Unilateral multilevel cervical radiculopathies as a late effect of poliomyelitis. A case report

Unilateral multilevel cervical radiculopathies as a late effect of poliomyelitis. A case report

94 CLINICAL NOTES Unilateral Multilevel Cervical Radiculopathies as a Late Effect of Poliomyelitis. A Case Report Allan J. Drapkin, MD, Walter S. Ro...

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CLINICAL NOTES

Unilateral Multilevel Cervical Radiculopathies as a Late Effect of Poliomyelitis. A Case Report Allan J. Drapkin, MD, Walter S. Rose, MD ABSTRACT. Drapkin A J, Rose WS. Unilateral multilevel cervical radiculpathies as a late effect of poliomyelitis. Arch Phys Med Rehabil 1995;76:94-6. • A severe left-sided cervical radiculopathy that developed after a work-related injury is reported. Because this involved the upper limb opposite to a long-standing postpolio sequela, it is suggestive of postpolio syndrome. Work-up showed left-sided multilevel acquired foraminal stenosis. These unilateral degenerative changes were very likely the result of overuse of the cervical apophyseal joints, the consequence of the muscle imbalance created by the poliomyelitis. It was successfully treated by appropriate surgical decompression.

© 1995 by the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation His mental status and his cranial nerve function were normal. A cervical curvature concave to the left was noted. On the right side, marked atrophy of the deltoid, supra and infraspinatus, pectoralis major, latissimus dorsi, and teres major was present. He was unable to abduct his right shoulder or extend his right elbow. The right biceps and more distal musculature was of normal bulk and power but no deep tendon reflexes were elicitable in that limb. These findings had been unchanged since his recovery from poliomyelitis. On the left, atrophy of the upper trapezius, deltoid, supra and infraspinatus, latissimus dorsi, as well as the biceps, was noted. Manual muscle testing in the proximal left upper limb revealed: shoulder flexion was poor-, shoulder abduction was poor-, internal rotation was poor+, external rotation 0, elbow extension was good, elbow flexion was fair+. All musculature distal to the elbow was normal. The left bicipital jerk was absent but the brachioradialis and tricipital reflexes, as well as both knee and ankle jerks, were normally elicited. Both plantar responses were flexor. No CASE REPORT deficits in deep or superficial modalities of sensation, nor in cereA 59-year-old, naturally left-handed man had poliomyelitis at bellar function, were detected. age 16. According to the patient, he was left with proximal atrophy Cervical spine x-rays confirmed a mild cervical curvature conand paralysis in his right upper extremity, apparently the only limb cave to the left with severe spondylotic changes, more marked on affected by the disease. Following his rehabilitation, he was able the left side. Magnetic resonance imaging of the cervical spine to function well, despite this sequela. Forty-three years later, he revealed multiple constrictions of the dural sac from C3 to C6 on was injured when, with his neck in an awkward position, he at- the basis of degenerative changes. On axial gradient image views, tempted to tighten a pipe connection. He developed pain that was narrowing of the left foraminal areas at the C3-C4, C4-C5 and C5centered in his left shoulder and that gradually extended into the C6 levels were noted (fig 1). A cervical myelogram showed minileft side of his neck and along the outer aspect of his left arm mal anterior ridging at C5-C6 and root changes at C4-C5 and C5and forearm. The pain was associated with tingling sensations. C6 on the left. A postmyelogram computerized tomography Coughing, sneezing, or straining did not alter the character nor the showed marked foraminal stenosis at C3-C4, C4-C5 and C5-C6 intensity of the pain. Abduction of the left upper limb above shoul- on the left side, the result of marked bony overgrowth on the der level lessened it, while rotating the neck or allowing the left left-sided facets, whereas the right-sided ones were spared. The arm to hang unsupported increased it. He gradually developed vertebral bodies showed overgrowth and sclerosis on the left side severe and persistent weakness and atrophy in the proximal muscle only, whereas no significant pathology was noted on the right side groups in the left upper extremity. Throughout this clinical course, (fig 2). On electromyography, the left paraspinal muscles at the levels of no symptoms involving his lower limbs nor sphincteric dysfunction occurred. A complete evaluation of his left shoulder, including C4 through C7 showed polyphasic, high-amplitude activity without fibrillations or sharp positive activity. Left supraspinatus, infraspimagnetic resonance imaging and arthrography, was negative. natus, deltoid, and biceps showed fibrillations and sharp positive From the Sectionof Neurosurgery,Departmentof Surgery(Dr. Drapkin),and the activity with motor units of high amplitude and long duration. The Departmentof Radiology(Dr. Rose), MonmouthMedicalCenter,LongBranch,NJ. interference pattern was diminished in these muscles. Because of Submitted for publicationMay 5, 1994. Accepted in revised form September6, severe atrophy the left trapezius could not be identified for testing. 1994. On December 10, 1992, the patient was operated on and leftNo commercialpartyhavinga directfinancialinterestin the resultsof the research supporting this article has or will confer a benefitupon the authors or upon any sided microforaminotomies at the three involved levels were perorganizationwith whichthe authors are associated. formed. Postoperatively, the preexisting pain immediately cleared. Reprint requests to AllanJ. Drapkin,MD, 1398 Highway#35, Ocean,NJ 07712. Once the operative wound healed he was started on a rehabilitation © 1995by the AmericanCongressof RehabilitationMedicineand the American program that consisted of physical therapy modalities to decrease Academyof PhysicalMedicineand Rehabilitation pain and spasm, including moist heat, massage, joint mobilization, 0003-9993/95/7601-306553.00/0

Since the advent and generalized use of polio vaccine, acute poliomyelitis has b e c o m e a rarity in the United States and Europe. 1 Nevertheless, there r e m a i n large n u m b e r s of disabled individuals who contracted poliomyelitis during the epidemics of the 1950s. Although their condition r e m a i n e d static for m a n y years, it has b e c o m e evident that as survivors grow older, they develop new symptoms, resulting in a decrease in their independence, work productivity and general level of functioning. This new disability is k n o w n as the postpolio syndrome [PPS] and its frequency is increasing. 14 Essential to the appropriate m a n a g e m e n t of PPS is the exclusion of other pathological conditions that can m i m i c it. This case report emphasizes the importance of m a k i n g that differential diagnosis.

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Fig 1--Axial magnetic resonance gradient images at the neural foraminal level of C4-C5. Note narrowing and compression of the root sleeves on the left (small arrows) compared with relative normalcy on the right (large arrows).

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Cervical spondylosis results from a combination of factors lead by intervertebral disc degeneration. This protracted process results in loss of disc turgescence and decrease in its vertical height together with mechanical instability of the motion segment involved. The progressive bulging of the annulus fibrosus, the abnormal mobility and the progressive approximation of the vertebral bodies and their uncinate processes which result, lead to reactive hyperostosis and osteophyte formation which, depending on their size and location, as well as on the dimensions of the spinal and foraminal canals, may result in spinal cord and/or nerve root compression. 9'I° Nerve root entrapment in the intervertebral foramen can occur as a consequence of: hypertrophy of the articular facets encroaching the posterior wall of the foramenH; telescoping of the apophyseal processes, accompanying the decrease in intervertebral disc height which decreases the foraminal height12; and/or hypertrophy of the uncovertebral process, or the development of osteophytes from that process, encroach on the anterior wall of the foramen. ~2 In the cervical spine, motion in the saggital plane is maximal at the C5-C6 and C6-C7 levels, which are the vertebrae usually most affected by spondylosis. Lateral bending, which is coupled with axial rotation, on the other hand, is maximal at the C3-C4 and C4-C5 levels. 1~ Circumstances leading to overuse of the cervical spine, such as intensive manual labor or dyskinesias have been implicated in the development of an earlier and more severe cervical spondylosis. 9'14-16In the previously mentioned movement disorders, with their repetitive lateral bending and rotation of the neck, the C3-C4 and C4-C5 segments are the areas of the cervical spine most severely affected, a4-16

and electric stimulation to the left shoulder, together with a complete exercise program including use of progressively increasing weights and aerobic activities. This program of rehabilitation resulted in a gradual improvement in function that continued for a period of 15 months. Manual muscle testing in the proximal left upper limb at completion of his rehabilitation showed: shoulder flexion was good, shoulder abduction was fair+, internal rotation was good, external rotation was good, elbow extension was good, elbow flexion was good-. Twelve months after the surgery he was able to return to gainful employment at his previous place of work, in a modified, lighter capacity. DISCUSSION Many postpolio survivors who experienced a good initial recovery following their acute illness, are presenting, more than 30 years later, with new major losses of function secondary to muscle weakness, fatigue, respiratory difficulties, and/or p a i n Y '5-7 This second disability or PPS has been encountered with increasing frequency. Current diagnostic criteria for PPS include: partial recovery of motor function after poliomyelitis and at least 15 years of functional disability or recovery; residual muscle atrophy, weakness and areflexia in at least one limb, with normal sensation; and new muscle weakness and other neuromuscular symptoms unrelated to any other neurological or medical disorder. 5'8 This frequently overlooked last criteria implies that a complete clinical and electrophysiological assessment of patients suspected of PPS should be supplemented with adequate neuroradiological studies, so that potentially reversible conditions other than PPS, can be detected and t r e a t e d . 3'4

Fig 2--Computerized tomographic myelography scans at the neural foraminal level of C41C5. Note marked neural foraminal narrowing on the left (thin white arrow), secondary to facet and vertebral body bony overgrowth (arrow heads), while on the right side, the neural foramen is normal (thick white arrow). Arch Phys Med RehabilVol 76, January 1995

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In our case report, the marked asymmetry of the polio sequela effected a very asymmetrical cervical muscle pull resulting in the cervical curvature noted. 17 The fact that this patient was left-handed and involved in a physically demanding occupation exacerbated the dynamic effects of overuse on the left-sided spinal joints leading to this unusual, strictly unilateral, severe multilevel foraminal stenosis. TM A posterior approach with microforaminotomies at the levels involved resulted in an immediate relief of pain and a gradual return of function, confirming reported experiences by others.19 Late involvement of the contralateral upper limb, apparently spared by poliomyelitis, has been reported previously, but none of these reported cases underwent neuroradiological evaluation. All of those cases were labeled as PPS, based on the clinical findings and results of electromyography, and failed to improve from their second disability. 7'2°'21 Symptoms related to cervical spondylosis were reported in 10% of cases in two series of postpolio patients but no sufficient data was provided to evaluate whether a cause-effect relationship existed between the spondylosis and the postpolio condition) ,4 With the increasing incidence of PPS, heightened awareness of this condition, as well as of its diagnostic pitfalls, is desirable. The case reported herewith underscores the importance of a complete work-up when evaluating new disabilities developing in postp01io patients. In this fashion, potentiaUy reversible conditions which may simulate PPS can be detected and treated, whereas a clearer picture of what truly constitutes PPS can emerge. 4 Acknowledgment: The authors thank Jeffrey D. Burke and John S. Walzer, RBP, (Audio-Visual Department, Monmouth Medical Center), for their photographic work; and Ms. Arlene Dietz for the preparation of the manuscript. References 1. Dean E. Clinical decision making in the management of the late sequelae of poliomyelitis. Phys Ther 1991 ;71:752-61.

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2. Agre JC, Rodriquez AA, Spefling KB. Symptoms and clinical impressions of patients seen in the postpolio clinic. Arch Phys Med Rehabil 1989; 70:367-70. 3. Dalakas M, Illa I. Post-polio syndrome: Concepts in clinical diagnosis, pathogenesis, and etiology. Adv Neurol 1991; 56:495-511. 4. Howard RS, Wiles CM, Spencer GT. The late sequelae of poliomyelitis. Q J Med 1988;251:219-32. 5. Halstead LS, Rossi CD. Post-polio syndrome: Clinical experience with 132 consecutive outpatients. In: Halstead LS, Wiechers DO, editors. Research and clinical aspects of the late effects of poliomyelitis. White Plains, NY: March of Dimes Birth Defects Foundation, 1987;23:1326. 6. Aston JW Jr. Post-polio syndrome. An emerging threat to polio survivors. Post Grad Med 1992;92:249-56. 7. Cosgrove JL, Alexander MA, Kitts EL, Swan BE, Klein MJ, Bauer RE. Late effects of poliomyelitis. Arch Phys Med Rehabil 1987;68:47. 8. Melchers W, deVisser M, Jongen P, vanLoon A, Nibbeling R, Oostvogel P, et al. The postpolio syndrome: no evidence for poliovirus persistence. Ann Neurol 1992;32:728-32. 9. Brain WR, Northfield D, Wilkinson M. The neurological manifestations of cervical spondylosis. Brain 1952;75:187-225. i0. Parke WW. Correlative anatomy of cervical spondylotic myelopathy. Spine 1988; 13:831-7. 11. Epstein JA, Epstein BS, Lavine LS, Carras R, Rosenthal AD. Cervical myeloradiculopathy caused by arthrotic hypertrophy of the posterior facets and laminae. J Neurosurg 1978;49:387-92. 12. Holt S, Yates PO. Cervical spondylosis and nerve root lesions. Incidence at routine necropsy. J Bone Joint Surg 1966;48B:407-23. 13. White AA III, Panjabi MM. Clinical biomechanics of the spine. Philadelphia: Lippincott, 1978. 14. E1-Mallakh RS, Rao K, Barwick M. Cervical myelopathy secondary to movement disorders: Case report. Neurosurg 1989;24:902-5. 15. Hirose G, Kadoya S. Cervical spondylotic radiculo-myelopathy in patients with athetoid-dystonic cerebral palsy: Clinical evaluation and surgical treatment. J Neurol Neurosurg Psychiatr 1984;47:775-80. 16. Levine RA, Rosenbaum AE, Waltz JM, Scheinberg LC. Cervical spondylosis and dyskinesias. Neurology 1970; 20:1194-9. 17. James JIP. Paralytic scoliosis. J Bone Joint Surg 1956;38B:660-85. 18. Garrett AL, Parry J, Nickel VL. Paralytic Scoliosis. Clin Orthop 1961;21:117-24. 19. Williams RW. Microcervical foraminotomy. A surgical alternative for intractable radicular pain. Spine 1983;8:708-16. 20. Campbell AMG, Williams ER, Pearce J. Late motor neuron degeneration following poliomyelitis. Neurology 1969; 19:1101-6. 21. Pinelli P, Ramelli E. Paralisi periferica controlaterale neuritica in paziente con postumi di poliomielite. Riv Sper Freniat 1964;88:349-91.