RSD Article # 10
Clinical Report
Reflex Sympathetic Dystrophy Associated With Multiple
Lumbar Laminectomies
Dennis W. Dobritt and Craig T. Hartrick
Providence Hospital, Southfield Michigan, U.S.A.
Abstract: Reflex sympathetic dystrophy (RSD) is an often devastating
chronic pain condition that can develop following relatively trivial traumatic events. The
precise mechanism and predisposing factors governing the development and progression of
this syndrome are not completely understood. However, RSD most commonly presents distally
in an extremity following injury to the limb. Rarely has it been reported following lumbar
laminectomy or ruptured lumbar disc (1,2). Of those cases reported. the RSD was relatively
acute, mild, and unilateral (1-3). We present a case of severe, chronic. bilateral RSD
following multiple laminectomies and propose a possible mechanism to explain these
findings. Key Words: Reflex sympathetic dystrophy-Causalgia-Sudet's atrophy- Lumbar
laminectomy
CASE REPORT
A 34-year-old man presented to the Pain Control Center with a 6-year history of low
back pain radiating into the left leg. The pain began acutely following a twisting fall at
work. Conservative therapy consisting of muscle relaxants, narcotic analgesics and
physical therapy failed to alleviate the pain. Orthopedic evaluation, computer tomography
(CT) scan and myelography of the lumbar spine revealed no evidence of pathology.
Discography of the L5 disc demonstrated diffuse bulging without extrusion of disc
material. He was not considered a candidate for surgery or chymopapain injection and
conservative modalities were resumed. Sixteen months following the injury, lumbar
laminectomy at L5-S1 was performed in an attempt to reduce the pain. No significant relief
was obtained following surgery or with subsequent acupuncture and transcutaneous nerve
stimulation. Over the next 3 years the patient underwent bilateral L5-S1 spinal fusion,
epidural steroid injections, and scleral therapy, all without improvement. Work up for
multiple sclerosis and connective tissue disease which included a muscle biopsy, was
negative. Repeat lumbar spine CT scan and myelography demonstrated epidural adhesions
extending into the left S1 nerve root sleeve. Electromyography (EMG) revealed mild left
L5-S1 radiculitis. A 3-day trial of intravenous procaine with vitamin B complex and
physical therapy failed to reduce the pain. Exploratory laminectomy with lysis of
adhesions was undertaken without substantial pain relief. Over the next 2 years, two
additional laminectomies for lysis of adhesions were performed without significant
improvement of the patient's symptoms.
The patient presented to the Pain Clinic complaining of a constant burning ache located in
the left lumbar area, radiating down the posterior left leg to the plantar aspect of his
foot. Several times monthly he experienced lancinating exacerbations into the left leg
described as "electrical jolts" followed by severe, debilitating muscle spasm
for several hours.
Burning pain in the right leg was present, hut to a much lesser degree. He was taking 60
mg Amitriptyline and six to eight tablets containing acetamenophen 325 mg with codeine 30
mg daily for pain relief.
Physical examination revealed severe limitations of motion in the lumbar spine. The skin
of both calves was pale and shiny with severe scaling. Allodynia was present in a stocking
distribution to the thigh on the left and to the knee on the right. The left leg was 2.8ºC colder than the right with atrophy and weakness. Deep tendon
reflexes were minimally decreased on the left. Straight leg raising was positive for
radicular pain at 30º and 45º in the
left and right legs, respectively. There was no sensory loss noted.
A recent CT scan and myelography of the lumbar spine demonstrated persistence of the
epidural adhesions at the left S1 nerve root. EMG remained positive for mild left L5-S1
radiculitis. Liquid crystal thermography confirmed the temperature discrepancy between the
legs. McGill pain rating index and present pain intensity were 40 and 3, respectively. A
visual analog scale consisting of a 10-cm line with I-cm graduations measured 7.5.
A retrograde differential spinal nerve block using I cc of 10% procaine with 1 cc of CSF
indicated that the pain was primarily sympathetically mediated with a mild somatic
component. Over the next 2 months, the patient underwent a series of two lumbar epidural
and one caudal injection of 10 cc 0.25% bupivicaine with depomethylprednisolone, followed
by five lumbar paravertebral sympathetic ganglion blocks with 15 cc of 0.25% bupivicaine.
On follow-up examination I month later, he reported 25% improvement of pain, no further
episodes of leg spasms, complete withdrawal from the acetomenophen with codeine and
improved mobility and improved sleep. The McGill pain rating index and present pain
intensity improved to 17 and 2 respectively. However, the visual analog scale remained at
7.5. The leg temperatures had equalized and the allodynia was markedly improved. At
present he continues to be treated at the Pain Control Center using a multidisciplinary
approach in-eluding temperature biofeedback.
DISCUSSION
RSD is a group of syndromes characterized by alteration in peripheral sympathetic
activity with severe persistent burning pain, vasomotor and sudomotor changes,
hyperesthesia, allodynia and trophic changes most commonly seen in a distal extremity
following trauma (4). Mitchell was the first to describe the burning pain associated with
peripheral nerve injuries sustained by soldiers during the Civil War, using the term
causalgia (5). Sudek, in 1900, defined the osteoporosis and radiographic changes seen with
RSD (6). The International Association for the Study of Pain and others have suggested
using the term causalgia specifically only if a demonstrable nerve lesion is present and
RSD for the syndrome in general (7).
Several theories have been proposed to explain the pathophysiology involved. The
proponents of the peripheral hypothesis contend that the pain and associated physiological
changes are due to a lesion present in a peripheral nerve (8,9). At the level of the
lesion, sprouting occurs from damaged axons which may form neuromas or ephapses between
sympathetic efferents and sensory or visceral afferents (8). The membrane of regenerating
sprouts are very unstable and may depolarize spontaneously (10). The chemosensitivity and
mechanosensitivity of these membranes is altered and may be stimulated by catecholamines,
touch, and blood flow (10). In addition, there is evidence suggesting that with high
velocity missile injuries, large myelinated fibers can be selectively damaged. This causes
a loss of the normal inhibition of the smaller unmyelinated pain fibers at the level of
the dorsal horn (9). Consequently, the rostral passage of these more slowly conducted
impulses creates abnormal activity in the CNS.
Those that postulate a central mechanism believe that the abnormal activity present in the
dorsal horn and higher centers arises due to the convergence of peripheral nociceptors and
mechanoreceptors on wide dynamic range dorsal horn cells leading to loss of inhibition or
misinterpretation of stimuli (11). This may cause retrograde neuronal activity or
turbulence in the dorsal horn as suggested by Sutherland (12). Melzack believes there is
loss of the central biasing mechanism involving the brain stem reticular formation
allowing normally inhibited impulses to reach higher centers (13). Some authorities feel
that there is a common underlying mechanism to all forms of RSD involving both peripheral
and central pathophysiology (4,14).
The relationship between lumbar spine surgery and RSD has rarely been reported (1,2,3,15).
The syndrome has been reported following myelography and chymopapain therapy (16,17).
Previously described cases have been relatively acute, i.e., present for <6 months,
mild in severity and unilateral. Our patient presented with severe, chronic. bilateral RSD
following multiple lumbar laminectomies.
The mechanism of bilateral RSD in this patient could be explained on either a peripheral
or a central basis. Below L3 the ventral and dorsal roots extending into the neural
foramen do not normally contain preganglionic sympathetic or peripherally directed
postganglionic sympathetic fibers (18). These structures would be necessarily involved in
a peripheral nerve injury for classic RSD (8). However, the sinu-vertebral nerve
(recurrent meningeal nerve of Luschka) innervates structures within the epidural space and
carries both afferent sensory and efferent postganglionic sympathetic fibers below L3
(19). Bilateral damage to the sinu-vertebral nerve from previous surgery or epidural
adhesions could have caused RSD on a peripheral basis in this patient.
A central mechanism can also be postulated. Increased afferent traffic from damaged neural
structures within the epidural space may lead to abnormal activity in the dorsal horn
causing a loss of the central biasing mechanism and allowing normally inhibited impulses
to reach higher centers. These pathways decussate at various levels within the CNS. Thus,
a unilateral lesion could, theoretically, develop into bilateral symptoms. The patient had
extensive epidural adhesions from L5 to S1. These adhesions extended into the left S1
neural foramen and could have damaged the left sinu-vertebral nerve at that level.
Furthermore, the patient had severe depression and this may have caused increased
susceptibility to pain as suggested by Pak (20).
Several treatment modalities have been suggested for RSD including sympathetic blockade,
physical therapy, TENS, acupuncture, biofeedback, and various drug therapies. However,
most authorities agree that prompt diagnosis and sympathetic blockade of the involved
extremity offers the best prognosis (1,4,7).
REFERENCES
1. Cayla J. Rondier J. Sudek's atrophy connected with pelvic or lumbar spine lesions
(Report of 23 cases). Sem Hop Paris 1974:50:275-86.
2. Bernini PM, Simeone FA. Reflex sympathetic dystrophy associated with low lumbar disc
herniation. Spine 1981:6:180-4.
3. Chodoroff B. Bail RD. Lumbosacral radiculothapy, reflex sympathetic dystrophy and
tarsal tunnel syndromes: an unusual presentation. Arch Phys Med Rehabil 1958:66:185-7.
4. Bonica JJ. Causalgia and other reflex sympathetic dystrophies. in: Bonica JJ,
Liebeskind IC, Albe-Fessard D, eds. Advances in pain research and therapy. New York: Raven
Press, 1979:41-66.
5. Mitchell SW. Morehouse GR. Keen WW. Gunshot wounds and other injuries of nerves
Philadelphia: JB Lippincott, 1864.
6. Sudek PHM. Ueber die acute entqundiche knockatrophie.Arch Klin Chir1900:62:147.
7. Rizzie R. Visentin M, Mazzetti C. Reflex sympathetic dystrophy. In: Beneditti C, et al
eds. Advances in pain research and therapy. New York: Raven Press, 1984:451-65.
8. Doupe J. Cullen CH, Chance GQ. Post-traumatic pain and the causalgic syndrome. J Neurol
Neurosurgery' Psychiatry 1944:7:33.
9. Noordenboos W. Pain. Amsterdam; Elsevier/North Holland, 1959.
10. Wall PD, Gutnick M. Ongoing activity in peripheral nerves: the physiology and
pharmacology of impulses originating from a neuroma. Exp Neurol 1974:43:580-93.
11. Nathan PW. Involvement of the sympathetic nervous system in pain. In: Kosterlitz HW.
Terenius LY eds. Pain and society. Florida, Deerfield Beach: Verlog Chemic, 1980:311-24.
12. Sutherland S. Pain mechanism in causalgia. J Neurol Neurosurg Psychiatry
1976:39:471-80.
13. Melzack R. Phantom limb pain: Implications for treatment of pathologic pain.
Anesthesiology197135:409-19.
14. Tohmoush AJ. Causalgia: Redefinition as a clinical pain syndrome. Pain 1981:10:187-97.
15. Carlson DH, Simon H, Wagner W. Bone scanning and diagnosis of RSD secondary to
herniated lumbar discs. Neurology 1977:791-93.
16. Morettin LB. Wilson M. Severe reflex algodystrophy (Sudek's atrophy) as a complication
of myelography: Report of two cases. Am J Roentgen 1970; 110:156-58.
17. Watts C, Knighton R, Roulhac G. Chymopapain treatment of intervertebral disc disease.
J Neurosurg 1975:42:374-83.
18. Williams PL, Warwick R. Neurology: The sympathetic nervous system. In: Gray's anatomy,
Philadelphia: Saunders. 1980:1123.
19. Williams PL, Warwick R. Neurology: The spinal nerves. In: Gray's anatomy,
Philadelphia: Saunders. 1980:1089.
20. Pak TJ. Martin GM, Magness JL, Kavanaugh GJ. Reflex sympathetic dystrophy. Minn Med
1970:53:507-12.
The Clinical Journal of Pain, Vol. 2, No. 2, 1986
Address correspondence and reprint requests to:
Dr. D. W. Dobritt
16001 West Nine Mile Road
Southfield, Ml 48075
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