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Glenohumeral joint subluxation and reflex sympathetic dystrophy in hemiplegic patients
944
Glenohumeral Joint Subluxation and Reflex Sympathetic Dystrophy in Hemiplegic Patients Erbil Dursun, MD, Nigar Dursun, MD, Canan Eksi Ural, MD, Aytu¨l C¸akci, MD ABSTRACT. Dursun E, Dursun N, Eksi Ural C, C¸akci A. Glenohumeral joint subluxation and reflex sympathetic dystrophy in hemiplegic patients. Arch Phys Med Rehabil 1999;81: 944-6. Objective: To examine the relation between glenohumeral joint subluxation and reflex sympathetic dystrophy (RSD) in hemiplegic patients. Design: Case-control study. Setting: Inpatient rehabilitation hospital. Patients: Thirty-five hemiplegic patients with RSD (RSD group) and 35 hemiplegic patients without RSD (non-RSD group) were included in the study. Patients with rotator cuff rupture, brachial plexus injury, or spasticity greater than stage 2 on the Ashworth scale were excluded. Main Outcome Measures: Both the RSD and non-RSD groups were assessed for presence and grade of subluxation from radiographs using a 5-point categorization. The degree of shoulder pain of the non-RSD group was assessed by a visual analogue scale of 10 points. Results: Glenohumeral subluxation was found in 74.3% of the RSD and 40% of the non-RSD group ( p ⫽ .004). In the non-RSD group, 78.6% of the patients with subluxation and 38.1% of the patients without subluxation reported shoulder pain ( p ⫽ .019). No correlation was found between the degree of shoulder pain and grade of subluxation in the non-RSD group ( p ⫽ .152). Conclusion: Findings from this study suggest that shoulder subluxation may be a causative factor for RSD. Therefore, prevention and appropriate treatment of glenohumeral joint subluxation should be included in rehabilitation of hemiplegic patients. Key Words: Hemiplegia; Reflex sympathetic dystrophy; Subluxation; Rehabilitation. 娀 2000 by the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation
D
EVELOPMENT OF reflex sympathetic dystrophy (RSD) in hemiplegic patients is a significant problem that may cause pain and function loss and seriously hamper their rehabilitation programs. Although many different treatment approaches have been described, the management of RSD remains quite difficult.1-11 Preventative measures to reduce the risk of RSD are essential. RSD is associated with a variety of precipitating factors, including immobilization of the upper extremity, trauma to the joint structures, rotator cuff tears, spasticity of the shoulder musculature, and glenohumeral joint From the Department of Physical Medicine and Rehabilitation, Kocaeli University Faculty of Medicine, Kocaeli (E. Dursun, N. Dursun) and the Department of Physical Medicine and Rehabilitation, Ankara Rehabilitation Center, Ankara (Eksi Ural, C¸akci), Turkey. Submitted January 13, 1999. Accepted in revised form June 18, 1999. The authors have chosen not to select a disclosure statement. ¨ niversitesi Tıp Faku¨ltesi, Fiziksel Reprint requests to Dr. Erbil Dursun, Kocaeli U Tıp ve Rehabilitasyon ABD, 41900, Kocaeli, Turkey. 0003-9993/00/8107-5375$3.00/0 doi:10.1053/apmr.2000.1761
Arch Phys Med Rehabil Vol 81, July 2000
subluxation. Most of these associations have not been obviously established. It is not clear why all of these factors cause the same clinical syndrome, but injury to neural tissue, either central or peripheral, may be the common mechanism.12,13 A persistent painful lesion must be present to develop RSD. Glenohumeral joint subluxation has been recognized as a major and frequent complication in patients with hemiplegia. It may be associated with shoulder pain, peripheral nerve damage, and autonomic dysfunction, and may interfere with functional activities.14-16 The association of glenohumeral joint subluxation and RSD is rarely mentioned in the literature. The aim of this study was to examine the relation between shoulder subluxation and RSD. In a non-RSD group, we also examined if subluxation is associated with shoulder pain, and if a correlation exists between the degree of shoulder pain and the grade of subluxation. MATERIALS AND METHODS One hundred sixteen consecutive stroke patients admitted to Ankara Rehabilitation Center, in a period of 36 months, were evaluated. Thirty-five patients with RSD were assigned to the RSD group and 35 patients without RSD were assigned to a non-RSD group. Forty-six patients were excluded because of bilateral involvement, multiple attacks, rotator cuff rupture, spacticity greater than stage 2 on the Ashworth scale, brachial plexus injury, major trauma after stroke, or cognitive dysfunction. The diagnosis of RSD was primarily based on the clinical entity and the staging was performed according to the classification of Steinbrocker and Argyros.17 Diagnosis was confirmed by a three-phase scintigraphic study if any suspicion of other factors such as positional edema or thrombophlebitis existed. According to Steinbrocker’s classification, Stage 1, the ‘‘acute’’ stage, is characterized by severe pain that has a burning or aching quality and is increased by dependency of the affected part, physical contact, or emotional upset. Edema, hyperthermia, hypothermia, and increased hair and nail growth occur in the affected part. Bony changes may be present on roentgenographs. Stage 2, the ‘‘dystrophic’’ stage, is characterized by the development of dystrophic changes such as nail changes and shiny skin with loss of normal wrinkling and the persistence of pain and disability. The edematous tissue becomes endurated and the skin is cool and hyperhidrotic. Roentgenographs may reveal diffuse osteoporosis. Stage 3, the ‘‘atrophic’’ stage, is characterized by progressive skin and subcutaneous tissue atrophy and occasionally proximal spread of pain. The skin is thin and shiny, the fascia becomes thickened, and flexion or Dupuytren’s contractures may occur. Roentgenographs show marked demineralization and ankylosis. Demographic properties including age, gender, side of involvement, etiology of the lesion, and duration of the disease were recorded, as were Brunnstrom functional classification scores of the patients. The presence and degree of subluxation in RSD patients was assessed from anterior-posterior radiographs centering on the glenohumeral joint with the hemiplegic arm unsupported. The degree of subluxation was determined by a 5-point categoriza-
945
SUBLUXATION AND RSD, Dursun
tion18-20 as: 0 (normal), the whole curvature of the glenoid fossa is opposed by and parallel to the humeral head; 1 (V-shaped widening), the whole curvature of the glenoid fossa is opposed by the humeral head, but a V-shaped widening is present in the superior intraarticular space; 2 (moderate subluxation), there is inferior subluxation of the humeral head, with the most superior margin of the humeral head not below the line perpendicularly bisecting the line connecting the most superior and inferior margins of the glenoid fossa; 3 (advanced subluxation), similar to moderate subluxation but the superior margin of the humeral head is level with or below the bisecting line; and 4 (dislocation), the most superior margin of the humeral head is level with or below the most inferior margin of the glenoid fossa. The degree of shoulder pain of the patients without RSD was assessed by a visual analogue scale of 10 points. This scale is a line taken to represent the continuum of pain, the ends defining the extremes of the experience, ie, ‘‘no pain’’ and ‘‘as severe as it could be.’’ Patients mark the line at a point corresponding to the estimate of their pain and the score is the length of the line to the mark. Demographic results were descriptive and expressed as percentage or as mean ⫾ standard error of the mean. Comparison of the demographic results, Brunnstrom functional classification, and the presence and degree of subluxation between the groups were performed by using unpaired t, Mann-Whitney U, and chi-square tests. The relation between the degree of pain and the grade of subluxation in the non-RSD group was performed by the correlation analysis of an Oxstat statistical program. RESULTS Table 1 shows the demographic results of the RSD and non-RSD groups. No significant differences were found between the two groups regarding these data. In the RSD group, 8 patients were in stage 1 and 27 in stage 2. The Brunnstrom functional classification of the RSD/non-RSD groups was as follows: grade 1, 14/14 patients; grade 2: 9/8 patients; grade 3, 5/6 patients, grade 4: 5/4 patients, grade 5, 2/3 patients. The Brunnstrom functional classification of the two groups was not significantly different ( p ⫽ .131). Glenohumeral subluxation was found in 26 patients (74.3%) of the RSD and 14 patients (40%) of the non-RSD group. The presence of shoulder subluxation in the RSD group was significantly higher than that of the non-RSD group ( p ⫽ .004). The comparison of the grade of shoulder subluxation of the RSD and non-RSD groups was found to be significantly different ( p ⫽ .03) (table 2). Among the non-RSD group, 11 (78.6%) of the 14 patients with subluxation and 8 (38.1%) of the 21 patients without subluxation reported shoulder pain ( p ⫽ .019), ie, the presence of shoulder pain was significantly higher in the patients with subluxation than in those without subluxation. No correlation Table 1: Demographic Findings
Age Sex Women Men Side of involvement Right Left Etiology Hemorrhagic Thromboembolic Duration of disease (mo)
RSD Group
Non-RSD Group
p
59.1 ⫾ 1.6
59.8 ⫾ 1.7
.758 .810
17 18
15 20
14 21
17 18
15 20 3.9 ⫾ 0.4
13 22 3.9 ⫾ 0.6
.630
.807
.919
Table 2: Grade of Shoulder Subluxation Grade of Subluxation
RSD Group
Non-RSD Group
0 1 2 3 4
9 (25.7%) 13 (37.1%) 7 (20%) 6 (17.1%) 0
21 (60%) 4 (11.4%) 6 (17.1%) 4 (11.4%) 0
was found between the degree of shoulder pain and grade of subluxation of the non-RSD group (correlation coefficient ⫽ .247, p ⫽ .152). DISCUSSION RSD syndrome, a difficult condition to manage, decreases the overall quality of life of many stroke patients. This serious complication can interfere with the patient’s rehabilitation program, including general mobility, ambulation training, and self-care activities such as rolling in bed, transferring, dressing the upper and lower body, eating, grooming, bathing, and toileting. Despite numerous hypotheses, the underlying mechanisms of RSD are still not clearly understood.12,21 Roberts22 refined the concepts and proposed that RSD is produced by sensitized wide dynamic range neurons in the spinal cord. These neurons are activated by mechanoreceptors that are continuously activated by sympathetic efferent stimulation. This hypothesis does not require an abnormality in the sympathetic nervous system, peripheral nerves, or other tissues, but a persistent painful stimulus capable of sensitizing the wide dynamic range neurons. RSD can be associated with a variety of precipitating factors like immobilization of the upper extremity, trauma to the joint structures, rotator cuff tears, and spasticity of the shoulder musculature. The role played by glenohumeral joint subluxation remains uncertain. The proposed possible mechanisms of how subluxation may cause RSD are overstretching of the periarticular tissues and impingement of the axillary nerve causing shoulder pain.19,23,24 Many authors have reported an association between shoulder pain and subluxation, claiming that anteroinferior subluxation of the humeral head can constitute a triggering factor in the hemiplegic patient25-29 and many have reported that no significant correlation exists.18,30-33 Van Langenberghe and Hogan18 investigated the correlation between degree of pain and grade of subluxation in 48 stroke patients. By finding no significant difference in degree of pain between patients with or without subluxation and no correlation between grade of subluxation and degree of pain, the investigators concluded that the role of subluxation in producing shoulder pain in hemiplegic patients might be negligible and subluxation must not necessarily be the cause of the pain in a painful hemiplegic shoulder. Joynt30 reported that the subacromial area of the shoulder is a location of pain-producing structures in many patients with hemiplegia; he evaluated the results of injecting 1% lidocaine into several sites in the shoulder area, and concluded that the amount of pain was related most to loss of motion, but unrelated to subluxation, spasticity, strength, or sensation. No statistical relationship between the presence of subluxation and either the severity or the amount of pain on passive movement was found in our study. Injury to rotator cuff or brachial plexus, marked spasticity, or major trauma to joint structures may be causative factors for shoulder pain, and precipitating factors for RSD. In our study, Arch Phys Med Rehabil Vol 81, July 2000
946
SUBLUXATION AND RSD, Dursun
to define the relation between shoulder subluxation and RSD more precisely, patients with a rotator cuff injury, spasticity greater than stage 2 on the Ashworth scale, brachial plexus injury, and major trauma were not included. In the subjects selected, the presence of shoulder subluxation was significantly higher in the RSD group than in the non-RSD group. We studied the correlation of degree of pain and grade of subluxation only in the non-RSD group, as RSD itself is characterized by severe pain. In the non-RSD group, no correlation was found between the degree of pain and grade of subluxation, but presence of pain was significantly higher in the patients with shoulder subluxation than those without subluxation. One should expect a positive correlation between the degree of pain and grade of subluxation when thinking that increased subluxation would coincide with increased stretching of tissue, increased ischemia, or increased nerve compression, leading to more severe pain. Our radiologic method to measure shoulder subluxation, also used by Van Langenberghe and Hogan,18 might lack precision because of visual inspection of the x-rays and classifying the subluxation into five predefined categories qualitatively. Therefore, a correlation might exist between the degree of pain and grade of subluxation that was not obtained by this methodology. Recently, Boyd and colleagues34 developed a new quantitative radiologic method named ‘‘plane of the scapula method’’ and concluded that three of the measures produced by this method were reliable and valid. Further studies by using this quantitative method for evaluating the subluxation might help reveal any correlation between the degree of pain and grade of subluxation. Although no direct correlation was found between degree of pain and grade of subluxation in our study, the presence of shoulder subluxation was significantly higher in the RSD group and presence of pain was significantly higher in patients with shoulder subluxation in the non-RSD group. This suggests that shoulder subluxation may be one of the factors causing pain and RSD. Therefore, preventative measures, and appropriate treatment of glenohumeral joint subluxation should be performed as early and as vigorously as possible to decrease possible complications. References 1. Richlin DM, Carron H, Rowlingson JC, Sussman MD, Baugher H, Goldner RD. Reflex sympathetic dystrophy: successful treatment by transcutaneous nerve stimulation. J Pediatr 1978;93:84-6. 2. Dunningham TH. The treatment of Sudeck’s atrophy in the upper limb by sympathetic blockade. Injury 1980;12:139-44. 3. Kozin F, Ryan LM, Carerra GF, Soin JS. The reflex sympathetic dystrophy syndrome. III. Scintigraphic studies, further evidence for the therapeutic efficacy of systemic corticosteroids, and proposed diagnostic criteria. Am J Med 1981;70:23-30. 4. Christensen K, Jensen EM, Noer I. The reflex dystrophy syndrome response to treatment with systemic corticosteroids. Acta Chir Scand 1982;148:653-5. 5. Ghostine SY, Comair YG, Turner DM, Kassel NF, Azar CG. Phenoxybenzamine in the treatment of causalgia. A report of 40 cases. J Neurosurg 1984;60:1263-8. 6. Prough DS, McLeskey CH, Poehling GG, Koman LA, Weeks DB, Whitworth T, et al. Efficacy of oral nifedipine in the treatment of reflex sympathetic dystrophy. Anesthesiology 1985;62:796-9. 7. Rocco AG, Kaul AF, Reisman RM, Gallo JP, Lief PA. A comparison of regional intravenous guanethidine and reserpine in reflex sympathetic dystrophy. A controlled, randomized, doubleblind crossover study. Clin J Pain 1989;5:205-9.
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8. van Laere M, Claessens M. The treatment of reflex sympathetic dystrophy syndrome: current concepts. Acta Orthop Belgica 1992;58 Suppl 1:259-61. 9. Gobelet C, Waldburger M, Meier JL. The effect of adding calcitonin to physical treatment on reflex sympathetic dystrophy. Pain 1992;48:171-5. 10. Esteve M. [Treatment of algodystrophies. The point of view of an anesthetist] [in French]. Cah Anesthesiol 1993;41:145-62. 11. Hamamci N, Dursun E, Ural C, C¸akci A. Calcitonin treatment in reflex sympathetic dystrophy: a preliminary study. Br J Clin Pract 1996;50:373-5. 12. Schwartzman RJ, McLellan TL. Reflex sympathetic dystrophy. Arch Neurol 1987;44:555-61. 13. Devor M. Nerve pathophysiology and mechanisms of pain in causalgia. J Auton Nerv Sys 1983;7:371-84. 14. Andresen LT. Shoulder pain in hemiplegia. Am J Occup Ther 1985;39:11-9. 15. Hall J, Dudgeon B, Guthrie M. Validity of clinical measures of shoulder subluxation in adults with post stroke hemiplegia. Am J Occup Ther 1995;49:526-33. 16. Brooke MM, DeLateur BJ, Diana-Rigby GC, Questad KA. Shoulder subluxation in hemiplegia: effects of three different supports. Arch Phys Med Rehabil 1991;72:582-6. 17. Steinbrocker O, Argyros TG. The shoulder-hand syndrome present status as a diagnostic and therapeutic entity. Med Clin North Am 1958;42:1538-53. 18. Van Langenberghe HVK, Hogan BM. Degree of pain and grade of subluxation in the painful hemiplegic shoulder. Scand J Rehabil Med 1988;20:161-6. 19. Ring H, Leillen B, Server S, Luz Y, Solzi P. Temporal changes in electrophysiological, clinical and radiological parameters in the hemiplegic’s shoulder. Scand J Rehabil Med 1985;12:124-7. 20. Smith RG, Cruikshank JG, Dunbar S, Akhtar AJ. Malalignment of the shoulder after stroke. Br Med J 1982;284:1224-6. 21. Kozin F. Reflex sympathetic dystrophy syndrome: a review. Clin Exp Rheumatol 1992;10:401. 22. Roberts WJ. A hypothesis on the physiological basis for causalgia and related pains. Pain 1986;24:297-311. 23. Caillet R. The shoulder in hemiplegia. Philadelphia: Davis; 1980. 24. Kioresku MA. [Innervation of the human shoulder joint] [in Russian]. Arkh Anat Gistol Embrol 1974;66(5):10-1. 25. Shai G, Ring H, Costeff H, Solzi P. Glenohumeral malalignment in the hemiplegic shoulder. Scand J Rehabil Med 1984;16:133-6. 26. Fitzgerald-Finch OP, Gibson I. Subluxation of the shoulder in hemiplegia. Age Ageing 1975;4:16-8. 27. Najensen T, Yavcubovich E, Pikielny S. Rotator cuff injury in shoulder joints of hemiplegic patients. Scand J Rehabil Med 1971;3:131-7. 28. Moskowitz E, Goodman CR, Smith E, Balthazar E, Mellins HZ. Hemiplegic shoulder. N Y State J Med 1969;69:548-50. 29. Poulin de Courval L, Barsauskas A, Berenbaum B, Dehaut F, Dussault R, Fontaine FS, et al. Painful shoulder in the hemiplegic and unilateral neglect. Arch Phys Med Rehabil 1990;71:673-6. 30. Joynt RL. The source of shoulder pain in hemiplegia. Arch Phys Med Rehabil 1992;73:409-13. 31. Davies PM. Steps to follow. A guide to the treatment of adult hemiplegia. Berlin: Springer-Verlag; 1985. 32. Bobath B. Adult hemiplegia: evaluation and treatment. 2nd ed. London: William Heinemann; 1978. 33. Braun RM, West F, Mooney V, Nickel VL, Roper B, Caldwell C. Surgical treatment of the painful shoulder contracture in the stroke patient. J Bone Joint Surg Am 1971;53:1307-12. 34. Boyd EA, Goudreau L, O’Riain MD, Grinnel DM, Torrance GM, Gaylard A. A radiological measure of shoulder subluxation in hemiplegia: its reliability and validity. Arch Phys Med Rehabil 1993;74:188-93.
Glenohumeral Joint Subluxation and Reflex Sympathetic Dystrophy in Hemiplegic Patients Erbil Dursun, MD, Nigar Dursun, MD, Canan Eksi Ural, MD, Aytu¨l C¸akci, MD ABSTRACT. Dursun E, Dursun N, Eksi Ural C, C¸akci A. Glenohumeral joint subluxation and reflex sympathetic dystrophy in hemiplegic patients. Arch Phys Med Rehabil 1999;81: 944-6. Objective: To examine the relation between glenohumeral joint subluxation and reflex sympathetic dystrophy (RSD) in hemiplegic patients. Design: Case-control study. Setting: Inpatient rehabilitation hospital. Patients: Thirty-five hemiplegic patients with RSD (RSD group) and 35 hemiplegic patients without RSD (non-RSD group) were included in the study. Patients with rotator cuff rupture, brachial plexus injury, or spasticity greater than stage 2 on the Ashworth scale were excluded. Main Outcome Measures: Both the RSD and non-RSD groups were assessed for presence and grade of subluxation from radiographs using a 5-point categorization. The degree of shoulder pain of the non-RSD group was assessed by a visual analogue scale of 10 points. Results: Glenohumeral subluxation was found in 74.3% of the RSD and 40% of the non-RSD group ( p ⫽ .004). In the non-RSD group, 78.6% of the patients with subluxation and 38.1% of the patients without subluxation reported shoulder pain ( p ⫽ .019). No correlation was found between the degree of shoulder pain and grade of subluxation in the non-RSD group ( p ⫽ .152). Conclusion: Findings from this study suggest that shoulder subluxation may be a causative factor for RSD. Therefore, prevention and appropriate treatment of glenohumeral joint subluxation should be included in rehabilitation of hemiplegic patients. Key Words: Hemiplegia; Reflex sympathetic dystrophy; Subluxation; Rehabilitation. 娀 2000 by the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation
D
EVELOPMENT OF reflex sympathetic dystrophy (RSD) in hemiplegic patients is a significant problem that may cause pain and function loss and seriously hamper their rehabilitation programs. Although many different treatment approaches have been described, the management of RSD remains quite difficult.1-11 Preventative measures to reduce the risk of RSD are essential. RSD is associated with a variety of precipitating factors, including immobilization of the upper extremity, trauma to the joint structures, rotator cuff tears, spasticity of the shoulder musculature, and glenohumeral joint From the Department of Physical Medicine and Rehabilitation, Kocaeli University Faculty of Medicine, Kocaeli (E. Dursun, N. Dursun) and the Department of Physical Medicine and Rehabilitation, Ankara Rehabilitation Center, Ankara (Eksi Ural, C¸akci), Turkey. Submitted January 13, 1999. Accepted in revised form June 18, 1999. The authors have chosen not to select a disclosure statement. ¨ niversitesi Tıp Faku¨ltesi, Fiziksel Reprint requests to Dr. Erbil Dursun, Kocaeli U Tıp ve Rehabilitasyon ABD, 41900, Kocaeli, Turkey. 0003-9993/00/8107-5375$3.00/0 doi:10.1053/apmr.2000.1761
Arch Phys Med Rehabil Vol 81, July 2000
subluxation. Most of these associations have not been obviously established. It is not clear why all of these factors cause the same clinical syndrome, but injury to neural tissue, either central or peripheral, may be the common mechanism.12,13 A persistent painful lesion must be present to develop RSD. Glenohumeral joint subluxation has been recognized as a major and frequent complication in patients with hemiplegia. It may be associated with shoulder pain, peripheral nerve damage, and autonomic dysfunction, and may interfere with functional activities.14-16 The association of glenohumeral joint subluxation and RSD is rarely mentioned in the literature. The aim of this study was to examine the relation between shoulder subluxation and RSD. In a non-RSD group, we also examined if subluxation is associated with shoulder pain, and if a correlation exists between the degree of shoulder pain and the grade of subluxation. MATERIALS AND METHODS One hundred sixteen consecutive stroke patients admitted to Ankara Rehabilitation Center, in a period of 36 months, were evaluated. Thirty-five patients with RSD were assigned to the RSD group and 35 patients without RSD were assigned to a non-RSD group. Forty-six patients were excluded because of bilateral involvement, multiple attacks, rotator cuff rupture, spacticity greater than stage 2 on the Ashworth scale, brachial plexus injury, major trauma after stroke, or cognitive dysfunction. The diagnosis of RSD was primarily based on the clinical entity and the staging was performed according to the classification of Steinbrocker and Argyros.17 Diagnosis was confirmed by a three-phase scintigraphic study if any suspicion of other factors such as positional edema or thrombophlebitis existed. According to Steinbrocker’s classification, Stage 1, the ‘‘acute’’ stage, is characterized by severe pain that has a burning or aching quality and is increased by dependency of the affected part, physical contact, or emotional upset. Edema, hyperthermia, hypothermia, and increased hair and nail growth occur in the affected part. Bony changes may be present on roentgenographs. Stage 2, the ‘‘dystrophic’’ stage, is characterized by the development of dystrophic changes such as nail changes and shiny skin with loss of normal wrinkling and the persistence of pain and disability. The edematous tissue becomes endurated and the skin is cool and hyperhidrotic. Roentgenographs may reveal diffuse osteoporosis. Stage 3, the ‘‘atrophic’’ stage, is characterized by progressive skin and subcutaneous tissue atrophy and occasionally proximal spread of pain. The skin is thin and shiny, the fascia becomes thickened, and flexion or Dupuytren’s contractures may occur. Roentgenographs show marked demineralization and ankylosis. Demographic properties including age, gender, side of involvement, etiology of the lesion, and duration of the disease were recorded, as were Brunnstrom functional classification scores of the patients. The presence and degree of subluxation in RSD patients was assessed from anterior-posterior radiographs centering on the glenohumeral joint with the hemiplegic arm unsupported. The degree of subluxation was determined by a 5-point categoriza-
945
SUBLUXATION AND RSD, Dursun
tion18-20 as: 0 (normal), the whole curvature of the glenoid fossa is opposed by and parallel to the humeral head; 1 (V-shaped widening), the whole curvature of the glenoid fossa is opposed by the humeral head, but a V-shaped widening is present in the superior intraarticular space; 2 (moderate subluxation), there is inferior subluxation of the humeral head, with the most superior margin of the humeral head not below the line perpendicularly bisecting the line connecting the most superior and inferior margins of the glenoid fossa; 3 (advanced subluxation), similar to moderate subluxation but the superior margin of the humeral head is level with or below the bisecting line; and 4 (dislocation), the most superior margin of the humeral head is level with or below the most inferior margin of the glenoid fossa. The degree of shoulder pain of the patients without RSD was assessed by a visual analogue scale of 10 points. This scale is a line taken to represent the continuum of pain, the ends defining the extremes of the experience, ie, ‘‘no pain’’ and ‘‘as severe as it could be.’’ Patients mark the line at a point corresponding to the estimate of their pain and the score is the length of the line to the mark. Demographic results were descriptive and expressed as percentage or as mean ⫾ standard error of the mean. Comparison of the demographic results, Brunnstrom functional classification, and the presence and degree of subluxation between the groups were performed by using unpaired t, Mann-Whitney U, and chi-square tests. The relation between the degree of pain and the grade of subluxation in the non-RSD group was performed by the correlation analysis of an Oxstat statistical program. RESULTS Table 1 shows the demographic results of the RSD and non-RSD groups. No significant differences were found between the two groups regarding these data. In the RSD group, 8 patients were in stage 1 and 27 in stage 2. The Brunnstrom functional classification of the RSD/non-RSD groups was as follows: grade 1, 14/14 patients; grade 2: 9/8 patients; grade 3, 5/6 patients, grade 4: 5/4 patients, grade 5, 2/3 patients. The Brunnstrom functional classification of the two groups was not significantly different ( p ⫽ .131). Glenohumeral subluxation was found in 26 patients (74.3%) of the RSD and 14 patients (40%) of the non-RSD group. The presence of shoulder subluxation in the RSD group was significantly higher than that of the non-RSD group ( p ⫽ .004). The comparison of the grade of shoulder subluxation of the RSD and non-RSD groups was found to be significantly different ( p ⫽ .03) (table 2). Among the non-RSD group, 11 (78.6%) of the 14 patients with subluxation and 8 (38.1%) of the 21 patients without subluxation reported shoulder pain ( p ⫽ .019), ie, the presence of shoulder pain was significantly higher in the patients with subluxation than in those without subluxation. No correlation Table 1: Demographic Findings
Age Sex Women Men Side of involvement Right Left Etiology Hemorrhagic Thromboembolic Duration of disease (mo)
RSD Group
Non-RSD Group
p
59.1 ⫾ 1.6
59.8 ⫾ 1.7
.758 .810
17 18
15 20
14 21
17 18
15 20 3.9 ⫾ 0.4
13 22 3.9 ⫾ 0.6
.630
.807
.919
Table 2: Grade of Shoulder Subluxation Grade of Subluxation
RSD Group
Non-RSD Group
0 1 2 3 4
9 (25.7%) 13 (37.1%) 7 (20%) 6 (17.1%) 0
21 (60%) 4 (11.4%) 6 (17.1%) 4 (11.4%) 0
was found between the degree of shoulder pain and grade of subluxation of the non-RSD group (correlation coefficient ⫽ .247, p ⫽ .152). DISCUSSION RSD syndrome, a difficult condition to manage, decreases the overall quality of life of many stroke patients. This serious complication can interfere with the patient’s rehabilitation program, including general mobility, ambulation training, and self-care activities such as rolling in bed, transferring, dressing the upper and lower body, eating, grooming, bathing, and toileting. Despite numerous hypotheses, the underlying mechanisms of RSD are still not clearly understood.12,21 Roberts22 refined the concepts and proposed that RSD is produced by sensitized wide dynamic range neurons in the spinal cord. These neurons are activated by mechanoreceptors that are continuously activated by sympathetic efferent stimulation. This hypothesis does not require an abnormality in the sympathetic nervous system, peripheral nerves, or other tissues, but a persistent painful stimulus capable of sensitizing the wide dynamic range neurons. RSD can be associated with a variety of precipitating factors like immobilization of the upper extremity, trauma to the joint structures, rotator cuff tears, and spasticity of the shoulder musculature. The role played by glenohumeral joint subluxation remains uncertain. The proposed possible mechanisms of how subluxation may cause RSD are overstretching of the periarticular tissues and impingement of the axillary nerve causing shoulder pain.19,23,24 Many authors have reported an association between shoulder pain and subluxation, claiming that anteroinferior subluxation of the humeral head can constitute a triggering factor in the hemiplegic patient25-29 and many have reported that no significant correlation exists.18,30-33 Van Langenberghe and Hogan18 investigated the correlation between degree of pain and grade of subluxation in 48 stroke patients. By finding no significant difference in degree of pain between patients with or without subluxation and no correlation between grade of subluxation and degree of pain, the investigators concluded that the role of subluxation in producing shoulder pain in hemiplegic patients might be negligible and subluxation must not necessarily be the cause of the pain in a painful hemiplegic shoulder. Joynt30 reported that the subacromial area of the shoulder is a location of pain-producing structures in many patients with hemiplegia; he evaluated the results of injecting 1% lidocaine into several sites in the shoulder area, and concluded that the amount of pain was related most to loss of motion, but unrelated to subluxation, spasticity, strength, or sensation. No statistical relationship between the presence of subluxation and either the severity or the amount of pain on passive movement was found in our study. Injury to rotator cuff or brachial plexus, marked spasticity, or major trauma to joint structures may be causative factors for shoulder pain, and precipitating factors for RSD. In our study, Arch Phys Med Rehabil Vol 81, July 2000
946
SUBLUXATION AND RSD, Dursun
to define the relation between shoulder subluxation and RSD more precisely, patients with a rotator cuff injury, spasticity greater than stage 2 on the Ashworth scale, brachial plexus injury, and major trauma were not included. In the subjects selected, the presence of shoulder subluxation was significantly higher in the RSD group than in the non-RSD group. We studied the correlation of degree of pain and grade of subluxation only in the non-RSD group, as RSD itself is characterized by severe pain. In the non-RSD group, no correlation was found between the degree of pain and grade of subluxation, but presence of pain was significantly higher in the patients with shoulder subluxation than those without subluxation. One should expect a positive correlation between the degree of pain and grade of subluxation when thinking that increased subluxation would coincide with increased stretching of tissue, increased ischemia, or increased nerve compression, leading to more severe pain. Our radiologic method to measure shoulder subluxation, also used by Van Langenberghe and Hogan,18 might lack precision because of visual inspection of the x-rays and classifying the subluxation into five predefined categories qualitatively. Therefore, a correlation might exist between the degree of pain and grade of subluxation that was not obtained by this methodology. Recently, Boyd and colleagues34 developed a new quantitative radiologic method named ‘‘plane of the scapula method’’ and concluded that three of the measures produced by this method were reliable and valid. Further studies by using this quantitative method for evaluating the subluxation might help reveal any correlation between the degree of pain and grade of subluxation. Although no direct correlation was found between degree of pain and grade of subluxation in our study, the presence of shoulder subluxation was significantly higher in the RSD group and presence of pain was significantly higher in patients with shoulder subluxation in the non-RSD group. This suggests that shoulder subluxation may be one of the factors causing pain and RSD. Therefore, preventative measures, and appropriate treatment of glenohumeral joint subluxation should be performed as early and as vigorously as possible to decrease possible complications. References 1. Richlin DM, Carron H, Rowlingson JC, Sussman MD, Baugher H, Goldner RD. Reflex sympathetic dystrophy: successful treatment by transcutaneous nerve stimulation. J Pediatr 1978;93:84-6. 2. Dunningham TH. The treatment of Sudeck’s atrophy in the upper limb by sympathetic blockade. Injury 1980;12:139-44. 3. Kozin F, Ryan LM, Carerra GF, Soin JS. The reflex sympathetic dystrophy syndrome. III. Scintigraphic studies, further evidence for the therapeutic efficacy of systemic corticosteroids, and proposed diagnostic criteria. Am J Med 1981;70:23-30. 4. Christensen K, Jensen EM, Noer I. The reflex dystrophy syndrome response to treatment with systemic corticosteroids. Acta Chir Scand 1982;148:653-5. 5. Ghostine SY, Comair YG, Turner DM, Kassel NF, Azar CG. Phenoxybenzamine in the treatment of causalgia. A report of 40 cases. J Neurosurg 1984;60:1263-8. 6. Prough DS, McLeskey CH, Poehling GG, Koman LA, Weeks DB, Whitworth T, et al. Efficacy of oral nifedipine in the treatment of reflex sympathetic dystrophy. Anesthesiology 1985;62:796-9. 7. Rocco AG, Kaul AF, Reisman RM, Gallo JP, Lief PA. A comparison of regional intravenous guanethidine and reserpine in reflex sympathetic dystrophy. A controlled, randomized, doubleblind crossover study. Clin J Pain 1989;5:205-9.
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