- Email: [email protected]
Rapid progression of acute sciatica to cauda equina syndrome
350
Journal of Manipulative and Physiological Therapeutics Volume 24 • Number 5 • June 2001 0161-4754/2001/$35.00 + 0 76/1/115261 © 2001 JMPT
CASE REPORTS Rapid Progression of Acute Sciatica to Cauda Equina Syndrome Jason W. Busse, DC,a and William S. Hsu, DCb
ABSTRACT Objective: To demonstrate the importance of clinical examination and continued vigilance for neurologic deterioration in patients with sciatica. Cauda equina syndrome, a rare sequela of sciatica, is considered a medical emergency requiring surgical decompression. Clinical Features: A 32-year-old woman had sciatica that rapidly progressed to cauda equina syndrome. Magnetic resonance imaging revealed the presence of a large nonsequestered disk fragment in the lower lumbar spine. Intervention and Outcome: The disk fragment was surgically excised. The patient experienced immediate pain relief after surgery but retained neurologic deficits. After 6 months of rehabilitation, neurologic integrity was restored, aside from patchy sensory loss of the left foot and buttocks. At the 6-month followup, the patient’s sciatica had not returned.
INTRODUCTION Sciatica is a generic term for pain along the distribution of the sciatic nerve, unilaterally or bilaterally, with or without back pain. It is a common condition among the general population, and the cause is often assumed to be lumbar disk prolapse.1 However, any intraspinal or extraspinal pathologic process along the course of the sciatic nerve can result in sciatica. Furthermore, not all causes of sciatica are benign in nature. The following report discusses a case of acute sciatica that progressed rapidly to cauda equina syndrome (CES). The diagnosis and management of this emergency condition are discussed.
CASE REPORT A 32-year-old woman had low back pain (LBP), left leg pain and numbness, and a secondary complaint of numbness
a
Clinical Sciences Resident, Department of Graduate Studies, Canadian Memorial Chiropractic College, Toronto, Ontario, Canada. b Faculty Radiologist, Department of Radiology, Canadian Memorial Chiropractic College, Toronto, Ontario, Canada. No funds were received during the preparation of this manuscript. Submit reprint requests to: J.W. Busse, DC, MSc, Consultant, Oncidium Health Group Inc., 3-5205 Harvester Rd, Burlington, Ontario, L7L 685, Canada. E-mail: [email protected]. Paper submitted June 16, 2000. doi:10.1067/mmt.2001.115261
Conclusions: Most cases of sciatica, regardless of cause, will self-resolve; as a result, there might be a tendency to maintain a low index of suspicion for serious, progressive disorders such as cauda equina syndrome. Patients need to be educated as to signs of this emergency condition and informed as to the possible consequences of delaying treatment. By maintaining a high index of suspicion for any case that fails to respond as expected to a course of conservative therapy or that demonstrates signs of cauda equina syndrome, chiropractors can assume a pivotal role by investigating and referring appropriately and by aiding in active rehabilitation postoperatively. (J Manipulative Physiol Ther 2001; 24:350-5) Key Indexing Terms: Cauda Equina Syndrome; Intervertebral Disk Herniation; Sciatica; Low Back Pain; Chiropractic
in her left arm. The left leg pain and LBP had developed 9 days before her visit when she rode her bicycle over a small bump. The pain was initially mild but progressed rapidly. At the time of presentation the pain was self-rated at 8/10 and described as sharp in the low back and dull and aching in the left leg. The pain, which originated centrally in the lumbosacral region and extended into the anterior left lower limb to the distal foot, was aggravated by sitting, walking, or standing; it was somewhat relieved if she lay supine or used Tylenol #3. The numbness in the patient’s left arm had come on insidiously 2 days before presentation and was described as extending from the elbow to the wrist in a nondermatomal pattern involving the entire forearm. She further reported a history of multiple shoulder dislocations, more frequently on the left. The numbness in her left lower limb was described as being present on the anterior aspect of the limb, extending to the toes and wrapping around the plantar surface of the left foot up to the proximal calf. The patient associated mild weakness of her left lower limb and a sensation of “cold” in her left foot with her complaint. Aside from her presenting complaint, she had been diagnosed with type II diabetes at the age of 31 years. She related that she did not smoke or drink and that she exercised by riding her bicycle approximately 10 km per day. Two days before visiting our clinic, she had sought treatment at her local hospital emergency clinic. An attendant
Journal of Manipulative and Physiological Therapeutics Volume 24 • Number 5 • June 2001 Cauda Equina Syndrome • Busse and Hsu
physician ordered radiographs, which were interpreted as unremarkable, and diagnosed the patient as having sciatica. She was released with instructions to rest at home and with a prescription for Tylenol #3 and muscle relaxants. The patient was overweight at 197 pounds and 5 feet 2 inches in height. Her blood pressure and heart rate were within normal parameters. Her posture was difficult to assess because of her hesitancy to bear weight on the left leg. Cervical spine range of motion was full and painless. Cervical anterior nerve root compression (ie, results of the cervical doorbell test) was unremarkable, as were the results of tests for thoracic outlet syndrome (EAST’s, Wright’s, Adson’s, and Eden’s). Global instability was revealed in the glenohumeral joints bilaterally, more so on the left. Orthopedic examination of her lumbar spine demonstrated (1) severely reduced motion with pain in flexion and extension and (2) moderately reduced motion with pain in right anterior rotation. There was significant muscular hypertonicity palpated in the left piriformis and gluteus medius and in the quadratus lumborum musculature bilaterally. Challenge of the L5 spinous process laterally or in a posteroanterior fashion and challenge of S1 in a posteroanterior fashion aggravated the patient’s LBP. Although pain was reported only on the anterior aspect of the left leg, palpation along the distribution of the sciatic nerve on the left resulted in pain that radiated from the point of challenge to the mid calf. The result of posterior joint provocation testing (Kemp’s test) of the lumbar spine was positive on the right. The patient’s straight leg raise (SLR) was 20° bilaterally, with reproduction of the LBP but with no radiation into the leg. The result of the bowstring test was positive on the left leg. Neurologic examination revealed normal (2+/2+) deep tendon reflexes (DTRs)2 bilaterally for the upper limb and on the right for the patellar and Achilles reflexes; areflexia was noted for the patellar and Achilles reflexes on the left. Normal strength (5/5) was recorded for the upper limb bilaterally3 and for the right lower limb. Mildly reduced strength (4/5) was recorded for the left lower limb. Results of sensory testing (sharp, dull, soft touch and vibration) for the upper and lower limbs were unremarkable, aside from a loss of vibration sense in the left lower limb—specifically, on the anterior aspect of the left leg and on the posterior aspect of the left leg and thigh. Results of Tinel’s test at the medial epicondyle of the elbow and at the carpal tunnel were unremarkable bilaterally. No pathologic reflexes were elicited. Results of Allen’s test for arterial sufficiency were negative bilaterally, and the dorsalis pedis pulse was well maintained bilaterally. Valsalva’s test did mildly aggravate the patient’s LBP. The patient denied any pain or difficulty in urination, defecation, or sexual function and reported no loss of sensation in the buttocks. Differential diagnoses at this time included sacroiliac syndrome, L5/S1 posterior joint dysfunction, and lumbar disk herniation/bulge with radiculopathy, all of which were discussed with the patient. The numbness in her left arm was determined to be unrelated to the primary complaint. The patient’s low back complaint was treated conservatively with transcutaneous elec-
tric nerve stimulation and mobilization, and she was asked to come to the clinic the next day for follow-up. Interestingly, she reported a transient decrease in the subjective numbness in her left lower limb during manual traction of her low back. On presentation the following day, her back pain had improved markedly and was now self-rated at 3/10. The left arm numbness had also improved considerably. The numbness in the left lower limb had become more pronounced below the knee, and there was evidence of foot drop on the left. Areflexia was still noted at the patellar and Achilles reflexes on the left, and the loss of vibration sense in the left lower limb was compounded by patchy loss of sharp sensation below the knee. Results of strength testing remained within normal limits (5/5) for the right lower limb, but strength in the left lower limb was now markedly decreased at 3/5. The patient was therefore diagnosed as having an acute, progressive disk herniation and was treated conservatively with transcutaneous electric nerve stimulation and mobilization for her LBP. After treatment, she was counseled as to the etiology of disk herniation-in-evolution and about signs of CES. She was instructed to return to the clinic the following day for reassessment of her neurologic status, and she was cautioned to report to the local hospital if symptoms of CES became manifest. The patient awoke the following day with complete loss of motor function of her left lower limb and admitted herself to the hospital. She began to manifest saddle paraesthesia approximately 4 hours after admission and was sent for magnetic resonance imaging (MRI). The images revealed a large, noncontained L4/L5 disk herniation, which had become sequestered in the spinal canal (Figs 1 and 2). Decompressive surgery was successful, and after 6 months of rehabilitation the patient made a full recovery, aside from patchy sensory loss in the left foot.
DISCUSSION Etiology and Pathogenesis Currently, there is no consensus on a precise definition of sciatica; however, it is not a diagnosis but rather a general descriptor for pain along the distribution of the sciatic nerve.4 Sciatica is usually the result of intraspinal pathosis, such as a herniated disk, spinal stenosis, or spondylolisthesis5; extraspinal causes of sciatica, such as pyriformis syndrome,6 aneurysm, and tumors,1,7 are rare. Disk herniations typically affect the nerve root exiting immediately below the disk level. Recent studies have supported the notion that inflammatory mechanisms are involved in sciatica because of lumbar disk herniation.8 Omarker and Myers9 have suggested that a combination of insults, including deformation of the nerve root/dorsal root ganglion and their simultaneous chemical irritation by herniated nucleus pulposus, is required to reliably produce sciatica pain. Disk herniation resulting in CES usually does not include injury to the spinal cord, inasmuch as the cauda equina is distal to the conus medullaris.
351
352
Journal of Manipulative and Physiological Therapeutics Volume 24 • Number 5 • June 2001 Cauda Equina Syndrome • Busse and Hsu
A
B
Fig 1. Proton density (A) and T2-weighted lumbar (B) sagittal images demonstrate a large extruded disk (arrow) that has migrated superiorly from L4/L5 disk and occluded most of spinal canal. Venous engorgement (bar arrow) is seen adjacent to extruded disk.
Epidemiology Sciatica is reported by approximately 25% of patients with back pain, and its incidence among the general population has been reported to range from 2% to 40%.5 Herniated disks are a common cause of sciatica and occur with equal frequency between L4/L5 and L5/S1. Fewer than 10% of herniated disks occur above these levels.10 Symptomatic disk herniation can occur at any age but is most common in patients aged 30 to 50 years.11 CES occurs in 1% to 15% of all herniated lumbar disks.12
Clinical Presentation Patients with sciatica describe pain that originates at the back or buttock and radiates below the knee, either unilaterally or bilaterally, typically involving the foot.13 Sciatica originating from neuropathy of the lumbar nerve root contributors to the sciatic nerve (L4 or L5 nerve root) occasionally result in radicular pain to the anterior thigh or the
groin area.14 No single test has a high diagnostic accuracy for sciatica resulting from a herniated lumbar disk; however, a predictive value of approximately 90% can be attained by combining history findings and physical test results.4,15 Coughing or bearing down often provokes sciatic pain associated with a herniated disk.9 This may be induced by Valsalva’s test. An SLR of less than 40° that is limited by pain radiating distal to the knee on the involved side can be indicative of underlying irritation of the sciatic nerve or its formative components (L4-S2 nerve roots).10 An SLR with pain proximal to the knee is often a sign of tight hamstring muscles. Ipsilateral SLR has a sensitivity of 0.8 and a specificity of 0.4, whereas a crossed SLR (well leg-raise test) has a sensitivity of 0.25 and a specificity of 0.9 in the diagnosis of herniated disks.4 Suspicion of sciatic nerve irritation can be further confirmed by the bowstring test, whereby at the painful range of SLR (1) the knee is bent until the pain is resolved and (2)
Journal of Manipulative and Physiological Therapeutics Volume 24 • Number 5 • June 2001 Cauda Equina Syndrome • Busse and Hsu
A
B
Fig 2. Proton density axial images at (A) and above (B) L4/L5 disk show large left paracentral disk herniation (white outline) occupying two thirds of spinal canal and severely compressing thecal sac (hatched area).
pressure is applied to the area of the tibial nerve at the popliteal fossa, which in the case of a positive test result elicits pain and/or paraesthesia. Heel and toe walking are also clinically useful tests. Asymmetry during heel walking can be caused by weakness of the L4/L5 nerve root innervated tibialis anterior and/or the L5 nerve root innervated extensor hallucis longus muscle. Inability to perform toe walking might reflect weakness of the S1 nerve root innervated gastroc-soleus muscle group. A patient with symptomatic lumbar disk herniation often experiences a brief history of back pain before the development of leg pain.11 Patients with sequestered lumbar disk herniations have a clinical appearance that is more severe than that of patients with incomplete disk herniations.8 Central lumbar disk rupture can result in neurologic compression of the sacral roots of the cauda equina, which manifests as CES.16 The pathognomonic signs of this lesion are bowel dysfunction, bladder dysfunction in the form of retention or incontinence, and saddle paraesthesia17; however, the classic presentation of the syndrome is uncommon.12 CES represents a medical emergency requiring prompt diagnosis and surgical decompression.
The Role of Imaging Diagnostic imaging is not recommended as a screening tool in cases of sciatica. Most causes of sciatica stem from the soft tissues (spondylolisthesis being the notable exception), which renders plain films of little value. MRI is therefore the imaging method of choice. Axial loading of the lumbar spine during MRI in a supine, psoas-relaxed position has been found to increase diagnostic specificity in patients with sciatica.18 Imaging studies are indicated if (1) symptoms persist 4 to 6 weeks after onset, (2) there are progressive neurologic deficits, or (3) a suitable index of suspi-
cion is raised concerning the possibility of organic pathosis by signs such as night pain or sudden weight loss.19 The importance of clinical imaging as a means of confirming a diagnosis rather than as a screening tool cannot be overstated. Investigation of 98 asymptomatic subjects by means of MRI found a high prevalence of abnormalities in the lumbar spine, only 36% of the subjects demonstrating normal disks at all levels.20 Grane et al21 have reported that no significant radiologic differences, including disk herniation, were found in a comparison of asymptomatic and symptomatic patients after lumbar disk surgery.
Treatment The approach to the management of sciatica depends on the underlying cause. However, in the case of sciatica due to disk herniation, the symptoms in most patients will resolve with conservative therapy; surgery is seldom indicated. Treatment is directed at reducing pain without prolonged use of narcotic medication. The efficacy of traction, corsets, or other spinal orthoses for the treatment of uncomplicated sciatica has not been convincingly demonstrated in the literature.22 Treatment with epidural corticosteriod injections23 or Maitland manipulation24 in patients with sciatica resulting from disk herniation has been shown to be effective for relief of symptoms in the short-term only, with no effect on the long-term course of the disorder. A recent randomized controlled trial on the effectiveness of bed rest for sciatica has found it to be no better than watchful waiting, and perhaps worse, inasmuch as extended bed rest has been associated with physical and psychologic adverse effects.25 In the only published controlled trial on lumbar side posture manipulation, such manipulation was shown to be superior to passive physiotherapy in the treatment of sciatica resulting from disk herniation.26 A retrospective case series
353
354
Journal of Manipulative and Physiological Therapeutics Volume 24 • Number 5 • June 2001 Cauda Equina Syndrome • Busse and Hsu
found that manipulative therapy might be effective and safe for uncomplicated sciatica, but further trials are necessary to confirm these findings.27 Cassidy et al28 have cautioned against manipulation in severe cases, recommending instead the use of mobilization in the first few treatments. Furthermore, in their experience, patients with nerve root entrapment from disk herniation respond best to gentle manipulations that maintain the lumbar lordosis. Manipulative therapy has been associated temporally with the development of CES in 3 cases but has not been established as a causative factor.29 Progression of sciatica to CES is a medical emergency and requires immediate referral for appropriate diagnosis and decompression. The urgency of decompression, however, is controversial.11,30 A meta-analysis of retrospective and observational studies by Ahn et al31 found improved outcomes in patients with CES who were treated within 48 hours of onset. Alternately, Delamarter et al,17 in a well-designed prospective animal study, found no differences in recovery from incomplete cauda equina compression in dogs regardless of whether decompression occurred 1 hour or 1 week after the onset of induced compression. A recent review of surgical procedures for lumbar disk prolapse found that diskectomy remains the surgical procedure of choice.32 Failure of lumbar disk surgery occurs in 10% to 20% of patients21; however, although 80% of the population will experience lower back pain during their lifetimes, only 1% to 3% will be considered candidates for surgery.33 After decompressive surgery, early return to activity is encouraged to increase muscle tone and improve the patient’s sense of well-being.
CONCLUSION Unacceptable delay in diagnosis, investigation, and referral of patients with CES can result in preventable deterioration in neurologic function before treatment. Numerous studies have found that primary contact clinicians make twice as many recommendations when confronted with a clinical vignette on low back pain than when confronted with a simulated patient having the same complaint.34 There is a need for ongoing education to encourage clinical colleagues in all disciplines to recognize the early signs and the need for urgent referral in suspected cases of CES. By maintaining a high index of suspicion for those patients with sciatica who fail to respond as expected to a course of conservative therapy or who demonstrate signs of CES, chiropractors can assume a pivotal role by investigating and referring appropriately and by aiding in active rehabilitation postoperatively.
REFERENCES 1. Dudeney S, O’Farrell D, Bouchier-Hayes D, Byrne J. Extraspinal causes of sciatica. Spine 1998;23:494-6. 2. Bates B, Bickley LS, Hoekelman RA. The nervous system: a guide to physical exam and history taking. 6th ed. Philadelphia: JB Lippincott; 1995. p. 491-554. 3. Walton J, Gilliatt R, Hutchinson M, O’Brian M, Thomas P, Willison R. Aids to the examination of the peripheral nervous system. London: Bailliere Tindall; 1990. p. 1-2.
4. Andersson GBJ, Deyo RA. History and physical examination in patients with herniated lumbar disks. Spine 1996;21: 10S-18S. 5. Kahanovitz N. Sciatica: Verifying the diagnosis, offering relief. J Musculoskeletal Med 1998;15:51-9. 6. Douglas S. Sciatic pain and piriformis syndrome. Nurse Pract 1997;22:166-80. 7. Servant CTJ. An unusual cause of sciatica. Spine 1998;19: 2134-6. 8. Nygaard OP, Mellgren SI, Osterud B. The inflammatory properties of contained and noncontained lumbar disk herniation. Spine 1997;22:2484-8. 9. Omarker K, Myers RR. Pathogenesis of sciatic pain: role of herniated nucleus pulposus and deformation of spinal nerve root and dorsal root ganglion. Pain 1998;78:99-105. 10. Frymoyer JW. Back pain and sciatica. N Engl J Med 1988; 318:291-300. 11. Murrey DB, Hanley EN. Surgery for lumbar disk herniation: what are the choices? J Musculoskeletal Med 1999;16:39-45. 12. Kostiuk JP, Harrington I, Alexander D, Rand W, Evans D. Cauda equina syndrome and lumbar disc herniation. J Bone Joint Surg 1986;68-A:386-91. 13. Olmarker K, Hasue M. Classification and pathophysiology of spinal pain syndromes. In: Weinstein JN, Rydevik B, editors. Essentials of the spine. New York: Raven Press; 1995. 14. Yukawa Y, Kato F, Kajino G, Nakamura S, Nitta H. Groin pain associated with lower lumbar disk herniation. Spine 1997;22: 1736-40. 15. Bogduk N. The lumbar disc and low back pain. Neurosurg Clin N Am 1991;2:791-806. 16. Bonaroti EA, Welch WC. Posterior epidural migration of an extruded lumbar disk fragment causing cauda equina syndrome. Spine 1998;23:378-81. 17. DeLamarter RB, Sherman JE, Carr JB. Cauda equina syndrome: neurologic recovery following immediate, early or late decompression. Spine 1992;16:1022-9. 18. Willen J, Danielson B, Gaulitz A, Niklason T, Schonstrom N, Hansson T. Dynamic effects on the lumbar spinal canal. Axially loaded CT-mylography and MRI in patients with sciatica and/or neurogenic claudication. Spine 1997;22:2968-76. 19. Bigos S, Bowyer O, Braen G, et al. Acute low back problems in adults. Clinical practice guideline no. 14. Rockville (MD): Agency for Health Care Policy and research, Public Health Service, US Department of Health and Human Services; 1994. AHCPR publication no. 95-0642. 20. Jensen MC, Brant-Zawadzki MN, Obuchowski N, Modic MT, Malkasian D, Ross JS. Magnetic resonance imaging of the lumbar spine in people without back pain. N Engl J Med 1994; 331:69-73. 21. Grane P, Tullberg T, Rydberg J, Lindgren L. Postoperative lumbar MR imaging with contrast enhancement. Comparisons between symptomatic and asymptomatic patients. Acta Radiol 1996;37:366-72. 22. Deyo RA, Loeser JD, Bigos SJ. Herniated lumbar intervertebral disk. Ann Intern Med 1990;112:598-603. 23. Carette S, Leclaire A, Marcoux S, et al. Epidural corticosteriod injections for sciatica due to herniated nucleus pulposus. N Engl J Med 1997;336:1634-40. 24. Coxhead CE, Meade TW, Inskip H, North WRS, Troup JDG. Multicentre trial of physiotherapy in the management of sciatic symptoms. Lancet 1981;1:1065-8. 25. Vroomen PCAJ, de Krom MCTFM, Wilmink JT, Kester ADM, Knottnerus JA. Lack of effectiveness of bed rest for sciatica. N Engl J Med 1999;340:418-23. 26. Nwuga VCB. Relative therapeutic efficacy of vertebral manipulation and conventional treatment in back pain management. Am J Phys Med 1982;61:273-8. 27. Stern PJ, Côté P, Cassidy JD. A series of cases of low back pain
Journal of Manipulative and Physiological Therapeutics Volume 24 • Number 5 • June 2001 Cauda Equina Syndrome • Busse and Hsu
28. 29. 30.
31.
with radiating leg pain treated by chiropractors. J Manipulative Physiol Ther 1995;18:335-42. Cassidy JD, Theil HW, Kirkaldy-Willis WH. Side posture manipulation for lumbar intervertebral disk herniation. J Manipulative Physiol Ther 1993;16:96-103. Haldeman S, Rubenstein SM. Cauda equina syndrome in patients undergoing manipulation of the lumbar spine. Spine 1992;17:1469-73. Busse JW, Bhandari M, Schnittker JB, Reddy K, Dunlop RB. Delayed presentation of cauda equina syndrome secondary to lumbar disk herniation: functional outcomes and health-related quality of life. Submitted for publication. Ahn UM, Buchowski JM, Ahn NU, Sieber A, Kostuik JP.
Cauda equina syndrome secondary to lumbar disk herniation: a meta-analysis of surgical outcomes. Presented at the American Academy of Orthopaedic Surgeons 1999 Annual Meeting; 1999 Feb 4-8; Anaheim (CA). 32. Gibson JNA, Grant IC, Waddell G. Surgery for lumbar disk prolapse (Cochrane Review). In: The Cochrane Library, Issue 3. Oxford: Update Software; 1999. 33. Frymoyer JW. Radiculopathies: Lumbar disk herniation and recess stenosis. In: Frymoyer JW, editor. The adult spine. 1st ed. New York: Raven Press; 1991. p. 1720. 34. Carey TS, Garrett J, North Carolina Back Pain Project. Patterns of ordering diagnostic tests for patients with acute low back pain. Ann Intern Med 1996;125:807-14.
CORRECTIONS In the March/April 2001 issue, the address of the author of the article “Evidence-based Clinical Guidelines for the Management of Acute Low Back Pain: Response to the Guidelines Prepared for the Australian Medical Health and Research Council” (2001;24:214-20) should have been listed as follows: Anthony L. Rosner, PhD, Foundation for Chiropractic Education and Research, 1330 Beacon St, Suite 315, Brookline, MA 02446-3203. In the May 2001 issue, the running heads for the article “Prognostic Values of Physical Examination Findings in Patients With Chronic Low Back Pain Treated Conservatively: A Systematic Literature Review” by Borge JA, LeBoeuf-Yde C, and Lothe J (2001;24:292-5) should read as follows: Examination Findings in Low Back Pain. We apologize for the errors and regret any confusion they may have caused.
355
Journal of Manipulative and Physiological Therapeutics Volume 24 • Number 5 • June 2001 0161-4754/2001/$35.00 + 0 76/1/115261 © 2001 JMPT
CASE REPORTS Rapid Progression of Acute Sciatica to Cauda Equina Syndrome Jason W. Busse, DC,a and William S. Hsu, DCb
ABSTRACT Objective: To demonstrate the importance of clinical examination and continued vigilance for neurologic deterioration in patients with sciatica. Cauda equina syndrome, a rare sequela of sciatica, is considered a medical emergency requiring surgical decompression. Clinical Features: A 32-year-old woman had sciatica that rapidly progressed to cauda equina syndrome. Magnetic resonance imaging revealed the presence of a large nonsequestered disk fragment in the lower lumbar spine. Intervention and Outcome: The disk fragment was surgically excised. The patient experienced immediate pain relief after surgery but retained neurologic deficits. After 6 months of rehabilitation, neurologic integrity was restored, aside from patchy sensory loss of the left foot and buttocks. At the 6-month followup, the patient’s sciatica had not returned.
INTRODUCTION Sciatica is a generic term for pain along the distribution of the sciatic nerve, unilaterally or bilaterally, with or without back pain. It is a common condition among the general population, and the cause is often assumed to be lumbar disk prolapse.1 However, any intraspinal or extraspinal pathologic process along the course of the sciatic nerve can result in sciatica. Furthermore, not all causes of sciatica are benign in nature. The following report discusses a case of acute sciatica that progressed rapidly to cauda equina syndrome (CES). The diagnosis and management of this emergency condition are discussed.
CASE REPORT A 32-year-old woman had low back pain (LBP), left leg pain and numbness, and a secondary complaint of numbness
a
Clinical Sciences Resident, Department of Graduate Studies, Canadian Memorial Chiropractic College, Toronto, Ontario, Canada. b Faculty Radiologist, Department of Radiology, Canadian Memorial Chiropractic College, Toronto, Ontario, Canada. No funds were received during the preparation of this manuscript. Submit reprint requests to: J.W. Busse, DC, MSc, Consultant, Oncidium Health Group Inc., 3-5205 Harvester Rd, Burlington, Ontario, L7L 685, Canada. E-mail: [email protected]. Paper submitted June 16, 2000. doi:10.1067/mmt.2001.115261
Conclusions: Most cases of sciatica, regardless of cause, will self-resolve; as a result, there might be a tendency to maintain a low index of suspicion for serious, progressive disorders such as cauda equina syndrome. Patients need to be educated as to signs of this emergency condition and informed as to the possible consequences of delaying treatment. By maintaining a high index of suspicion for any case that fails to respond as expected to a course of conservative therapy or that demonstrates signs of cauda equina syndrome, chiropractors can assume a pivotal role by investigating and referring appropriately and by aiding in active rehabilitation postoperatively. (J Manipulative Physiol Ther 2001; 24:350-5) Key Indexing Terms: Cauda Equina Syndrome; Intervertebral Disk Herniation; Sciatica; Low Back Pain; Chiropractic
in her left arm. The left leg pain and LBP had developed 9 days before her visit when she rode her bicycle over a small bump. The pain was initially mild but progressed rapidly. At the time of presentation the pain was self-rated at 8/10 and described as sharp in the low back and dull and aching in the left leg. The pain, which originated centrally in the lumbosacral region and extended into the anterior left lower limb to the distal foot, was aggravated by sitting, walking, or standing; it was somewhat relieved if she lay supine or used Tylenol #3. The numbness in the patient’s left arm had come on insidiously 2 days before presentation and was described as extending from the elbow to the wrist in a nondermatomal pattern involving the entire forearm. She further reported a history of multiple shoulder dislocations, more frequently on the left. The numbness in her left lower limb was described as being present on the anterior aspect of the limb, extending to the toes and wrapping around the plantar surface of the left foot up to the proximal calf. The patient associated mild weakness of her left lower limb and a sensation of “cold” in her left foot with her complaint. Aside from her presenting complaint, she had been diagnosed with type II diabetes at the age of 31 years. She related that she did not smoke or drink and that she exercised by riding her bicycle approximately 10 km per day. Two days before visiting our clinic, she had sought treatment at her local hospital emergency clinic. An attendant
Journal of Manipulative and Physiological Therapeutics Volume 24 • Number 5 • June 2001 Cauda Equina Syndrome • Busse and Hsu
physician ordered radiographs, which were interpreted as unremarkable, and diagnosed the patient as having sciatica. She was released with instructions to rest at home and with a prescription for Tylenol #3 and muscle relaxants. The patient was overweight at 197 pounds and 5 feet 2 inches in height. Her blood pressure and heart rate were within normal parameters. Her posture was difficult to assess because of her hesitancy to bear weight on the left leg. Cervical spine range of motion was full and painless. Cervical anterior nerve root compression (ie, results of the cervical doorbell test) was unremarkable, as were the results of tests for thoracic outlet syndrome (EAST’s, Wright’s, Adson’s, and Eden’s). Global instability was revealed in the glenohumeral joints bilaterally, more so on the left. Orthopedic examination of her lumbar spine demonstrated (1) severely reduced motion with pain in flexion and extension and (2) moderately reduced motion with pain in right anterior rotation. There was significant muscular hypertonicity palpated in the left piriformis and gluteus medius and in the quadratus lumborum musculature bilaterally. Challenge of the L5 spinous process laterally or in a posteroanterior fashion and challenge of S1 in a posteroanterior fashion aggravated the patient’s LBP. Although pain was reported only on the anterior aspect of the left leg, palpation along the distribution of the sciatic nerve on the left resulted in pain that radiated from the point of challenge to the mid calf. The result of posterior joint provocation testing (Kemp’s test) of the lumbar spine was positive on the right. The patient’s straight leg raise (SLR) was 20° bilaterally, with reproduction of the LBP but with no radiation into the leg. The result of the bowstring test was positive on the left leg. Neurologic examination revealed normal (2+/2+) deep tendon reflexes (DTRs)2 bilaterally for the upper limb and on the right for the patellar and Achilles reflexes; areflexia was noted for the patellar and Achilles reflexes on the left. Normal strength (5/5) was recorded for the upper limb bilaterally3 and for the right lower limb. Mildly reduced strength (4/5) was recorded for the left lower limb. Results of sensory testing (sharp, dull, soft touch and vibration) for the upper and lower limbs were unremarkable, aside from a loss of vibration sense in the left lower limb—specifically, on the anterior aspect of the left leg and on the posterior aspect of the left leg and thigh. Results of Tinel’s test at the medial epicondyle of the elbow and at the carpal tunnel were unremarkable bilaterally. No pathologic reflexes were elicited. Results of Allen’s test for arterial sufficiency were negative bilaterally, and the dorsalis pedis pulse was well maintained bilaterally. Valsalva’s test did mildly aggravate the patient’s LBP. The patient denied any pain or difficulty in urination, defecation, or sexual function and reported no loss of sensation in the buttocks. Differential diagnoses at this time included sacroiliac syndrome, L5/S1 posterior joint dysfunction, and lumbar disk herniation/bulge with radiculopathy, all of which were discussed with the patient. The numbness in her left arm was determined to be unrelated to the primary complaint. The patient’s low back complaint was treated conservatively with transcutaneous elec-
tric nerve stimulation and mobilization, and she was asked to come to the clinic the next day for follow-up. Interestingly, she reported a transient decrease in the subjective numbness in her left lower limb during manual traction of her low back. On presentation the following day, her back pain had improved markedly and was now self-rated at 3/10. The left arm numbness had also improved considerably. The numbness in the left lower limb had become more pronounced below the knee, and there was evidence of foot drop on the left. Areflexia was still noted at the patellar and Achilles reflexes on the left, and the loss of vibration sense in the left lower limb was compounded by patchy loss of sharp sensation below the knee. Results of strength testing remained within normal limits (5/5) for the right lower limb, but strength in the left lower limb was now markedly decreased at 3/5. The patient was therefore diagnosed as having an acute, progressive disk herniation and was treated conservatively with transcutaneous electric nerve stimulation and mobilization for her LBP. After treatment, she was counseled as to the etiology of disk herniation-in-evolution and about signs of CES. She was instructed to return to the clinic the following day for reassessment of her neurologic status, and she was cautioned to report to the local hospital if symptoms of CES became manifest. The patient awoke the following day with complete loss of motor function of her left lower limb and admitted herself to the hospital. She began to manifest saddle paraesthesia approximately 4 hours after admission and was sent for magnetic resonance imaging (MRI). The images revealed a large, noncontained L4/L5 disk herniation, which had become sequestered in the spinal canal (Figs 1 and 2). Decompressive surgery was successful, and after 6 months of rehabilitation the patient made a full recovery, aside from patchy sensory loss in the left foot.
DISCUSSION Etiology and Pathogenesis Currently, there is no consensus on a precise definition of sciatica; however, it is not a diagnosis but rather a general descriptor for pain along the distribution of the sciatic nerve.4 Sciatica is usually the result of intraspinal pathosis, such as a herniated disk, spinal stenosis, or spondylolisthesis5; extraspinal causes of sciatica, such as pyriformis syndrome,6 aneurysm, and tumors,1,7 are rare. Disk herniations typically affect the nerve root exiting immediately below the disk level. Recent studies have supported the notion that inflammatory mechanisms are involved in sciatica because of lumbar disk herniation.8 Omarker and Myers9 have suggested that a combination of insults, including deformation of the nerve root/dorsal root ganglion and their simultaneous chemical irritation by herniated nucleus pulposus, is required to reliably produce sciatica pain. Disk herniation resulting in CES usually does not include injury to the spinal cord, inasmuch as the cauda equina is distal to the conus medullaris.
351
352
Journal of Manipulative and Physiological Therapeutics Volume 24 • Number 5 • June 2001 Cauda Equina Syndrome • Busse and Hsu
A
B
Fig 1. Proton density (A) and T2-weighted lumbar (B) sagittal images demonstrate a large extruded disk (arrow) that has migrated superiorly from L4/L5 disk and occluded most of spinal canal. Venous engorgement (bar arrow) is seen adjacent to extruded disk.
Epidemiology Sciatica is reported by approximately 25% of patients with back pain, and its incidence among the general population has been reported to range from 2% to 40%.5 Herniated disks are a common cause of sciatica and occur with equal frequency between L4/L5 and L5/S1. Fewer than 10% of herniated disks occur above these levels.10 Symptomatic disk herniation can occur at any age but is most common in patients aged 30 to 50 years.11 CES occurs in 1% to 15% of all herniated lumbar disks.12
Clinical Presentation Patients with sciatica describe pain that originates at the back or buttock and radiates below the knee, either unilaterally or bilaterally, typically involving the foot.13 Sciatica originating from neuropathy of the lumbar nerve root contributors to the sciatic nerve (L4 or L5 nerve root) occasionally result in radicular pain to the anterior thigh or the
groin area.14 No single test has a high diagnostic accuracy for sciatica resulting from a herniated lumbar disk; however, a predictive value of approximately 90% can be attained by combining history findings and physical test results.4,15 Coughing or bearing down often provokes sciatic pain associated with a herniated disk.9 This may be induced by Valsalva’s test. An SLR of less than 40° that is limited by pain radiating distal to the knee on the involved side can be indicative of underlying irritation of the sciatic nerve or its formative components (L4-S2 nerve roots).10 An SLR with pain proximal to the knee is often a sign of tight hamstring muscles. Ipsilateral SLR has a sensitivity of 0.8 and a specificity of 0.4, whereas a crossed SLR (well leg-raise test) has a sensitivity of 0.25 and a specificity of 0.9 in the diagnosis of herniated disks.4 Suspicion of sciatic nerve irritation can be further confirmed by the bowstring test, whereby at the painful range of SLR (1) the knee is bent until the pain is resolved and (2)
Journal of Manipulative and Physiological Therapeutics Volume 24 • Number 5 • June 2001 Cauda Equina Syndrome • Busse and Hsu
A
B
Fig 2. Proton density axial images at (A) and above (B) L4/L5 disk show large left paracentral disk herniation (white outline) occupying two thirds of spinal canal and severely compressing thecal sac (hatched area).
pressure is applied to the area of the tibial nerve at the popliteal fossa, which in the case of a positive test result elicits pain and/or paraesthesia. Heel and toe walking are also clinically useful tests. Asymmetry during heel walking can be caused by weakness of the L4/L5 nerve root innervated tibialis anterior and/or the L5 nerve root innervated extensor hallucis longus muscle. Inability to perform toe walking might reflect weakness of the S1 nerve root innervated gastroc-soleus muscle group. A patient with symptomatic lumbar disk herniation often experiences a brief history of back pain before the development of leg pain.11 Patients with sequestered lumbar disk herniations have a clinical appearance that is more severe than that of patients with incomplete disk herniations.8 Central lumbar disk rupture can result in neurologic compression of the sacral roots of the cauda equina, which manifests as CES.16 The pathognomonic signs of this lesion are bowel dysfunction, bladder dysfunction in the form of retention or incontinence, and saddle paraesthesia17; however, the classic presentation of the syndrome is uncommon.12 CES represents a medical emergency requiring prompt diagnosis and surgical decompression.
The Role of Imaging Diagnostic imaging is not recommended as a screening tool in cases of sciatica. Most causes of sciatica stem from the soft tissues (spondylolisthesis being the notable exception), which renders plain films of little value. MRI is therefore the imaging method of choice. Axial loading of the lumbar spine during MRI in a supine, psoas-relaxed position has been found to increase diagnostic specificity in patients with sciatica.18 Imaging studies are indicated if (1) symptoms persist 4 to 6 weeks after onset, (2) there are progressive neurologic deficits, or (3) a suitable index of suspi-
cion is raised concerning the possibility of organic pathosis by signs such as night pain or sudden weight loss.19 The importance of clinical imaging as a means of confirming a diagnosis rather than as a screening tool cannot be overstated. Investigation of 98 asymptomatic subjects by means of MRI found a high prevalence of abnormalities in the lumbar spine, only 36% of the subjects demonstrating normal disks at all levels.20 Grane et al21 have reported that no significant radiologic differences, including disk herniation, were found in a comparison of asymptomatic and symptomatic patients after lumbar disk surgery.
Treatment The approach to the management of sciatica depends on the underlying cause. However, in the case of sciatica due to disk herniation, the symptoms in most patients will resolve with conservative therapy; surgery is seldom indicated. Treatment is directed at reducing pain without prolonged use of narcotic medication. The efficacy of traction, corsets, or other spinal orthoses for the treatment of uncomplicated sciatica has not been convincingly demonstrated in the literature.22 Treatment with epidural corticosteriod injections23 or Maitland manipulation24 in patients with sciatica resulting from disk herniation has been shown to be effective for relief of symptoms in the short-term only, with no effect on the long-term course of the disorder. A recent randomized controlled trial on the effectiveness of bed rest for sciatica has found it to be no better than watchful waiting, and perhaps worse, inasmuch as extended bed rest has been associated with physical and psychologic adverse effects.25 In the only published controlled trial on lumbar side posture manipulation, such manipulation was shown to be superior to passive physiotherapy in the treatment of sciatica resulting from disk herniation.26 A retrospective case series
353
354
Journal of Manipulative and Physiological Therapeutics Volume 24 • Number 5 • June 2001 Cauda Equina Syndrome • Busse and Hsu
found that manipulative therapy might be effective and safe for uncomplicated sciatica, but further trials are necessary to confirm these findings.27 Cassidy et al28 have cautioned against manipulation in severe cases, recommending instead the use of mobilization in the first few treatments. Furthermore, in their experience, patients with nerve root entrapment from disk herniation respond best to gentle manipulations that maintain the lumbar lordosis. Manipulative therapy has been associated temporally with the development of CES in 3 cases but has not been established as a causative factor.29 Progression of sciatica to CES is a medical emergency and requires immediate referral for appropriate diagnosis and decompression. The urgency of decompression, however, is controversial.11,30 A meta-analysis of retrospective and observational studies by Ahn et al31 found improved outcomes in patients with CES who were treated within 48 hours of onset. Alternately, Delamarter et al,17 in a well-designed prospective animal study, found no differences in recovery from incomplete cauda equina compression in dogs regardless of whether decompression occurred 1 hour or 1 week after the onset of induced compression. A recent review of surgical procedures for lumbar disk prolapse found that diskectomy remains the surgical procedure of choice.32 Failure of lumbar disk surgery occurs in 10% to 20% of patients21; however, although 80% of the population will experience lower back pain during their lifetimes, only 1% to 3% will be considered candidates for surgery.33 After decompressive surgery, early return to activity is encouraged to increase muscle tone and improve the patient’s sense of well-being.
CONCLUSION Unacceptable delay in diagnosis, investigation, and referral of patients with CES can result in preventable deterioration in neurologic function before treatment. Numerous studies have found that primary contact clinicians make twice as many recommendations when confronted with a clinical vignette on low back pain than when confronted with a simulated patient having the same complaint.34 There is a need for ongoing education to encourage clinical colleagues in all disciplines to recognize the early signs and the need for urgent referral in suspected cases of CES. By maintaining a high index of suspicion for those patients with sciatica who fail to respond as expected to a course of conservative therapy or who demonstrate signs of CES, chiropractors can assume a pivotal role by investigating and referring appropriately and by aiding in active rehabilitation postoperatively.
REFERENCES 1. Dudeney S, O’Farrell D, Bouchier-Hayes D, Byrne J. Extraspinal causes of sciatica. Spine 1998;23:494-6. 2. Bates B, Bickley LS, Hoekelman RA. The nervous system: a guide to physical exam and history taking. 6th ed. Philadelphia: JB Lippincott; 1995. p. 491-554. 3. Walton J, Gilliatt R, Hutchinson M, O’Brian M, Thomas P, Willison R. Aids to the examination of the peripheral nervous system. London: Bailliere Tindall; 1990. p. 1-2.
4. Andersson GBJ, Deyo RA. History and physical examination in patients with herniated lumbar disks. Spine 1996;21: 10S-18S. 5. Kahanovitz N. Sciatica: Verifying the diagnosis, offering relief. J Musculoskeletal Med 1998;15:51-9. 6. Douglas S. Sciatic pain and piriformis syndrome. Nurse Pract 1997;22:166-80. 7. Servant CTJ. An unusual cause of sciatica. Spine 1998;19: 2134-6. 8. Nygaard OP, Mellgren SI, Osterud B. The inflammatory properties of contained and noncontained lumbar disk herniation. Spine 1997;22:2484-8. 9. Omarker K, Myers RR. Pathogenesis of sciatic pain: role of herniated nucleus pulposus and deformation of spinal nerve root and dorsal root ganglion. Pain 1998;78:99-105. 10. Frymoyer JW. Back pain and sciatica. N Engl J Med 1988; 318:291-300. 11. Murrey DB, Hanley EN. Surgery for lumbar disk herniation: what are the choices? J Musculoskeletal Med 1999;16:39-45. 12. Kostiuk JP, Harrington I, Alexander D, Rand W, Evans D. Cauda equina syndrome and lumbar disc herniation. J Bone Joint Surg 1986;68-A:386-91. 13. Olmarker K, Hasue M. Classification and pathophysiology of spinal pain syndromes. In: Weinstein JN, Rydevik B, editors. Essentials of the spine. New York: Raven Press; 1995. 14. Yukawa Y, Kato F, Kajino G, Nakamura S, Nitta H. Groin pain associated with lower lumbar disk herniation. Spine 1997;22: 1736-40. 15. Bogduk N. The lumbar disc and low back pain. Neurosurg Clin N Am 1991;2:791-806. 16. Bonaroti EA, Welch WC. Posterior epidural migration of an extruded lumbar disk fragment causing cauda equina syndrome. Spine 1998;23:378-81. 17. DeLamarter RB, Sherman JE, Carr JB. Cauda equina syndrome: neurologic recovery following immediate, early or late decompression. Spine 1992;16:1022-9. 18. Willen J, Danielson B, Gaulitz A, Niklason T, Schonstrom N, Hansson T. Dynamic effects on the lumbar spinal canal. Axially loaded CT-mylography and MRI in patients with sciatica and/or neurogenic claudication. Spine 1997;22:2968-76. 19. Bigos S, Bowyer O, Braen G, et al. Acute low back problems in adults. Clinical practice guideline no. 14. Rockville (MD): Agency for Health Care Policy and research, Public Health Service, US Department of Health and Human Services; 1994. AHCPR publication no. 95-0642. 20. Jensen MC, Brant-Zawadzki MN, Obuchowski N, Modic MT, Malkasian D, Ross JS. Magnetic resonance imaging of the lumbar spine in people without back pain. N Engl J Med 1994; 331:69-73. 21. Grane P, Tullberg T, Rydberg J, Lindgren L. Postoperative lumbar MR imaging with contrast enhancement. Comparisons between symptomatic and asymptomatic patients. Acta Radiol 1996;37:366-72. 22. Deyo RA, Loeser JD, Bigos SJ. Herniated lumbar intervertebral disk. Ann Intern Med 1990;112:598-603. 23. Carette S, Leclaire A, Marcoux S, et al. Epidural corticosteriod injections for sciatica due to herniated nucleus pulposus. N Engl J Med 1997;336:1634-40. 24. Coxhead CE, Meade TW, Inskip H, North WRS, Troup JDG. Multicentre trial of physiotherapy in the management of sciatic symptoms. Lancet 1981;1:1065-8. 25. Vroomen PCAJ, de Krom MCTFM, Wilmink JT, Kester ADM, Knottnerus JA. Lack of effectiveness of bed rest for sciatica. N Engl J Med 1999;340:418-23. 26. Nwuga VCB. Relative therapeutic efficacy of vertebral manipulation and conventional treatment in back pain management. Am J Phys Med 1982;61:273-8. 27. Stern PJ, Côté P, Cassidy JD. A series of cases of low back pain
Journal of Manipulative and Physiological Therapeutics Volume 24 • Number 5 • June 2001 Cauda Equina Syndrome • Busse and Hsu
28. 29. 30.
31.
with radiating leg pain treated by chiropractors. J Manipulative Physiol Ther 1995;18:335-42. Cassidy JD, Theil HW, Kirkaldy-Willis WH. Side posture manipulation for lumbar intervertebral disk herniation. J Manipulative Physiol Ther 1993;16:96-103. Haldeman S, Rubenstein SM. Cauda equina syndrome in patients undergoing manipulation of the lumbar spine. Spine 1992;17:1469-73. Busse JW, Bhandari M, Schnittker JB, Reddy K, Dunlop RB. Delayed presentation of cauda equina syndrome secondary to lumbar disk herniation: functional outcomes and health-related quality of life. Submitted for publication. Ahn UM, Buchowski JM, Ahn NU, Sieber A, Kostuik JP.
Cauda equina syndrome secondary to lumbar disk herniation: a meta-analysis of surgical outcomes. Presented at the American Academy of Orthopaedic Surgeons 1999 Annual Meeting; 1999 Feb 4-8; Anaheim (CA). 32. Gibson JNA, Grant IC, Waddell G. Surgery for lumbar disk prolapse (Cochrane Review). In: The Cochrane Library, Issue 3. Oxford: Update Software; 1999. 33. Frymoyer JW. Radiculopathies: Lumbar disk herniation and recess stenosis. In: Frymoyer JW, editor. The adult spine. 1st ed. New York: Raven Press; 1991. p. 1720. 34. Carey TS, Garrett J, North Carolina Back Pain Project. Patterns of ordering diagnostic tests for patients with acute low back pain. Ann Intern Med 1996;125:807-14.
CORRECTIONS In the March/April 2001 issue, the address of the author of the article “Evidence-based Clinical Guidelines for the Management of Acute Low Back Pain: Response to the Guidelines Prepared for the Australian Medical Health and Research Council” (2001;24:214-20) should have been listed as follows: Anthony L. Rosner, PhD, Foundation for Chiropractic Education and Research, 1330 Beacon St, Suite 315, Brookline, MA 02446-3203. In the May 2001 issue, the running heads for the article “Prognostic Values of Physical Examination Findings in Patients With Chronic Low Back Pain Treated Conservatively: A Systematic Literature Review” by Borge JA, LeBoeuf-Yde C, and Lothe J (2001;24:292-5) should read as follows: Examination Findings in Low Back Pain. We apologize for the errors and regret any confusion they may have caused.
355