Chinese Medical Journal 2009;122(10):1214-1222
Cauda equina syndrome: a review of clinical progress

MA Bin,  WU Hong,  JIA Lian-shun,  YUAN Wen,  SHI Guo-dong ,  SHI Jian-gang

MA Bin (Division of Orthopedics, Orthopedics Institute of PLA, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China)

WU Hong (Division of Endocrinology, Changhai Hospital, Second Military Medical University, Shanghai 200433, China)

JIA Lian-shun (Division of Orthopedics, Orthopedics Institute of PLA, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China)

YUAN Wen (Division of Orthopedics, Orthopedics Institute of PLA, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China)

SHI Guo-dong (Division of Orthopedics, Orthopedics Institute of PLA, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China)

SHI Jian-gang (Division of Orthopedics, Orthopedics Institute of PLA, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China)

Correspondence to:SHI Jian-gang,Division of Orthopedics, Orthopedics Institute of PLA, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China (Tel: 86-21-81886999 ext 885636. Fax:86-21-63720099.
cauda equina syndrome; diagnosis; treatment; prognosis; evidence-based medicine

Objective To review the literature on the clinical progress in cauda equina syndrome (CES), including the epidemic history, pathogenesis, diagnosis, treatment policy and prognosis.

Data sources All reports on CES in the literature were searched in PubMed, Ovid, Springer, Elsevier, and the Chinese Biomedical Literature Disk using the key terms “cauda equina syndrome”, “diagnosis”, “treatment”, “prognosis” and “evidence-based medicine”.

Study selection Original milestone articles and critical reviews written by major pioneer investigators about the cauda equina syndrome were selected.

Results CES is rare, both atraumatically and traumatically. Males and females are equally affected. The incidence of CES is variable, depending on the etiology of the syndrome. The most common cause of CES is herniation of a lumbar intervertebral disc. CES symptoms may have sudden onset and evolve rapidly or sometimes chronic ally. Each type of CES has different typical signs and symptoms. Low back pain may be the most significant symptoms, accompanied by sciatica, lower extremities weakness, saddle or perianal hypoesthesia, sexual impotence, and sphincter dysfunction. MRI is usually the preferred investigation approach. Patients who have had CES are difficult to return to a normal status.

Conclusions The diagnosis of CES is primarily based on a careful history inquiry and clinical examination, assisted by elective radiologic investigations. Early diagnosis and early surgical decompression are crucial for a favorable outcome in most CES cases.

The spinal cord terminates at the level of the intervertebral disc between the first and second lumbar vertebrae, forming the conus medullaris, below which is the filum terminale and a bundle of nerve roots constituting the cauda equina (CE). Cauda equina syndrome (CES), a rare neurological disorder, is a combination of signs and symptoms resulting from lesion of the nerves in the CE. Typical manifestations can be associated variably with the disorders characterized by low back pain, unilateral or usually bilateral sciatica, bilateral weakness of the lower extremities, saddle or perianal hypoesthesia or anesthesia, sexual impotence, together with rectal and bladder sphincter dysfunction.1-5

The term “cauda equina” was first described by a French anatomist Lazarius more than four centuries ago.6 Three centuries later, Mixter and Barr7 gave the definition of CES in the English-language literature.


CES is rare, both atraumatically as well as traumatically. Males and females are equally affected, and it can occur at any age but primarily in adults. The incidence of CES is variable, depending on the etiology of the syndrome. The prevalence among the general population has been estimated between 1:100 000 and 1:33 000.8 The most common cause of CES is herniation of a lumbar intervertebral disc. It is reported by approximately 1% to 10% of patients with herniated lumbar disks.4,5,9-15 The prevalence among patients with low back pain is approximately four in 10 000.16


The pathophysiological mechanisms of CES are not completely understood. It may result from any lesion to CE nerve roots such as direct mechanical compression, inflammation, and venous congestion or ischemia.

CE nerve roots are especially vulnerable to injury of compressive and tensile stresses. Two reasons responsible for this: firstly, CE nerve roots have no Schwann cell covered; secondly, the microvascular systems of CE nerve roots have a region of relative hypovascularity formed by the combined areas of anastomoses in the proximal one-third of the root. It may provide an anatomical rationale for the suspected neuroischemic manifestations concurrent with degenerative changes.17 In a case-control retrospective analysis, Kou et al18 proposed the theory that multilevel procedures and the presence of a preoperative coagulopathy were significant risk factors for the development of a compressive spinal epidural hematoma in patients who underwent spinal surgery. Groen and his group members19 analyzed 199 cases of spontaneous spinal epidural hematoma, and hypothesized that rupture of the posterior internal vertebral venous plexus of Batson plays an important part in the etiology of the idiopathic hematomas.

All kinds of lesions to the CE may cause CES. Of the numerous causes reported, the most common one is disc herniation in the lumbar region. It may also be caused by traumatic injury, lumbar spinal stenosis, primary or metastatic tumors, epidural abscess, ankylosing spondylitis, idiopathic causes, inferior vena cava thrombosis, spinal subdural or epidural hematoma, spinal manipulation, vascular problems, spinal or epidural anaesthesia, and iatrogenic causes (Table 1).

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Table 1. Causes of CES


There are no broadly accepted definite diagnostic criteria of CES up to now. Though early diagnosis and treatment are of extremely importance to prevent permanent neurological damage, it may be difficult to assess the presence of CES timely. Its low morbility attributes to the first reason. Moreover, its initial signs and symptoms are often subtle and may vary in intensity and evolvement according to different etiologies.

Timely diagnosis of CES requires the evaluation of multiple variables including clinical history, physical examination, and radiologic investigations.

Clinical history and physical examination
For patients with low-back pain or sciatica, the presence of one of the following symptoms, including saddle anesthesia, recent onset of bladder dysfunction (such as urinary retention or incontinence), bowel incontinence, sensory or motor weakness in either of the lower extremities, suggests the diagnosis of CES.

Initial evaluation of urinary retention, saddle anesthesia, rectal tone, and bulbocavernosus reflex is most important according to Della-Giustina,77 who deems that the failure of emergency room evaluation and subsequent reliance by health care workers on that evaluation are the greatest cause of litigation because of missed CES. Assessment of bladder function and perianal sensation is extremely important for the diagnosis and prognosis in those patients in whom CES is suspected, and urodynamic studies should be performed at initial presentation.5,78

Although sexual impotence in the affected males with CES was a significant feature, it was usually difficult to assess whether this was of origin or due to other causes such as psychological factors.79

Only by careful history taking and examination of the patient can CES be diagnosed early and therefore treated early to avoid preventable life-long disability (Table 2).

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Table 2. Clinical history and physical examination of CES

Imaging studies
Radiologic investigations such as plain radiography, plain myelography, magnetic resonance imaging (MRI), computed tomography (CT) or computed tomography- myelography may be obtained to help assess the presence of CES quickly in patients with a history and examination that strongly suggest a serious cause for CES. These examinations each have their advantages and disadvantages. Plain radiography is often helpless in detecting the cause of CES but useful in search of destructive changes, disk-space narrowing, or spondylolysis. Myelography was routinely performed before CT and MRI become universally accepted, but it has lot of complications, such as pain, infection, and headache due to hypo-intracranial pressure. Computed tomography, magnetic resonance imaging, and computed tomography-myelography have equivalent overall sensitivities and diagnostic accuracies, and they are complimentary to some extent.80 By comparing with the surgically confirmed abnormality, MRI may be slightly more sensitive than CT and CT myelography, though they have roughly equivalent sensitivities and specificities, and all the above three appear superior to plain myelography in the diagnosis of intervertebral disc herniation.81,82 Similarly, sensitivities and specificities of CT and MRI appear comparable in the diagnosis of lumbar spinal stenosis, and both are significantly higher than plain myelography.81,83 MRI may be most helpful in differentiating recurrent disc herniation from postoperative fibrosis.84 MRI also has the advantage of not using ionizing radiation or contrast injection and provides better resolution. So magnetic resonance imaging should be the best initial procedure for patients with suspected CES. Bell et al85 recommend emergency MRI be assessed in all patients who present with new onset of urinary symptoms in the context of lumbar back pain or sciatica in order to avoid misdiagnosis or missed diagnosis of CES.

Other tests
Other tests such as urodynamic investigations and electromyography are also important for the early diagnosis and the assessment of the prognosis. Electromyography may reveal the severity and early recovery of CE conduction function. Urodynamic investigation may be used to assess recovery of bladder function before and following decompression surgery. Residual urine volume may monitor urinary retention suggesting a neurogenic bladder by catheterization.


Several classifications with regard to onset of CES are reported. Tandon and Sankaren,86 and Tay and Chacha79 identify three groups of CES: group I, in which the symptoms arose suddenly without previous history of backache; group II, in which there was an acute onset of bladder dysfunction following a long history of low back pain; and group III, in which CES arose gradually from a background of chronic low back pain and sciatica. Shephard87 and Kostuik et al5 identified two types of presentation in patients with CES secondary to a central disc lesion: type I was an acute mode, in which there were abrupt, more severe symptoms and signs and a slightly poorer prognosis after decompression, especially for the return of bladder function; type II was a slower onset, characterized by prior symptoms for varying time-intervals before the more gradual onset.

Patients with CES were assigned to two stages by Gleave and Macfarlane10 in terms of urinary function: stage I, CES with retention, characterized by painless urinary retention and overflow incontinence; stage II, incomplete CES, characterized by altered urinary sensation, loss of desire to void, poor urinary stream, and the need to strain in order to micturate.

In the study of Shi et al,88 patients with CES were assigned to four stages according to electrophysiology and clinical symptoms. Stage I, laboratory stage or pre-clinical stage, in which patients had no clinical symptoms while electrophysiology had changed; Stage II, early clinical stage, in which there was a decreased saddle or perianal sensation; Stage III, intermediate clinical stage, in which there was a lax anal sphincters and change in sexual function; Stage IV, advanced clinical stage, in which there was a sensory loss and sexual impotence.


CES is often misdiagnosed as other disorders for its symptoms mimic those of other conditions. For some less experienced medical workers, it is difficult to discriminate CES from conus medullaris syndrome, which is characterized by urinary retention and constipation. The presentation of CES resembles that of conus medullaris syndrome; however, with the exception that symptoms may be asymmetric.1,89 Other conditions with similar symptoms to CES include peripheral neuropathy, lumbosacral plexopathy, low back pain, Guillain-Barr syndrome, lumbar disk disorders, neoplasms of spinal cord, spinal cord infections, spinal cord injuries, and spinal cord compression, etc.


Several therapeutic options are available for patients with CES, but some have not yet been rigorously tested. Two main conservative treatments have been reported, which are anti-inflammatory treatment and vasodilatatory treatment.90

Vasodilatatory agents
Many studies showed that vasodilatatory agents had a significant therapeutical effect for CES.91-93 In an experimental study, Yamamoto and his colleagues94 demonstrated that systemic treatment with OP-1206 α-CD, a prostaglandin E1 analogue, could significantly improve local nerve blood flow and attenuate thermal hyperalgesia induced by nerve constriction injury in rats. Yone et al95 performed myeloscopic examination in patients with lumbar spinal canal stenosis, and dilation of the running blood vessels was observed immediately after the administration of lipoprostaglandin E1 in six of 11 patients. The authors believed that lipoprostaglandin E1 might enhance blood flow in the CE and improve clinical symptoms in some patients with lumbar spinal stenosis. Nakai and co-worker′s experiments demonstrated that orally administered OP-1206 α-CD improved walking dysfunction and alleviated restricted spinal cord blood flow in the rat neuropathic intermittent claudication model.91-97

Anti-inflammatory agents
Anti-inflammatory agents, including steroids and nonsteroidal anti-inflammatory drugs (NSAIDs), might be effective in CES patients with inflammatory causes and have been broadly used in treatment of back pain,98-102 but no evidence suggests that they have shown significant benefit.103

The mechanism of anti-inflammatory properties of steroids includes the inhibition of cytokines, lipid peroxidation, and hydrolysis.104,105 NSAIDs work by inhibiting the enzyme cyclo-oxygenase, which is responsible for the synthesis of prostaglandins.106,107

In a study of adhesive arachnoiditis in rats, Nakano et al108 found that methylprednisolone administration before and after laminectomy suppressed CE adhesion and facilitated recovery from CE adhesion. Della-Giustina77 advocated steroid use in patients suspected of CES because it can rapidly decrease the severity of pain while appropriate diagnostic studies are being performed.

One possible regimen of steroid may be the dose similar to that for traumatic spinal cord injury, but no studies have shown significant benefit supporting this over any other regimen. The recommended regimen of dexamethasone is usally an initial dose of 10 mg intravenously, followed by 4 mg intravenous dose every six hours. The regimen of dexamethasone was commonly given intravenously at doses of 4 to 100 mg.77

NSAIDs have been proven useful in prevention of the calcification of the soft tissues, heterotopic ossification and adherence.109,110 In a recent data in the rabbit model, Sandoval et al111 have demonstrated that aceclofenac, a kind of NSAIDs, may also be helpful in prevention of the formation of the peridural fibrosis.

Some authors also pointed out the potential risks of steroid use. Disadvantages are reported by Jacobs et al,112 that the anti-inflammatory drugs may delay healing and frequently result in abscess formation.


Emergency department care
Patients who are suspected CES should be treated immediately with a neurologic evaluation. Once CES is diagnosed, emergent surgical decompression is recommended for most patients to avoid potential permanent neurological damage, except for some late stage patients. Surgical therapy is somewhat directed at the underlying cause of CES. For those caused by trauma, immobilision of spine is the first step.

Timing of surgery
Most authors advocate that emergency surgical decompression plays an important role in improving the outcome of CES. In a recent meta-analysis of the timing of surgery for CES with urinary retention, DeLong et al113 reviewed 16 available studies, and the result suggested early surgery for CES. Although most series recommend emergent surgery, the timing of surgery still remains controversial. No study has convincingly demonstrated the “best” timing of decompression for CES up to date. The majority of authors agree that urgent decompression can improve outcome of CES while others hold a contrary idea.

Before the mid-1980s, most authors believed that decompression should be carried out within six hours after onset in patients who have an acute cauda-equina lesion. But this view was overthrowed by Kostuik et al,5 who perfomed a retrospective chart review, and found that decompression did not have to be performed in less than six hours if recovery was to occur, although decompression should be done as soon as possible to allow maximum recovery.

Some authors suggest decompression be proceeded within 24 hours of presentation, especially in the presence of complete perianal anaesthesia and significant sphincter disturbance.43,78,114

More authors recommend within 48 hours of symptom onset. Nielsen et al115 reported that decompression within 48 hours after onset of CES reduced the late bladder abnormalities in comparison with decompression after 48 hours. Shapiro et al4,9 also reported reduced chronic sciatica and good sexual potency after early depression within 48 hours. Hellström′s experience suggests that early surgery within 48 hours may improve bladder function and the ability to regain or retain erections.116 In a meta-analysis of surgical outcomes, Ahn et al117 draw the conclusion that patients who underwent decompression within 48 hours could reserve a better outcome in sensory and motor as well as urinary and bowel functions than those after 48 hours. For CES due to low lumbar injuries, surgery is also recommended to be performed within 48 hours of syndrome onset.118

Notwithstanding, it seems not always the truth that the earlier surgical depression is taken since CES onset the better outcome may be obtained. Kohles et al119 reported no benefit of an early surgical decompression in less than 24 hours compared with surgery within a period between 24 and 48 hours in a meta-analysis. Hussain et al120 reported on 20 CES patients, in whom nine were operated on within 5 hours, eleven between 8 and 24 hours after neurosurgical admission. Their study revealed no difference between the two groups and that urgent surgery within 5 hours of onset was not associated with reduced permanent disability compared with those between 8 and 24 hours.

However, a few authors argued that no benefit could be obtained from urgent decompression, conflicting with those previously addressed.41,121-122 In their series of studies, Gleave and Macfarlane10,11 drew the conclusion that urgent decompression conferred no benefit when urinary retention with overflow incontinence existed at presentation. They even believed that emergent surgery might add to rather than alleviate morbidity when performed under less than optimal conditions. Hussain et al120 demonstrated no benefit from emergent decompression compared with a more delayed approach. McCarthy et al123 also demonstrated that no significant difference existed in outcomes between those patients operated less than 48 hours and those over 48 hours from initial onset of sphincteric symptoms.

Surgical procedure
Surgical strategy is usually focused on the underlying causes. Generally spine posterior decompression is often adequate, unless there is a lesion such as vertebrae destruction, neoplasm or large abscess in the anterior spine as well. Multiple surgical approaches of decompression are recommended such as diskectomy, microdiskectomy, microscopic decompression, fenestrations, laminectomy, hemisemilaminotomy, distraction laminoplasty, multilevel laminectomies, neurolysis of CE, and intradural exploration of the nerve roots.5,9,115,124,125 However, there is no sufficient evidence on the effectiveness of any form of surgical decompression compared to another. Different modus operandi is applicable for different causes of CES according to history, physical signs and imaging study of the patient.

Kostuik et al5 performed a wide laminectomy and bilateral decompression in the CES patients due to lumbar disc herniation, and found that these patients generally had an excellent result, particularly in terms of the recovery of motor function. Surgery by Shapiro et al9 consisted of a laminectomy before discectomy to facilitate delivery of the disc herniation without undue manipulation of the neural elements, and then an aggressive removal of remaining material in the disc space was performed. They also performed foraminotomies on the stenotic patients. One patient was treated via a unilateral microdiscectomy approach.

For patients with CES and ankylosing spondylitis (the CES-AS syndrome), Ahn et al68 recommended either lumboperitoneal shunting or laminectomy to improve neurologic dysfunction or halt the progression of neurologic deficit.

As a postoperative complication, repeated surgery appears to provide a best recovery for CES. It was estimated about 80% of CES patients could make either a complete or a delayed partial recovery.43,45 Jensen44 reviewed pertinent literature concerning postoperative CES, and he recommended surgical exploration and further decompression in all situations, especially when the symptoms were progressive.


The prognosis for CES is traditionally considered to be heavily weighted by multiple factors such as etiology, speed of onset, duration of compression, degree of neurological deficit, symptoms and signs, and levels of spinal involvement.1,77,118

There is much controversy within the literature regarding the urgency of depression and the prognosis. Some researchers claimed no clear correlation between symptom duration before surgery and functional recovery.5,10,11,121,123,126,127 McCarthy et al123 performed a retrospective cohort study and found that the symptom duration before operation and the speed of onset do not affect the outcome more than 2 years after surgery. Gleave and Macfarlane10,11 retrospectively reviewed 33 CES cases and found that the duration of bladder paralysis prior to surgery did not influence the outcome. This view was confirmed by a prospective longitudinal inception cohort study of 33 patients performed by Qureshi and Sell. They found a significantly better outcome in patients who were continent of urine at presentation compared with those who were incontinent. The authors concluded that the severity of bladder dysfunction at the time of surgery was the dominant factor in recovery of bladder function.121 In a review of a case series of 19 patients surgically treated for CES, Kennedy et al78 found that no correlation existed between presence of initial motor dysfunction, bilateral sciatica, level of injury as predictors of a poor outcome. The authors emphasized initial urodynamic studies as bladder function assessment in those patients in whom CES was suspected. Bohlman128 even reported significant recovery from late surgical decompression performed 11 years following the initial injury.

However, many authors believe that recovery of neurologic dysfunction for CES patients seems to be very difficult when CES has been diagnosed.123,129 McCarthy et al70 reviewed a case series of 56 patients and drew the conclusion that patients who have had CES do not return to a normal status based on the SF-36, ODI, and Low Back Outcome Scores.


1. Scott PJ. Bladder paralysis in cauda equina lesions from disc prolapse. J Bone Joint Surg Br 1965; 47: 224-235.

2. Floman Y, Wiesel SW, Rothman RH. Cauda equina syndrome presenting as a herniated lumbar disk. Clin Orthop Relat Res 1980; 147: 234-237.

3. Byrne TN. Disorders of the spinal cord and cauda equina. Curr Opin Neurol Neurosurg 1993; 6: 545-548.

4. Shapiro S. Cauda equina syndrome secondary to lumbar disc herniation. Neurosurg 1993; 32: 743-747.

5. Kostuik JP, Harrington I, Alexander D, Rand W, Evans D. Cauda equina syndrome and lumbar disc herniation. J Bone Joint Surg Am 1986; 68: 386-391.

6. Lazarius A. Historia anatomica humani corporis. Frankfurt Germany: Becker; 1600: 178.

7. Mixter WJ, Barr JS. Rupture of the intervertebral disc with involvement of the spinal canal. N Engl J Med 1934; 211: 210-215.

8. Mooney V. Differential diagnosis of low back disorders: principles of classification. In: Frymore JW, eds. The adult spine. New York: Raven Press; 1991: 1559-1560.

9. Shapiro S. Medical realities of cauda equina syndrome secondary to lumbar disc herniation. Spine 2000; 25: 348-352.

10. Gleave JR, Macfarlane R. Cauda equina syndrome: what is the relationship between timing of surgery and outcome? Br J Neurosurg 2002; 16: 325-328.

11. Gleave JR, MacFarlane R. Prognosis for recovery of bladder function following lumbar central disc prolapse. Br J Neurosurg 1990; 4: 205-209.

12. Raaf J. Removal of protruded lumbar intervertebral discs. J Neurosurg 1970; 32: 604-611.

13. Chang HS, Nakagawa H, Mizuno J. Lumbar herniated disc presenting with cauda equina syndrome. Long-term follow-up of four cases. Surg Neurol 2000; 53: 100-104.

14. O′Connell JE. Protrusions of the lumbar intervertebral discs: a clinical review based on five hundred cases treated by excision of the protrusion. J Bone Joint Surg Br 1951; 33: 8-30.

15. Kostuik JP. Medicolegal consequences of cauda equina syndrome: an overview. Neurosurg Focus 2004; 16: 39-41.

16. Deyo RA, Rainville J, Kent DL. What can the history and physical examination tell us about low back pain. JAMA 1992; 268: 760-765.

17. Parke WW, Gammell K, Rothman RH. Arterial vascularization of the cauda equina. J Bone Joint Surg Am 1981; 63: 53-62.

18. Kou J, Fischgrund J, Biddinger A, Herkowitz H. Risk factors for spinal epidural hematoma after spinal surgery. Spine 2002; 27: 1670-1673.

19. Groen RJ, Ponssen H. The spontaneous spinal epidural hematoma. A study of the etiology. J Neurol Sci 1990; 98: 121-138.

20. Lenehan B, Sullivan P, Street J, Dudeney S. Epidural abscess causing cauda equina syndrome. Ir J Med Sci 2005; 174: 88-91.

21. Reihsaus E, Waldbaur H, Seeling W. Spinal epidural abscess: a meta-analysis of 915 patients. Neurosurg Rev 2000; 23: 175-205.

22. Rigamonti D, Liem L, Sampath P, Knoller N, Namaguchi Y, Schreibman DL, et al. Spinal epidural abscess: contemporary trends in etiology, evaluation, and management. Surg Neurol 1999; 52: 189-197.

23. Tang HJ, Lin HJ, Liu YC, Li CM. Spinal epidural abscess-experience with 46 patients and evaluation of prognostic factors. J Infect 2002; 45: 76-81.

24. Yilmaz C, Selek HY, Gürkan I, Erdemli B, Korkusuz Z. Anterior instrumentation for the treatment of spinal tuberculosis. J Bone Joint Surg Am 1999; 81: 1261-1267.

25. Govender S, Parbhoo AH. Support for the anterior column with allografts in tuberculosis of the spine. J Bone Joint Surg Br 1998; 81: 106-109.

26. Cohen DB. Infectious origins of cauda equina syndrome. Neurosurg Focus 2004; 16: e2.

27. Faraj A, Krishna M, Mehdian SM. Cauda equina syndrome secondary to lumbar spondylodiscitis caused by streptococcus milleri. Eur Spine J 1996; 5: 134-136.

28. Brecker SJ, Pugey CD. Nocardia asteroides infection of the cauda equina. J Neurol Neurosurg Psychiatry 1988; 51: 309-311.

29. Kapoor SK, Garg V, Dhaon BK, Jindal M. Tuberculosis of the posterior vertebral elements: a rare cause of compression of the cauda equina. A case report. J Bone Joint Surg Am 2005; 87: 391-394.

30. Carod-Artal FJ. Neurological complications of Schistosoma infection. Trans R Soc Trop Med Hyg 2008; 102: 107-116.

31. Chen HJ, Liang CL, Lu K, Liliang PC, Tsai YD. Cauda equina syndrome caused by delayed traumatic spinal subdural haematoma. Injury 2001; 32: 505-507.

32. Harrop JS, Hunt GE Jr, Vaccaro AR. Conus medullaris and cauda equina syndrome as a result of traumatic injuries: management principles. Neurosurg Focus 2004; 16: e4.

33. Schoenecker PL, Cole HO, Herring JA, Capelli AM, Bradford DS. Cauda equina syndrome after in situ arthrodesis for severe spondylolisthesis at the lumbosacral junction. J Bone Joint Surg Am 1990; 72: 369-377.

34. Cheung EV, Herman MJ, Cavalier R, Pizzutillo PD. Spondylolysis and spondylolisthesis in children and adolescents: II. Surgical management. J Am Acad Orthop Surg 2006; 14: 488-498.

35. Shaw M, Birch N. Facet joint cysts causing cauda equina compression. J Spinal Disord Tech 2004; 17: 442-445.

36. Johnsson KE, Sass M. Cauda equina syndrome in lumbar spinal stenosis: case report and incidence in Jutland, Denmark. J Spinal Disord Tech 2004; 17: 334-335.

37. Schatzker J, Pennal GF. Spinal stenosis, a cause of cauda equina compression. J Bone Joint Surg Br 1968; 50: 606-618.

38. Storm PB, Chou D, Tamargo RJ. Lumbar spinal stenosis, cauda equina syndrome, and multiple lumbosacral radiculopathies. Phys Med Rehabil Clin N Am 2002; 13: 713-733.

39. Rubenstein DJ, Ghelman B. Case report 477: Cauda equina syndrome (CES) complicating long-standing ankylosing spondylitis (AS). Skeletal Radiol 1988; 17: 212-215.

40. Baba H, Maezawa Y, Furusawa N, Imura S, Tomita K. The role of calcium deposition in the ligamentum flavum causing a cauda equina syndrome and lumbar radiculopathy. Paraplegia 1995; 33: 219-223.

41. Buchner M, Schiltenwolf M. Cauda equina syndrome caused by intervertebral lumbar disk prolapse: mid-term results of 22 patients and literature review. Orthopedics 2002; 25: 727-731.

42. Jauslin PA, Müller AF, Myers P, Velebit V. Cauda equina syndrome associated with an aorto-caval fistula. Eur J Vasc Surg 1991; 5: 471-473.

43. McLaren AC, Bailey SI. Cauda equina syndrome: a complication of lumbar discectomy. Clin Orthop Relat Res 1986; 204: 143-149.

44. Jensen RL. Cauda equina syndrome as a postoperative complication of lumbar spine surgery. Neurosurg Focus. 2004; 16: e7.

45. Ramirez LF, Thisted R. Complications and demographic characteristics of patients undergoing lumbar discectomy in community hospitals. Neurosurgery 1989; 25: 226-231.

46. Henriques T, Olerud C, Petrén-Mallmin M, Ahl T. Cauda equina syndrome as a postoperative complication in five patients operated for lumbar disc herniation. Spine 2001; 26: 293-297.

47. Dimopoulos V, Fountas KN, Machinis TG, Feltes C, Chung I, Johnston K, et al. Postoperative cauda equina syndrome in patients undergoing single-level lumbar microdiscectomy. Report of two cases. Neurosurg Focus 2005; 19: e11.

48. Strömqvist B, Jönsson B, Annertz M, Holtås S. Cauda equina syndrome caused by migrating fat graft after lumbar spinal decompression. A case report demonstrated with magnetic resonance imaging. Spine 1991; 16: 100-101.

49. Prusick VR, Lint DS, Bruder WJ. Cauda equina syndrome as a complication of free epidural fat-grafting. A report of two cases and a review of the literature. J Bone Joint Surg Am 1988; 70: 1256-1258.

50. Mayer PJ, Jacobsen FS. Cauda equina syndrome after surgical treatment of lumbar spinal stenosis with application of free autogenous fat graft. A report of two cases. J Bone Joint Surg Am 1989; 71: 1090-1093.

51. Onik G, Maroon JC, Jackson R. Cauda equina syndrome secondary to an improperly placed nucleotome probe. Neurosurgery 1992; 30: 412-415.

52. Dickman CA, Shedd SA, Spetzler RF, Shetter AG, Sonntag VK. Spinal epidural hematoma associated with epidural anesthesia: complications of systemic heparinization in patients receiving peripheral vascular thrombolytic therapy. Anesthesiology 1990; 72: 947-950.

53. Liu YC, Wu RS, Wong CS. Unexpected complication of attempted epidural anaesthesia: cauda equina syndrome. Anaesth Intensive Care 2003; 31: 461-464.

54. Rigler ML, Drasner K, Krejcie TC, Yelich SJ, Scholnick FT, DeFontes J, et al. Cauda equina syndrome after continuous spinal anesthesia. Anesth Analg 1991; 72: 275-281.

55. Auroy Y, Benhamou D, Bargues L, Ecoffey C, Falissard B, Mercier F, et al. Complications of regional anesthesia in France: the SOS regional anesthesia hotline service. Anesthesiology 2002; 97: 1274-1280.

56. Oppenheim JS, Spitzer DE, Segal DH. Nonvascular complications following spinal manipulation. Spine J 2005; 5: 660-667.

57. Marhouitz HD, Dloce DT. Cauda equina syndrome due to sequestrated recurrent disk herniation after chiropractic manipulation. Orthopedics 1997; 20: 652-653.

58. Haldeman S, Rubinstein SM. Cauda equina syndrome in patients undergoing manipulation of the lumbar spine. Spine 1992; 17: 1469-1473.

59. Simou N, Zioga A, Zygouris A, Pahatouridis D, Charalabopoulos K, Batistatou A. Plexiform neurofibroma of the cauda equina: a case report and review of the literature. Int J Surg Pathol 2008; 16: 78-80.

60. Gaetani P, Di Ieva A, Colombo P, Tancioni F, Aimar E, Debernardi A, et al. Intradural spinal metastasis of renal clear cell carcinoma causing cauda equina syndrome. Acta Neurochir (Wien) 2004; 146: 857-861.

61. Lampl Y, Eshel Y, Gilad R, Sarova-Pinchas I. Glioblastoma multiforme with bone metastase and cauda equina syndrome. J Neurooncol 1990; 8: 167-172.

62. Bagley CA, Gokaslan ZL. Cauda equina syndrome caused by primary and metastatic neoplasms. Neurosurg Focus 2004; 16: e3.

63. Kotil K, Kilinc BM, Bilge T. Spinal metastasis of occult lung carcinoma causing cauda equina syndrome. J Clin Neurosci 2007; 14: 372-375.

64. Poncelet A. The neurologic complications of Paget’s disease. J Bone Miner Res 1999; 14(Suppl 2): 88-91.

65. Richter RL, Semble EL, Turner RA, Challa VR. An unusual manifestation of Paget’s disease of bone: spinal epidural hematoma presenting as acute cauda equina syndrome. J Rheumatol 1990; 17: 975-978.

66. Frenay J, Lambooy N. Cauda equina syndrome following spondylolisthesis by low lumbar involvement of chronic rheumatoid arthritis. Neurochirurgie 1974; 20: 431-440.

67. Kawaji H, Miyamoto M, Gembun Y, Ito H. A case report of rapidly progressing cauda equina symptoms due to rheumatoid arthritis. J Nippon Med Sch 2005; 72: 290-294.

68. Ahn NU, Ahn UM, Nallamshetty L, Springer BD, Buchowski JM, Funches L, et al. Cauda equina syndrome in ankylosing spondylitis (the CES-AS syndrome): meta-analysis of outcomes after medical and surgical treatments. J Spinal Disord 2001; 14: 427-433.

69. Tullous MW, Skerhut HE, Story JL, Brown WE Jr, Eidelberg E, Dadsetan MR, et al. Cauda equina syndrome of long-standing ankylosing spondylitis. Case report and review of the literature. J Neurosurg 1990; 73: 441-447.

70. Sant SM, O’Connell D. Cauda equina syndrome in ankylosing spondylitis: a case report and review of the literature. Clin Rheumatol 1995; 14: 224-226.

71. Schröder R, Urbach H, Zierz S. Cauda equina syndrome with multiple lumbar diverticula complicating long-standing ankylosing spondylitis. Clin Investig 1994; 72: 1056-1059.

72. Groen RJ, Ponssen H. The spontaneous spinal epidural hematoma: a study of the etiology. J Neurol Sci 1990; 98: 121-138.

73. Mohit AA, Fisher DJ, Matthews DC, Hoffer E, Avellino AM. Inferior vena cava thrombosis causing acute cauda equina syndrome. Case report. J Neurosurg 2006; 104(1 Suppl): 46-49.

74. Domenicucci M, Ramieri A, Ciappetta P, Delfini R. Nontraumatic acute spinal subdural hematoma: report of five cases and review of the literature. J Neurosurg 1999; 91(1 Suppl): 65-73.

75. Morandi X, Riffaud L, Chabert E, Brassier G. Acute nontraumatic spinal subdural hematomas in three patients. Spine 2001; 26: E547-551.

76. Russell NA, Benoit BG. Spinal subdural hematoma. A review. Surg Neurol 1983; 20: 133-137.

77. Della-Giustina. Emergency department evaluation and treatment of back pain. Emerg Med Clin North Am 1999; 17: 877-893.

78. Kennedy JG, Soffe KE, McGrath A, Stephens MM, Walsh MG, McManus F. Predictors of outcome in cauda equina syndrome. Eur Spine J 1999; 8: 317-322.

79. Tay EC, Chacha PB. Midline prolapse of a lumbar intervertebral disc with compression of the cauda equina. J Bone Joint Surg Br 1979; 61: 43-46.

80. Saint-Louis LA. Lumbar spinal stenosis assessment with computed tomography, magnetic resonance imaging, and myelography. Clin Orthop Relat Res 2001; 384: 122-136.

81. Bischoff RJ, Rodriguez RP, Gupta K, Righi A, Dalton JE, Whitecloud TS. A comparison of computed tomography-myelography, magnetic resonance imaging, and myelography in the diagnosis of herniated nucleus pulposus and spinal stenosis. J Spinal Disord 1993; 6: 289-295.

82. Modic MT, Masaryk T, Boumphrey F, Goormastic M, Bell G. Lumbar herniated disk disease and canal stenosis: prospective evaluation by surface coil MR, CT, and myelography. Am J Roentgenol 1986; 147: 757-765.

83. Kent DL, Haynor DR, Larson EB, Deyo RA. Diagnosis of lumbar spinal stenosis in adults: a metaanalysis of the accuracy of CT, MR, and myelography. Am J Roentgenol 1992; 158: 1135-1144.

84. Bundschuh CV, Modic MT, Ross JS, Masaryk TJ, Bohlman H. Epidural fibrosis and recurrent disk herniation in the lumbar spine: MR imaging assessment. Am J Roentgenol 1988; 150: 923-932.

85. Bell DA, Collie D, Statham PF. Cauda equina syndrome: what is the correlation between clinical assessment and MRI scanning? Br J Neurosurg 2007; 21: 201-203.

86. Tandon PN, Sankaren B. Cauda equina syndrome due to lumbar disc prolapse. Indian J Orthop 1967; 1: 112-116.

87. Shephard RH. Diagnosis and prognosis of cauda equina syndrome produced by protrusion of lumbar disk. Br Med J 1959; 2: 1434-1439.

88. Shi JG, Jia LS, Yuan W, Ye XJ, Chen DY, Ni B, et al. Clinical stages and early diagnosis of cauda equina syndrome due to lumbo-sacral nerve injury. Orthop J Chin (Chin) 2005; 7: 491-493.

89. Jaradeh S. Cauda equina syndrome: a neurologist’s perspective. Reg Anesth 1993; 18(6 Suppl): 473-480.

90. Orendácová J, Cízková D, Kafka J, Lukácová N, Marsala M, Sulla I, et al. Cauda equina syndrome. Prog Neurobiol 2001; 64: 613-637.

91. Nakai K, Takenobu Y, Takimizu H, Akimaru S, Maegawa H, Ito H, et al. Effects of OP-1206 alpha-CD on walking dysfunction in the rat neuropathic intermittent claudication model: comparison with nifedipine, ticlopidine and cilostazol. Prostaglandins Other Lipid Mediat 2003; 71: 253-263.

92. Murakami M, Takahashi K, Sekikawa T, Yasuhara K, Yamagata M, Moriya H. Effects of intravenous lipoprostaglandin E1 on neurogenic intermittent claudication. J Spinal Disord 1997; 10: 499-504.

93. Konno S, Kayama S, Olmarker K, Kikuchi S. Effects of OP-1206 (prostaglandin E1) on nerve-conduction velocity in the dog cauda equina subjected to acute experimental compression. J Spinal Disord 1996; 9: 103-106.

94. Yamamoto T, Shimoyama N, Asano H, Mizuguchi T. OP-1206, a prostaglandin E1 derivative, attenuates the thermal hyperesthesia induced by constriction injury to the sciatic nerve in the rat. Anesth Analg 1995; 80: 515-520.

95. Yone K, Sakou T, Kawauchi Y. The effect of Lipoprostaglandin E1 on cauda equina blood flow in patients with lumbar spinal canal stenosis: myeloscopic observation. Spinal Cord 1999; 37: 269-274.

96. Nakai K, Takenobu Y, Eguchi K, Takimizu H, Honjo K, Akimaru S, et al. The effects of OP-1206 alpha-CD on walking dysfunction in the rat neuropathic intermittent claudication model. Anesth Analg 2002; 94: 1537-1541.

97. Nakai K, Takenobu Y, Takimizu H, Akimaru S, Ito H, Maegawa H, et al. Effects of orally administered OP-1206 alpha-CD with loxoprofen-Na on walking dysfunction in the rat neuropathic intermittent claudication model. Prostaglandins Leukot Essent Fatty Acids 2003; 69: 269-273.

98. Koes BW, Scholten RJ, Mens JM, Bouter LM. Efficacy of non-steroidal anti-inflammatory drugs for low back pain: a systematic review of randomised clinical trials. Ann Rheum Dis 1997; 56: 214-223.

99. Pohjolainen T, Jekunen A, Autio L, Vuorela H. Treatment of acute low back pain with the COX-2-selective anti-inflammatory drug nimesulide: Results of a randomized, double-blind comparative trial versus ibuprofen. Spine 2000; 25: 1579-1585.

100. van Tulder MW, Scholten RJ, Koes BW, Deyo RA. Nonsteroidal anti-inflammatory drugs for low back pain: a systematic review within the framework of the Cochrane Collaboration Back Review Group. Spine 2000; 25: 2501-2513.

101. Roelofs PD, Deyo RA, Koes BW, Scholten RJ, van Tulder MW. Nonsteroidal anti-inflammatory drugs for low back pain: an updated cochrane review. Spine 2008; 33: 1766-1774.

102. Abram SE, O’Connor TC. Complications associated with epidural steroid injections. Reg Anesth 1996; 21: 149-162.

103. Fukusaki M, Kobayashi I, Hara T, Sumikawa K. Symptoms of spinal stenosis do not improve after epidural steroid injection. Clin J Pain 1998; 14: 148-151.

104. Hirata F, Schiffmann E, Venkatasubramanian K, Salomon D, Axelrod J. A phospholipase A2 inhibitory protein in rabbit neutrophils induced by glucocorticoids. Proc Natl Acad Sci USA 1980; 77: 2533-2536.

105. Tsurufuji S, Sugio K, Takemasa F. The role of glucocorticoid receptor and gene expression in the anti-inflammatory action of dexamethasone. Nature 1979; 280: 408-410.

106. Vane J, Botting R. Inflammation and the mechanism of action of anti-inflammatory drugs. FASEB J 1987; 1: 89-96.

107. Ardoin SP, Sundy JS. Update on nonsteriodal anti-inflammatory drugs. Curr Opin Rheumatol 2006; 18: 221-226.

108. Nakano M, Matsui H, Miaki K, Tsuji H. Postlaminectomy adhesion of the cauda equina: inhibitory effects of anti-inflammatory drugs on cauda equina adhesion in rats. Spine 1998;23: 298-304.

109. MacKay MA, Fischgrund JS, Herkowitz HN, Kurz LT, Hecht B, Schwartz M. The effect of interposition membrane on the outcome of lumbar laminectomy and discectomy. Spine 1995; 20: 1793-1796.

110. Einhaus SL, Robertson JT, Dohan FC Jr, Wujek JR, Ahmad S. Reduction of peridural fibrosis after lumbar laminotomy and discectomy in dogs by a resorbable gel (ADCON-L). Spine 1997; 22: 1440-1447.

111. Sandoval MA, Hernandez-Vaquero D. Preventing peridural fibrosis with nonsteroidal anti-inflammatory drugs. Eur Spine J 2008; 17: 451-455.

112. Jacobs RR, McClain O, Neff J. Control of postlaminectomy scar formation: an experimental and clinical study. Spine 1980; 5: 223-229.

113. DeLong WB, Polissar N, Neradilek B. Timing of surgery in cauda equina syndrome with urinary retention: meta-analysis of observational studies. J Neurosurg Spine 2008; 8: 305-320.

114. Mangialardi R, Mastorillo G, Minoia L, Garofalo R, Conserva F, Solarino GB. Lumbar disc herniation and cauda equina syndrome. Considerations on a pathology with different clinical manifestations. Chir Organi Mov 2002; 87: 35-42.

115. Nielsen B, de Nully M, Schmidt K, Hansen RI. A urodynamic study of cauda equina syndrome due to lumbar disc herniation. Urol Int 1980; 35: 167-170.

116. Hellström P, Kortelainen P, Kontturi M. Late urodynamic findings after surgery for cauda equina syndrome caused by a prolapsed lumbar intervertebral disk. J Urol 1986; 135: 308-312.

117. Ahn UM, Ahn NU, Buchowski JM, Garrett ES, Sieber AN, Kostuik JP. Cauda equina syndrome secondary to lumbar disc herniation: a meta-analysis of surgical outcomes. Spine 2000; 25: 1515-1522.

118. Thongtrangan I, Le H, Park J, Kim DH. Cauda equina syndrome in patients with low lumbar fractures. Neurosurg Focus 2004; 16: e6.

119. Kohles SS, Kohles DA, Karp AP, Erlich VM, Polissar NL. Time-dependent surgical outcomes following cauda equina syndrome diagnosis: comments on a meta-analysis. Spine 2004; 29: 1281-1287.

120. Hussain SA, Gullan RW, Chitnavis BP. Cauda equina syndrome: outcome and implications for management. Br J Neurosurg 2003; 17: 164-167.

121. Qureshi A, Sell P. Cauda equina syndrome treated by surgical decompression: the influence of timing on surgical outcome. Eur Spine J 2007; 16: 2143-2151.

122. Borovich B, Zaaroor M, Gruszkiewicz J. The syndrome of the central L-3-herniated disc with special emphasis on motor involvement. Acta Neurochir (Wien) 1984; 70: 115-125.

123. McCarthy MJ, Aylott CE, Grevitt MP, Hegarty J. Cauda equina syndrome: factors affecting long-term functional and sphincteric outcome. Spine 2007; 32: 207-216.

124. Bartels RH, de Vries J. Hemi-cauda equina syndrome from herniated lumbar disc: a neurosurgical emergency? Can J Neurol Sci 1996: 23; 296-299.

125. Jones DL, Moore T. The types of neuropathic bladder dysfunction associated with prolapsed lumbar intervertebral discs. Br J Urol 1973; 45: 39-43.

126. Foo D, Rossier AB. Preoperative neurological status in predicting surgical outcome of spinal epidural hematomas. Surg Neurol 1981; 15: 389-401.

127. Deyo RA, Cherkin DC, Loeser JD, Biqos SJ, Ciol MA. Morbidity and mortality in association with operations on the lumbar spine. The influence of age, diagnosis, and procedure. J Bone Joint Surg Am 1992; 74: 536-543.

128. Bohlman HH, Kirkpatrick JS, Delamarter RB, Leventhal M. Anterior decompression for late pain and paralysis after fractures of the thoracolumbar spine. Clin Orthop Relat Res 1994; 300: 24-29.

129. Schaeffer HR. Cauda equina compression resulting from massive lumbar disc extrusion. Aust N Z J Surg 1966; 35: 300-306.

  1. Shanghai Scientific and Technological Committee,No. 07JC14072;