(Stroke. 1995;26:2277-2280.)
© 1995 American Heart Association, Inc.
Articles |
From the Department of Physical Medicine and Rehabilitation, Chang Gung Memorial Hospital, Chang Gung College of Medicine and Technology, Taiwan (P.-T.C.), and the Department of Physical Medicine and Rehabilitation, University of California, Irvine (C.-Z.H).
Correspondence to Pao-Tsai Cheng, MD, Department of Physical Medicine and Rehabilitation, Chang Gung Memorial Hospital, 5 Fu-Hsing St, Kuei-Shan Hsiang, Tao-Yuan, Taiwan.
| Abstract |
|---|
|
|
|---|
Methods An EMG and nerve conduction velocity study of the weak upper limb was conducted on 70 hemiplegic patients at 3 to 4 weeks after cerebrovascular disease (either cerebral hemorrhage or infarction). Clinical assessment for development of the RSDS was done during the following 6 months. The correlation of RSDS development with the presence of spontaneous EMG activity and certain clinical parameters (including sex, age, side affected, cause of stroke, sensory impairment, spasticity, and shoulder subluxation) was analyzed statistically.
Results Of the 46 patients who exhibited spontaneous activity, 30 (65%) developed clinical RSDS in their hemiplegic upper extremity, whereas only 1 (4%) of the other 24 patients with no spontaneous EMG activity developed clinical RSDS within 6 months after the onset of hemiplegia (P<.001). The correlation of RSDS development with the presence of shoulder subluxation and sensory impairment in the hemiplegic side was statistically significant. Neither age, sex, severity of spasticity, nor etiology of stroke had a significant correlation with the development of clinical RSDS.
Conclusions There is significant correlation between the presence of spontaneous EMG activity and the development of clinical RSDS in the hemiplegic upper extremity after stroke. It is concluded that spontaneous EMG activity in the hemiplegic hands of stroke patients might be a good predictor of the future development of clinical RSDS.
Key Words: electromyography hemiplegia reflex sympathetic dystrophy
| Introduction |
|---|
|
|
|---|
| Subjects and Methods |
|---|
|
|
|---|
Electrodiagnostic Procedures
All 70 patients underwent needle EMG examination of the
hemiplegic upper extremity and a motor nerve conduction study of
bilateral median nerves at 3 to 4 weeks after onset of hemiplegia.
Nicolet Viking IIe EMG apparatus was used. The concentric
needle was inserted into the muscles of the hemiplegic upper extremity,
including the abductor pollicis brevis, abductor digiti minimi, and
extensor digitorum communis. The above muscles were selected based on
the findings of a previous study.11
Spontaneous activity was quantitatively recorded for each examined muscle with the following grading system: absent, no spontaneous activity; few, spontaneous activity present at one or two sites for longer than 1 second after moving the needle electrode; moderate, present in three or four sites for longer than 1 second; and many, present in more than four sites for longer than 2 seconds or continuously at all sites.12 13
We conducted a median motor nerve conduction study using a standard technique.13 The compound muscle action potential (CMAP) amplitude and distal latency of median nerve in affected side were compared with the unaffected side.
Assessment of RSDS
The clinical diagnosis of RSDS was based on (1) shoulder pain at
rest or with mobilization, (2) swelling of wrist and hand, (3)
vasomotor change in the hand, and (4) tenderness to palpation of wrist,
metacarpopharyngeal, and interpharyngeal joints.
All 70 patients were assigned to one of the following groups according to Tepperman et al8 at the time of EMG study and follow-up: (1) definite RSDS, showing all shoulder and hand criteria; (2) probable RSDS, showing all hand criteria without shoulder involvement; (3) possible RSDS, displaying hand swelling with metacarpopharyngeal and/or wrist tenderness; and (4) non-RSDS. The first three groups were considered "clinical RSDS."
Clinical Assessment at the Time of Follow-up
Physical and neurological examinations were performed at the
time of EMG study as well as at a later follow-up at 6 months;
motor and sensory function, the presence of spasticity, passive range
of motion of the shoulder in all planes, the intensity of pain with
shoulder motion or tenderness by palpation, and the presence of hand
swelling and shoulder subluxation were recorded. The clinical data
and the appearance of spontaneous EMG activity were then correlated
with the presence of RSDS.
Data Analysis
Statistically, the data were analyzed for association
among variables, with the
2 test and
Fisher's exact test used for small sample size. Student's
t test was also used for data analysis. A value of
P<.05 was considered significant.
| Results |
|---|
|
|
|---|
Correlation Between RSDS and Clinical Characteristics
The correlation of development of RSDS with clinical
characteristics of the 70 hemiplegic patients at follow-up
evaluation is shown in Table 1
. Hemiplegic patients with
sensory impairment and/or shoulder subluxation had a higher incidence
of RSDS. Patients with left hemiplegia patients had an increased risk
of RSDS, although this did not reach statistical significance. Neither
age, sex, severity of spasticity, or cause of stroke had any bearing on
subsequent RSDS development.
|
Correlation Between RSDS and EMG Findings
Table 2
shows the correlation between the presence
of spontaneous EMG activity and the probability of developing RSDS.
Thirty of the 31 patients (97%) with clinical RSDS had EMG evidence of
fibrillation or positive sharp wave compared with 16 non-RSDS patients
(41%). On the other hand, of the 46 patients who displayed few,
moderate, or many instances of spontaneous EMG activity in the
hemiplegic hand, 30 (65%) later developed clinical RSDS. Only 1 (4%)
of the other 24 patients with no spontaneous EMG activity developed
clinical RSDS afterward. A significant correlation (P<.001)
was found: the larger the amount of spontaneous EMG activity that
appeared, the higher the incidence of subsequently developed RSDS.
|
Correlation Between RSDS and Nerve Conduction Study
The mean CMAP amplitude was lower in the hemiplegic hand compared
with the healthy side. The thenar CMAP amplitude difference between the
hemiplegic and healthy sides was larger for the patients who
subsequently developed clinical RSDS than for those without RSDS,
although it did not reach statistical significance
(P=.0668). The difference in distal latency was not
statistically significant (P>.5).
| Discussion |
|---|
|
|
|---|
Although some earlier authors have reported seeing no spontaneous activity on EMG examination of hemiplegic extremities after stroke,14 15 16 most authors have observed spontaneous EMG activity in hemiplegic limbs,11 17 18 19 20 21 especially in the distal muscles of the paralyzed upper extremity.11 17 18 Cheng et al11 found a close correlation between spontaneous EMG activity and poststroke shoulder-hand syndrome, with spontaneous EMG activity primarily in the abductor pollicis brevis, abductor digiti minimi, and extensor digitorum communis. Our study further confirms the correlation between spontaneous EMG activity and the later development of RSDS. Almost all the patients who had no EMG evidence of spontaneous activity did not develop RSDS, and those with more spontaneous EMG activity had a higher incidence of RSDS. This suggests that spontaneous EMG activity might be a good predictor of the risk of developing clinical RSDS after stroke.
The etiology of RSDS is still unknown. Hooshmand22 reported that the origins of sympathetic pain include inactivity, impaired circulation, and damaged peripheral nerve. A paralyzed shoulder may be overstretched during transfer of a patient, particularly when a patient has concomitant loss of central proprioception. Many authors have suspected a possible brachial plexus lesion related to a hemiplegic shoulder. Partial nerve root avulsions are quite frequently accompanied by spontaneous pathological hyperpathic pain and RSDS.23
Chalsen et al3 and Griffen7 reported that patients with decreased sensation and/or shoulder subluxation in the hemiplegic upper extremity had a higher probability of developing RSDS. Our study confirmed this finding. One may speculate that a hemiplegic patient with sensory impairment and/or shoulder subluxation may have higher incidence of brachial plexus injury, which subsequently causes RSDS. In this study the mean CMAP amplitude, which was diminished in the hemiplegic hand, was similar to findings in previous reports.19 20 It was also found that the difference in CMAP amplitude between hemiplegic and healthy sides is higher for the clinical RSDS group than for the non-RSDS group (although the difference is not statistically significant). These findings are in agreement with the studies cited above, although some studies did not support that hypothesis.24
Joynt5 and Weiss et al9 reported that patients with left hemiplegia had a greater tendency to develop RSDS. In this study patients with left hemiplegia did show an increased tendency to develop RSDS compared with patients with right hemiplegia, but the difference was not statistically significant. As for age, sex, spasticity of the hemiplegic limb, or cause of stroke, no clear relation to clinical RSDS development was found.
In conclusion, for those patients who were asymptomatic for RSDS at the time of EMG examination within the first month after stroke, the appearance of diffuse spontaneous EMG activity may be a good predictor of the future development of clinical RSDS. More research in a larger population may be helpful to confirm this hypothesis. Early aggressive measures to prevent and/or diagnose RSDS for these high-risk patients are particularly important.
Received July 10, 1995; revision received September 1, 1995; accepted September 1, 1995.
| References |
|---|
|
|
|---|
2. Andersen LT. Shoulder pain in hemiplegia. Am J Occup Ther.. 1985;39:11-19. [Medline] [Order article via Infotrieve]
3. Chalsen GG, Fitzpatrick KA, Navia RA, Bean SA, Reding MJ. Prevalence of the shoulder-hand pain syndrome in an in-patient stroke rehabilitation population: a quantitative cross-sectional study. J Neurol Rehab. 1987;1:137-141.
4. Van Ouwenaller C, Laplace PM, Chantraine A. Painful shoulder in hemiplegia. Arch Phys Med Rehabil. 1986;67:23-26. [Medline] [Order article via Infotrieve]
5. Joynt RL. The source of shoulder pain in hemiplegia. Arch Phys Med Rehabil. 1992;73:409-413. [Medline] [Order article via Infotrieve]
6. Escobar P. Reflex sympathetic dystrophy. Orthop Rev. 1986;15:646-651. [Medline] [Order article via Infotrieve]
7. Griffin JW. Hemiplegic shoulder pain. Phys Ther.. 1986;66:1884-1893.
8. Tepperman PS, Greyson ND, Hilbert L, Jimenez J, Williams JI. Reflex sympathetic dystrophy in hemiplegia. Arch Phys Med Rehabil. 1984;65:442-447. [Medline] [Order article via Infotrieve]
9. Weiss L, Alfano A, Bardfeld P, Weiss J, Friedmann LW. Prognostic value of triple phase bone scanning for reflex sympathetic dystrophy in hemiplegia. Arch Phys Med Rehabil. 1993;74:716-719. [Medline] [Order article via Infotrieve]
10. Davidoff G, Werner R, Cremer S, Jackson MD, Ventocilla C, Wolf L. Predictive value of the three-phase technetium bone scan in diagnosis of reflex sympathetic dystrophy syndrome. Arch Phys Med Rehabil. 1989;70:135-137. [Medline] [Order article via Infotrieve]
11. Cheng PT, Lee CE, Liaw MY, Wong MK. Electrophysiological study of shoulder pain in stroke patients. J Rehabil Med Assoc. 1994;22:67-74.
12. Johnson EW, Denny ST, Kelley JP. Sequence of electromyographic abnormalities in stroke syndrome. Arch Phys Med Rehabil. 1975;56:468-473. [Medline] [Order article via Infotrieve]
13. Kimura J. Electrodiagnosis in Diseases of Nerve and Muscle: Principles and Practice. Philadelphia, Pa: FA Davis Co; 1989:249-274.
14. Alpert S, Idarroga S, Orbegozo J, Rosenthal A. Absence of electromyographic evidence of lower motor neuron involvement in hemiplegic patients. Arch Phys Med Rehabil. 1971;52:179-181. [Medline] [Order article via Infotrieve]
15. Alpert S, Jarrett S, Lerner I, Rosenthal A. Electromyographic findings in early hemiplegia. Arch Phys Med Rehabil. 1973;54:464-465. [Medline] [Order article via Infotrieve]
16. Rizk TE, Christopher RP, Pianls RS, Salazar JE, Higgins C. Arthrographic studies in painful hemiplegic shoulders. Arch Phys Med Rehabil. 1984;65:254-256. [Medline] [Order article via Infotrieve]
17. Spaans F, Wilts G. Denervation due to lesions of the central nervous system: an EMG study in cases of cerebral contusion and cerebrovascular accidents. J Neurol Sci.. 1982;57:291-305. [Medline] [Order article via Infotrieve]
18. Benecke R, Berthold A, Conrad B. Denervation activity in the EMG of patients with upper motor neuron lesions: time course, local distribution and pathogenetic aspects. J Neurol. 1983;230:143-151. [Medline] [Order article via Infotrieve]
19. Zalis AW, Lafratta CW, Fauls LB, Oester YT. Electrophysiological studies in hemiplegia: lower motor neuron findings and correlates. Electromyogr Clin Neurophysiol.. 1976;16:151-162. [Medline] [Order article via Infotrieve]
20. Kingery WS, Date ES, Bocobo CR. The absence of brachial plexus injury in stroke. Am J Phys Med Rehabil. 1993;72:127-135. [Medline] [Order article via Infotrieve]
21. Bhala RP. Electromyographic evidence of lower motor neuron involvement in hemiplegics. Arch Phys Med Rehabil. 1969;50:632-637. [Medline] [Order article via Infotrieve]
22. Hooshmand H. Chronic Pain: Reflex Symphathetic Dystrophy Prevention and Management. Ann Arbor, Mich: CRC Press; 1993:35-55.
23. Wynn Parry CB. Pain in avulsion lesions of brachial plexus. Pain.. 1980;9:41-53. [Medline] [Order article via Infotrieve]
24. Myers SJ, Lovelace RE. The motor unit and muscle action potentials. In: Downey JA, Myers SJ, Gonzalez EG, Lieberman JS, eds. The Physiological Basis of Rehabilitation Medicine. 2nd ed. Boston, Mass: Butterworth-Heinemann; 1994:243-282.
This article has been cited by other articles:
![]() |
A. Griffin and J. Bernhardt Strapping the hemiplegic shoulder prevents development of pain during rehabilitation: a randomized controlled trial Clinical Rehabilitation, April 1, 2006; 20(4): 287 - 295. [Abstract] [PDF] |
||||
![]() |
H C Hanger, P Whitewood, G Brown, M C Ball, J Harper, R Cox, and R Sainsbury A randomized controlled trial of strapping to prevent post-stroke shoulder pain Clinical Rehabilitation, April 1, 2000; 14(4): 370 - 380. [Abstract] [PDF] |
||||
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
Stroke Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 1995 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |