin time, sequential multiple analyzer,, sequential multiple analyzer,,, and urinalysis, all of which yielded results within the normal range, except for a white blood cell count of 3.8 X 10’/mm3 and microcytic hypochromic anemia.

The patient’s neurologist was consulted to evaluate the patient before surgery. He recommended that her orthope- dist be consulted for an injection of anesthetic into the subscapular bursa to relieve the neck and occipital pains and that a medical service grant presurgical medical clearance. Such clearance was obtained.

Because of the patient’s low Hb/Hct, morning surgery was deferred until the hematology service assured us that this anemia was usual for our patient and that it posed no obstacle to the intended surgery; parenteral iron supple- mentation after surgery was recommended because the patient’s response to enteral iron was suboptimal.

On Oct. 20, 1983, the patient was given a general anesthetic via nasotracheal intubation for excision of four third and two fourth molars. The surgery and anesthesia were atraumatic and completed without difficulty. The patient’s head and neck were maintained in a neutral position and the arms were tucked against the sides throughout the intubation and surgery. She received 80 mg of methylprednisolone sodium succinate and 2 million units of aqueous penicillin intravenously before incision. On extubation in the operating room the patient complain- ed of spasm and severe pain in the neck, radiating into the fingers of the left hand, but sparing the thumb, and pins-and-needles paresthesia of the left arm with profound weakness. The Neurology Department was consulted

immediately from the recovery room; the impression was that of severe RSDS, rather than cervical myelopathy secondary to disc herniation. A cervical collar was placed and x-ray films were immediately taken of the cervical spine; they demonstrated no acute changes, Postoperative orders included continuation of the steroid, 80 mg every 4 hours and penicillin, 2 million units every 4 hours. For the remainder of the day the patient’s intraoral status was excellent but the pain of the left upper extremity necessi- tated increasing doses of narcotic for adequate analgesia.

On the first postoperative day the neurologist suspected that the symptoms represented exacerbation of RSDS and he recommended analgesics and EMG testing of the left arm. The orthopedist suspected cervical strain as the source of the pain and dysfunction and he recommended anti-inflammatory medication. The patient received a final dose of 80 mg of methylprednisolone sodium succinate, followed later by 80 mg of methylprednisolone acetate as a single intramuscular injection.

By the fourth postoperative day the patient’s mouth was healing well, but the pain and dysfunction of the left arm and neck remained unabated and the neurologist accepted her for treatment. EMG results indicated reduced volun- tary effort, as is seen in cases of extreme discomfort, without evidence of neuropathy or radiculopathy. The physical therapy service was consulted; it recommended range-of-motion therapy and moist heat to the left shoul- der and neck, followed by ice massage if moist heat was ineffective. The regimen was initiated the same day. The patient was given 300 mg of lidocaine via slow intravenous infusion by an anesthesiologist to reduce the pain and spasm; it gave only minor improvement. She was started on intravenous iron supplement for treatment of the iron- deficiency anemia. The patient received physical and occupational therapy sessions, and frequent analgesics with slightly improved function and pain control.

By the tenth day after surgery the patient started complaining of pain in the right shoulder, aggravated by function. Ice packs were applied to treat this problem. That night the patient’s temperature rose to 104” F, and this nocturnal fever was decrementally repeated, with her temperature returning to a normal level 3 days later; negative blood and urine cultures, chest x-ray films, and a negative antinuclear antibody titer suggested a viral cause. The patient also started complaining of bilateral medial knee pain.

Fourteen days after oral surgery the pains and dysfunc- tion were without change. The patient was interviewed by a psychiatrist from the hospital’s chronic pain clinic. He suggested that the patient might have a hysterical type of personality and recommended hypnosis and consideration of propranolol for possible vasospasm. That day the patient was started on a tricyclic antidepressant for her increasing depression. By this time the patient’s neurologist noted, “ . The spinal x-rays, tomograms, EMG, are negative and . (he sees) no physiological reason for pain.” He was concerned with the narcotic dosage and ordered a decrease of dosage and frequency. The patient complained often about this decrease in medication.

By Nov. 7, 1984, the patient reported a sudden absence

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Reflex sympathetic dystrophy syndrome 25

of pain in the right shoulder. It was believed that at this time she would benefit from her home environment, with outpatient follow-up by a psychiatrist. Discharge was arranged with the patient on oral analgesics and with psychiatric follow-up. She was discharged the next day, 19 days after oral surgery, without improvement of the pain, dysfunction and paresthesia of the left arm. On follow-up more than a year after discharge the patient reported persistence of the pain and dysfunction.

REVIEW OF LITERATURE

RSDS represents a symptom complex that in one form or another and by a multitude of names was known since Mitchell et al3 reported it is wounded soldiers of the American Civil War in 1864. RSDS has numerous signs and symptoms, and may be considered a collective term under which various diseases have been included, for example, Steinbrok- er’s shoulder-hand syndrome, Sudeck’s atrophy, posttraumatic osteoporosis, traumatic angiospasm, chronic traumatic edema, peripheral trophoneurosis, algodystrophy, and minor causalgia.4-8

The classic signs and symptoms are pain and swelling in an extremity, trophic skin changes in the same limb, and typically a precipitating event that usually involves injury to a peripheral nerve.4, 5*9. ‘O In addition, hypertrichosis and osteoporosis of the limb may be noted.5 The pain and dysesthesias are not restricted to the distribution of the injured nerve and often temporally endure beyond the nerve deficit.”

The age and sex distribution reported in the 125 cases of Subbarao and Stillwell* agree with other studies; the incidence increased with age, peaking in the fifth decade. The male-female ratio is 1: 2.9.* The actual prevalence is not known, but Plewes’* reported one case in every 2000 accidents (approxi- mately 12 a year) treated in a busy trauma center. De Takats4 estimated that 5% to 15% of all trauma cases will result in a form of minor to severe RSDS.

Initiation of RSDS has been attributed to trauma, often of a minor nature, drugs, nerve injury, surgery, carcinoma, cervical osteoarthritis, myocardial ische- mia and infarct, and cerebrovascular and other neurologic lesions. I’, I33 I4 In the study by Subbarao et al.,* about 9.5% of the cases had no identifiable cause.

Several theories have arisen in an attempt to explain the various clinical stigmata and test results found in RSDS. Bonicals and others thought that damage to peripheral nerves led to a reflex aberra- tion of vasomotor function in autonomic efferent nerves. This may occur by cross-stimulation between sympathetic efferents and damaged, demyelinated, or unmyelinated sensory fibers by way of a choliner-

gic vasodilator chemical mediator.4 Livingstoni pos- tulated that this short-circuiting of neural transmis- sion occurred in self-sustaining neuronal loops within the spinal dorsal horn. More recently, the “gate control” mechanism of Melzack and Wall’ has been cited to explain the beginning of RSDS; specialized cells within the substantia gelatinosa of the spine’s dorsal column modulate sensory transmission to higher centers by closing the gate in response to large, myelinated afferent fiber input, and by open- ing this gate with input from small C fibers. In addition, fibers descending from higher neural cen- ters modulate this gate. Thus mild stimuli transmit- ted along C fibers may be felt as intense pain, especially when input from large fibers is faulty or when descending impulses fail to close the gate.l. IO. 13. I7 C-S involvement in RSDS is supported by a case of diffuse RSDS reported by Bentley and Hameroff” and by consistent findings of bilateral limb involvement in RSDS.5

De Takats4 pointed out that in the primary phase of RSDS a sympathetic block will relieve the pain because of its restriction to the first-order neurons. This is the vasodilation phase, with hot throbbing and burning pain, and is relieved by elevation and cold, wet packs. However, as with other long- standing painful states, the second-order sensory neuron becomes involved, making peripheral auto- nomic or somatic blocks ineffectual, and spinal anesthesia is the least anesthesia required for pain relief. This is the secondary or vasoconstrictive phase, with cold, tense, sweaty, glossy skin, limited range of motion secondary to pain and contracture, and patchy osteoporosis. RSDS may continue to the tertiary phase, with higher centers involved, namely, the reflex tuning of the hypothalamus to minor or subliminal stimuli, which results in exaggerated autonomic outbursts.18 When RSDS reaches the highest sensory level, drug addiction, insanity, and even suicide may ensue.4

Histologic study of RSDS has thus far centered on the articular tissues because of the accentuated symptomatic involvement of limb joints. Synovial specimens from four RSDS patient were histologi- cally abnormal when compared with age-matched, fresh cadaver tissues. Kozin et al.5 report, “Varying degrees of synovial edema, proliferation and disarray of synovial lining cells, proliferation of capillaries, fibrosis of the subsynovium and slight perivascular infiltration with chronic inflammatory cells (chiefly lymphocyte) were noted.”

There is a conspicuous absence of consistently abnormal laboratory findings in RSDS. In fact, laboratory studies are best used to rule out other disease in a differential diagnosis, such as infectious

26 Mark&-and Farole Oral Surg. January, 19%

Table I. Diagnostic criteria of RSDS Table II. Treatment modalities used for RSDS

Description: Neurovascular pain complex affecting limbs; pain and edema

exceeding stimulus in severity and duration. Antecedent event:

Signs and symptoms:

Laboratory findings:

Age:

Sex: Histology:

Radiographic findings:

Trauma, systemic disease, drugs, nerve injury, myocardial infarc- tion, unrelated surgery; IO% with- out identifiable cause.

Pain and swelling of limb, leading to protective immobility: eventual tro- phic skin changes, patchy osteopor- osis, permanent limb contractures.

Nondiagnostic; exclude other diagno- ses.

Increased prevalence with age; peaks in fifth decade.

Males to females, 1:2.9. Synovial edema, proliferation and

disarray of synovial lining cells, proliferation of capillaries, fibrosis of subsynovium, slight perivascular lymphocytosis.

Soft tissue swelling; patchy osteopor- osis in some patients.

Diagnostic sympathetic Relieves vasomotor component and nerve block: usually pain in primary phase.

Psychological factors: Abnormal hysteria, hypochondriasis, and/or depression in majority of cases.

Radioisotope scan: Juxta-articular (increase) in 99mTc uptake.

arthritis (especially staphylococcal and gonococcal), early rheumatoid arthritis, scleroderma, and lym- phedema.19

Radiographically, the usual findings in RSDS are soft tissue swelling with patchy osteoporosis (which can resemble regional migratory osteoporosis). When fine-detail radiography is used, juxta-articular osseous resorption of trabecular, intracortical, sub- chondral, subperiosteal, and endosteal bone can be noted. Scintigraphy is a most useful study in the early identification of suspected cases of RSDS. Before plain films or symptoms indicate RSDS, scans may demonstrate bilaterality of the condition with increased 99mTc uptake, especially by juxta- articular tissues.20, *’

Diagnosis of RSDS is based on history (a sus- pected predisposing event had been identified in up to 65% of the cases of Kozin et a1.,9 the clinical picture, scintigraphic and/or radiographic evidence, and normal or nonspecific laboratory values. In addition, a local anesthetic block of appropriate sympathetic ganglia will relieve the vasomotor com- ponent, and usually the pain, for a duration appropri- ate for the life of the anesthetic, whereas a placebo saline block will not.

Prevention: Care in the selection of surgical candidates who have a history ol RSDS; awareness of those at grcatcr risk.

Corticosteroids Sympathetic blockade Sympathectomy Pharmacologic agents: Analgesics, fl-adrenergic blockade.

calcitonin, localized intravenous reserpine, guanethidine.

The literature on RSDS offers as many different regimens for treatments there are synonyms and subgroups of RSDS. Some authors claim that corti- costeroid therapy is the most effective therapy.22 Others recommend sympathetic blockade with lido- Caine; according to De Takats,14 “Two successive blocks resulting in subjective and objective improve- ment constitute an indication of sympathetectomy.” Still others advocate hydrocortisone-lidocaine injec- tions into painful trigger zones (e.g., a subscapular bursa),4 analgesics, physical therapy, @-adrenergic blockade, calcitonin” or localized intravenous reser- pine,” or guanethidine*’ treatments. However, throughout this variety several points of agreement emerge. The most promising approach is that of prevention, consisting of early mobilization of the extremities for all high-risk patients. Early recogni- tion and aggressive treatment of RSDS while it is in its early stages are essential in preventing ascent of neuronal involvement toward progressive morbidity and intractability.*, 14. ” Despite adequate therapy, nearly 60% of the 125 cases in the survey of Subbarao and Stillwell’ retained some persistent symptoms in the upper limb, with an equal percent- age requiring modification of work or other daily activities.*

Although any “normal” individual can develop RSDS, HillI states that it is more often seen in inadequate personality types and in outright neurot- ics. The use of the MMPI (Minnesota Multiphasic Personality Inventory) by Subbarao and Stillwell* showed abnormal hysteria, hypochondriasis, and/or depression in 80% of the 45 cases studied. Just as there are documented correlations between adult RSDS and psychosocial situations, so there are correlations noted in childhood patients. Bernstein et a1.6 showed that an overwhelming majority of chil- dren afflicted with RSDS had a history of overt parental conflict in their families, accepted responsi- bility beyond their years, had difficulty expressing anger or being assertive, and were indifferent to the implications of their condition to future activities.

Volume 6 I Number I

RSDS in children and adolescents is comparative- ly rare. Data from more than 30 patients indicate several key differences between this form of the malady and RSDS affecting adults. There is a lack of trophic changes of the affected limbs in children, and the patchy osteoporosis pattern of adult RSDS is absent.6, lo. ” Also, there is a lower frequency of identifiable initiating events and a greater frequency of knee involvement in childhood patients.6 Child- hood RSDS appears to be a self-limiting disease, typically responding well to mild analgesics and physical therapy. I’ The diagnostic criteria and treat- ment modalities used for RSDS are summarized in Tables I and II.

CONCLUSIONS

The case presented illustrates the different approaches to preventing and treating exacerbated. RSDS. The patient’s age places her on the younger end of the statistical spectrum for RSDS; in fact, the original diagnosis of RSDS was made 3 years prior to this admission, when the patient was 17 years of age. At the time of this hospital admission the patient was an “A” student in nursing school, a daughter from a broken marriage, and periodically had expressed lack of concern for her inability to continue her training in this debilitated condition.

The treatment of the patient’s condition was in many ways like those treatments prescribed for adolescent RSDS. The question then arises, “At what age should a patient cease to be treated for adolescent RSDS, with conservative therapy and an excellent prognosis?” This question has yet to be addressed in the English language literature.

Because the literature does not discuss the perio- perative management of patients for surgery unre- lated to their RSDS, some recommendations are made in this article on the basis of the information provided by the literature to date, combined with common sense.

1. In light of potential RSDS relapse or exacerba- tion the surgeon should carefully weigh the altered risk: benefit ratio of intended surgery.

2. Consideration should be given to patients at high risk for RSDS development (see earlier).

3. Consider use of local anesthesia with or without sedation when practical, thereby avoiding the trau- ma of intubation and avoiding chemical agents that might cause a relapse or exacerbation (i.e., agents with direct neuromuscular and/or vasomotor effects).

4. The patient’s physician(s) and a staff neurolo- gist and anesthesiologist should be consulted, to provide as atraumatic a perioperative phase as possi-

Reflex sympathetic dystrophy syndrome 27

ble. Nurses interacting with the patient should be informed about the do’s and don’ts of the patient’s disorder. Psychiatric consultations may be consid- ered.

5. Particular attention ought to be paid to the intraoperative physical position of the patient, so that no nerve or circulatory compression or tension results. Arm boards should be at less than a 90- degree angle of abduction from the body, to prevent tension on the brachial plexus.

6. Perioperative steroids are not contraindicated as yet and could conceivably help prevent or lessen the severity of RSDS relapse. Regimens should be discussed with the patient’s neurologist and general physician.

The case reported here and an extensive review of the literature serve as guidelines for clinicians in assessing and planning the perioperative course of a patient with a history of RSDS. Finally, clinicians should realize that this is an example of a disorder in which the psyche affects the soma. Organized physi- ologic responses to stresses in everyday life can have dramatic clinical manifestations of which we need to cognizant.

REFERENCES

1.

2.

3.

4.

5.

6

I

8

9

IO.

II

12.

13.

14.

Melzack R, Wall P: Pain mechanisms: A new theory. Science 150: 971-979, 1965. Subbarao J, Stillwell GK: Relfex sympathetic dystrophy syndrome of the upper extremity: Analysis of total outcome of management of 125 cases. Arch Phys Med Rehabil 62: 549-554, 198 I. Mitchell SW, Morehouse GR, Keen WW: Gunshot wounds and other injuries to nerves. Philadelphia, 1964, J.B. Lippin- cott Company. De Takats G: Sympathetic reflex dystrophy. Med Clin North Am 49: 117-129, 1965. Kozin F, McCarty D, Sims J, Genant H: The reflex sympa- thetic dystrophy syndrome. I. Am J Med 60: 321-330, 1976. Bernstein BH, Singsen BH, Kent JT, Kornreich H, King R, Hanson V: Reflex neurovascuiar dystrophy in childhood. J Pediatr 93: 21 l-215, 1978. Abert J, Ott H: Three brothers with algodystrophy of the hip. Ann Rheum Dis 42: 421-424, 1983. Homans J: Minor causalgia, a hyperesthetic neurovascular syndrome. N Engl J Med 222: 870, 1940. Kozin F, Ryan LM, Caressa GF, Soin JS, Wortmann RL: The reflex sympathetic dystrophy syndrome. 111. Am J Med 70: 23-30, 198 I. Buckta RM: Reflex sympathetic dystrophy in a ICyear-old female. J Adolesc Health Care 4: 121-122, 1983. Ruggeri SB, Athreya BH, Doughty R, Gregg JR, Das MM: Reflex sympathetic dystrophy in children. Clin Orthop 163: 225-230, 1982. Plewes LW: Sudeck’s atrophy in the hand. J Bone Joint Surg [Br] 38: 195-203, 1956. Chuinard RG, Dabezies EJ, Gould JS, Murphy GA, Mat- thews RE: Intravenous reserpine for treatment of reflex sympathetic dystrophy. South Med J 74: 1481-1484, 1981. Hill GJ: Outpatient surgery, ed 2, Philadelphia, 1980 W.B. Saunders Company, pp. 624 and 684.

28 iUarko$and Farole Oral Surg. January, 1986

15. Bonica JJ: Causalgia and other reflex sympathetic dystro- phies. Postgrad Med 53: 143-170, 1973.

16. Livingston WK: Pain mechanism: A physiologic interpreta- tion of causalgia and its related states. New York, 1943, Macmillan Publishing Company, pp. 224-230.

17. Bentley JB, Hameroff SR: Diffuse reflex sympathetic dystro- phy. Anesthesiology 53: 256-257, 1980.

18. Steinbrocker 0: Shoulder-hand syndrome: Present perspec- tive. Arch Phys Med Rehabil 49: 388-394, 1968.

19. Kozin F: Two unique shoulder disorders. Postgrad Med 73: 207-215, 1983.

20. Kozin F, Genant HK, Bekerman C, McCarty D: The reflex sympathetic dystrophy syndrome. II. Am J Med 60: 332-338, 1976.

2 I. Karasick S, Karasick D: Case report 193. Skeletal Radio] 8: 151-152, 1982.

22. Christensen K, Jensen EM, Noer I: The reflex dystrophy syndrome response to treatment with systemic corticosteroids. Acta Chir Stand 148: 653-655, 1982.

23. Bonelli S, Conoscente F, Movilia PC, Restelli L, Franucci B, Grossi E: Regional intravenous guanethidine vs stellate gan- glion block in reflex sympathetic dystrophies: A random trial. Pain 16: 297-307. 1983.

Reprint requests to: Anthony Farole, D.M.D. Division of Oral and Maxillofacial Surgery Department of Dentistry Suite II20 Edison Building I30 South 9th St. Philadelphia, PA 19107

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