cauda equina

1214Chin Med J 2009;122(10):1214-1222 Review article Cauda equina syndrome: a review of clinical progress MA Bin, WU Hong, JIA Lian-shun, YUAN Wen, SHI Guo-dong and SHI Jian-gang Keywords: 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. Chin Med J 2009;122(10):1214-1222 T he 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. EPIDEMIOLOGY 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 PATHOGENESIS 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 DOI: 10.3760/cma.j.issn.0366-6999.2009.10.019 Division of Orthopedics, Orthopedics Institute of PLA, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China (Ma B, Jia LS, Yuan W, Shi GD and Shi JG) Division of Endocrinology, Changhai Hospital, Second Military Medical University, Shanghai 200433, China (Wu H) Correspondence to: Dr. 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. Email: [email protected] Drs. MA Bin and WU Hong contributed equally to this article. This research was supported by a grant from Shanghai Scientific and Technological Committee (No. 07JC14072). Clinical history and physical examination of CES Items Details Medical history Disorders involving the intervertebral discs. Causes of CES Causes Lesions Congenital Spinal dysraphism: spina bifida. All kinds of lesions to the CE may cause CES. magnetic resonance imaging (MRI). and radiologic investigations.28 Tuberculosis. it was usually difficult to assess whether this was of origin or due to other causes such as psychological factors. such as vertebral fractures. epidural abscess. including saddle anesthesia. Of the numerous causes reported. plain myelography. History of a lumbar surgery Chronic low back pain or sciatica. rectal tone. teratoma. primary or metastatic tumors. ranging from minimal to severe Lower extremity motor and/or sensory abnormality: unilateral or bilateral. bowel incontinence. neurofibroma.65 Inflammatory Rheumatoid arthritis66. its initial signs and symptoms are often subtle and may vary in intensity and evolvement according to different etiologies. idiopathic causes. and bulbocavernosus reflex Decreased saddle or perianal sensation or sensory loss Lax anal sphincters: inability to initiatively contract anus and decreased anal tone and sensation when rectal touch Motor and/or sensory weakness of lower extremities. and urodynamic studies should be performed at initial presentation.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). Moreover. depending on level of compression DIAGNOSIS There are no broadly accepted definite diagnostic criteria of CES up to now. such as urinary retention or overflow incontinence. spinal or epidural anaesthesia. Saddle or perianal anesthesia Bladder dysfunction: acute or chronic. Imaging studies Radiologic investigations such as plain radiography. or numbness of the extremities.13. epidermoid. 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.34 Lumbar spinal stenosis35-40 Herniated intervertebral disc /Lumbar disk disease4. vascular problems.9. presented with a hugely distended insensate bladder. the most common one is disc herniation in the lumbar region. and iatrogenic causes (Table 1). Though early diagnosis and treatment are of extremely importance to prevent permanent neurological damage. Assessment of bladder function and perianal sensation is extremely important for the diagnosis and prognosis in those patients in whom CES is suspected. sensory or motor weakness in either of the lower extremities. lumbar spinal stenosis. ankylosing spondylitis. such as incontinence and constipation Sexual impotence or loss of ejaculation or orgasm Physical signs Loss or diminution of reflexes: one or both ankle jerks. . knee extension weakness. schwannoma. meningioma. vertebrae or CE. spinal manipulation.17 In a case-control retrospective analysis. Initial evaluation of urinary retention.32 Degenerative Spondylolisthesis33. recent onset of bladder dysfunction (such as urinary retention or incontinence). anal reflex. Dwarfing syndromes. Morquio′s syndrome. often presents earlier as difficulty in starting or stopping a stream of urine Bowel disturbances. Achilles tendon reflex. such as foot drop. It may also be caused by traumatic injury. patella tendon reflex. Clinical history and physical examination For patients with low-back pain or sciatica. spinal subdural or epidural hematoma.41 Vascular Arteriovenous malformations42 Iatrogenic Secondary to surgery43-51 Spinal or epidural anaesthesia52-55 Spinal manipulation56-58 Lumbar arachnoiditis following radiculogram Neoplastic Primary: ependymoma. and hypothesized that rupture of the posterior internal vertebral venous plexus of Batson plays an important part in the etiology of the idiopathic hematomas. lymphoma59 Secondary metastasis60-63 Endocrine Osteoporotic collapse Biochemical Paget’s disease64.78 Although sexual impotence in the affected males with CES was a significant feature. lumbar spinal stenosis.67 Ankylosing spondylitis68-71 Idiopathic Spontaneous spinal epidural hematoma72 Thrombotic Inferior vena cava thrombosis73 Hemorrhagic Spinal subdural hematoma74-76 Spinal epidural hematoma18 Timely diagnosis of CES requires the evaluation of multiple variables including clinical history. it may be difficult to assess the presence of CES timely. Groen and his group members19 analyzed 199 cases of spontaneous spinal epidural hematoma. the presence of one of the following symptoms.Chinese Medical Journal 2009. tuberculous epidural infections29 Schistosomiasis30 Traumatic Spinal fractures or fracture dislocation31. diastematomyelia Vertebral body malformation: hemivertebra. saddle anesthesia. lumbar disc herniation. Its low morbility attributes to the first reason. physical examination. inferior vena cava thrombosis.5. suggests the diagnosis of CES. and bulbocavernosus reflex is most important according to Della-Giustina. lipoma Acquired Infective Pyogenic or nonpyogenic20-26 Bacterial abscess formation27.122(10):1214-1222 1215 manifestations concurrent with degenerative changes. spondylo-epiphyseal dysplasia Congenital tumors: dermoid. but sometimes normal power examination. Table 1.77 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. Table 2. 81. but it has lot of complications. in which there was an acute onset of bladder dysfunction following a long history of low back pain. Electromyography may reveal the severity and early recovery of CE conduction function. Guillain-Barr syndrome. lumbar disk disorders. loss of desire to void.1. and all the above three appear superior to plain myelography in the diagnosis of intervertebral disc herniation. MRI may be slightly more sensitive than CT and CT myelography. magnetic resonance imaging. Patients with CES were assigned to two stages by Gleave and Macfarlane10 in terms of urinary function: stage I. low back pain. These examinations each have their advantages and disadvantages. though they have roughly equivalent sensitivities and specificities. in which there was a lax anal sphincters and change in sexual function. DIFFERENTIAL DIAGNOSIS CES is often misdiagnosed as other disorders for its symptoms mimic those of other conditions.80 By comparing with the surgically confirmed abnormality. and spinal cord compression.88 patients with CES were assigned to four stages according to electrophysiology and clinical symptoms. Yone et al95 performed myeloscopic examination in . etc. and computed tomography-myelography have equivalent overall sensitivities and diagnostic accuracies. could significantly improve local nerve blood flow and attenuate thermal hyperalgesia induced by nerve constriction injury in rats. intermediate clinical stage.86 and Tay and Chacha79 identify three groups of CES: group I. especially for the return of bladder function. incomplete CES. which is characterized by urinary retention and constipation. spinal cord infections. neoplasms of spinal cord. Yamamoto and his colleagues94 demonstrated that systemic treatment with OP-1206 α-CD. group II. in which there were abrupt. 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. characterized by altered urinary sensation. Myelography was routinely performed before CT and MRI become universally accepted. The presentation of CES resembles that of conus medullaris syndrome. a prostaglandin E1 analogue. Stage I. Urodynamic investigation may be used to assess recovery of bladder function before and following decompression surgery. CES with retention. disk-space narrowing. in which patients had no clinical symptoms while electrophysiology had changed.1216 Chin Med J 2009. Plain radiography is often helpless in detecting the cause of CES but useful in search of destructive changes. more severe symptoms and signs and a slightly poorer prognosis after decompression. infection. Residual urine volume may monitor urinary retention suggesting a neurogenic bladder by catheterization. early clinical stage.89 Other conditions with similar symptoms to CES include peripheral neuropathy. Two main conservative treatments have been reported. such as pain. in which the symptoms arose suddenly without previous history of backache. sensitivities and specificities of CT and MRI appear comparable in the diagnosis of lumbar spinal stenosis.82 Similarly. in which CES arose gradually from a background of chronic low back pain and sciatica. Tandon and Sankaren. So magnetic resonance imaging should be the best initial procedure for patients with suspected CES. stage II. and headache due to hypo-intracranial pressure. advanced clinical stage. and the need to strain in order to micturate. lumbosacral plexopathy. laboratory stage or pre-clinical stage. For some less experienced medical workers. Stage IV. In the study of Shi et al.91-93 In an experimental study.84 MRI also has the advantage of not using ionizing radiation or contrast injection and provides better resolution. and group III. type II was a slower onset. and they are complimentary to some extent. which are anti-inflammatory treatment and vasodilatatory treatment. CLASSIFICATION AND STAGING Several classifications with regard to onset of CES are reported. it is difficult to discriminate CES from conus medullaris syndrome.83 MRI may be most helpful in differentiating recurrent disc herniation from postoperative fibrosis. in which there was a sensory loss and sexual impotence. Stage II. and both are significantly higher than plain myelography. with the exception that symptoms may be asymmetric. in which there was a decreased saddle or perianal sensation.122(10):1214-1222 computed tomography (CT) or computed tomographymyelography 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. however.81.90 Vasodilatatory agents Many studies showed that vasodilatatory agents had a significant therapeutical effect for CES. characterized by prior symptoms for varying time-intervals before the more gradual onset. Computed tomography. characterized by painless urinary retention and overflow incontinence. poor urinary stream. CONSERVATIVE TREATMENT Several therapeutic options are available for patients with CES. 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. spinal cord injuries. Other tests Other tests such as urodynamic investigations and electromyography are also important for the early diagnosis and the assessment of the prognosis. but some have not yet been rigorously tested. or spondylolysis. Stage III. 103 The mechanism of anti-inflammatory properties of steroids includes the inhibition of cytokines. The recommended regimen of dexamethasone is usally an initial dose of 10 mg intravenously. immobilision of spine is the first step. But this view was overthrowed by Kostuik et al.116 In a meta-analysis of surgical outcomes. Disadvantages are reported by Jacobs et al. 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. Some authors suggest decompression be proceeded within 24 hours of presentation. Although most series recommend emergent surgery.77 NSAIDs have been proven useful in prevention of the calcification of the soft tissues. In a recent meta-analysis of the timing of surgery for CES with urinary retention. and the result suggested early surgery for CES. DeLong et al113 reviewed 16 available studies. 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.104.107 In a study of adhesive arachnoiditis in rats.9 also reported reduced chronic sciatica and good sexual potency after early depression within 48 hours. Surgical therapy is somewhat directed at the underlying cause of CES. emergent surgical decompression is recommended for most patients to avoid potential permanent neurological damage. Once CES is diagnosed.43. Shapiro et al4. The authors believed that lipoprostaglandin E1 might enhance blood flow in the CE and improve clinical symptoms in some patients with lumbar spinal stenosis. might be effective in CES patients with inflammatory causes and have been broadly used in treatment of back pain.110 In a recent data in the rabbit model.105 NSAIDs work by inhibiting the enzyme cyclo-oxygenase. Kohles et al119 reported no benefit of an early surgical decompression in less than 24 hours compared with surgery within a period between . the timing of surgery still remains controversial.5 who perfomed a retrospective chart review. except for some late stage patients. especially in the presence of complete perianal anaesthesia and significant sphincter disturbance.106. and dilation of the running blood vessels was observed immediately after the administration of lipoprostaglandin E1 in six of 11 patients. and found that decompression did not have to be performed in less than six hours if recovery was to occur. followed by 4 mg intravenous dose every six hours. SURGICAL TREATMENT Emergency department care Patients who are suspected CES should be treated immediately with a neurologic evaluation. Sandoval et al111 have demonstrated that aceclofenac. including steroids and nonsteroidal anti-inflammatory drugs (NSAIDs). and hydrolysis. surgery is also recommended to be performed within 48 hours of syndrome onset. For CES due to low lumbar injuries. Before the mid-1980s. but no studies have shown significant benefit supporting this over any other regimen. 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. heterotopic ossification and adherence. which is responsible for the synthesis of prostaglandins. 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.98-102 but no evidence suggests that they have shown significant benefit. Timing of surgery Most authors advocate that emergency surgical decompression plays an important role in improving the outcome of CES.112 that the anti-inflammatory drugs may delay healing and frequently result in abscess formation. The regimen of dexamethasone was commonly given intravenously at doses of 4 to 100 mg.78.91-97 Anti-inflammatory agents Anti-inflammatory agents. although decompression should be done as soon as possible to allow maximum recovery. it seems not always the truth that the earlier surgical depression is taken since CES onset the better outcome may be obtained.122(10):1214-1222 1217 patients with lumbar spinal canal stenosis.118 Notwithstanding. For those caused by trauma. Some authors also pointed out the potential risks of steroid use.114 More authors recommend within 48 hours of symptom onset. lipid peroxidation. a kind of NSAIDs. most authors believed that decompression should be carried out within six hours after onset in patients who have an acute cauda-equina lesion.109. 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.Chinese Medical Journal 2009. One possible regimen of steroid may be the dose similar to that for traumatic spinal cord injury. Hellström′s experience suggests that early surgery within 48 hours may improve bladder function and the ability to regain or retain erections. may also be helpful in prevention of the formation of the peridural fibrosis. there is no sufficient evidence on the effectiveness of any form of surgical decompression compared to another.11 drew the conclusion that urgent decompression conferred no benefit when urinary retention with overflow incontinence existed at presentation. and intradural exploration of the nerve roots. Gleave and Macfarlane10. distraction laminoplasty. They even believed that emergent surgery might add to rather than alleviate morbidity when performed under less than optimal conditions. Bladder paralysis in cauda equina lesions from disc . and Low Back Outcome Scores.10. particularly in terms of the recovery of motor function. and he recommended surgical exploration and further decompression in all situations. One patient was treated via a unilateral microdiscectomy approach.126. level of injury as predictors of a poor outcome. However. Kostuik et al5 performed a wide laminectomy and bilateral decompression in the CES patients due to lumbar disc herniation. microdiskectomy. Different modus operandi is applicable for different causes of CES according to history.5. and levels of spinal involvement. 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.121. 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. Hussain et al120 reported on 20 CES patients. The authors concluded that the severity of bladder dysfunction at the time of surgery was the dominant factor in recovery of bladder function. laminectomy. They found a significantly better outcome in patients who were continent of urine at presentation compared with those who were incontinent.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.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-36.124. Gleave and Macfarlane10.123. Hussain et al120 demonstrated no benefit from emergent decompression compared with a more delayed approach.9. and then an aggressive removal of remaining material in the disc space was performed. 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.45 Jensen44 reviewed pertinent literature concerning postoperative CES. PROGNOSIS The prognosis for CES is traditionally considered to be heavily weighted by multiple factors such as etiology. This view was confirmed by a prospective longitudinal inception cohort study of 33 patients performed by Qureshi and Sell. Some researchers claimed no clear correlation between symptom duration before surgery and functional recovery. As a postoperative complication.77. conflicting with those previously addressed.1218 Chin Med J 2009.121-122 In their series of studies. and found that these patients generally had an excellent result.43. The authors emphasized initial urodynamic studies as bladder function assessment in those patients in whom CES was suspected. microscopic decompression. Bohlman128 even reported significant recovery from late surgical decompression performed 11 years following the initial injury. unless there is a lesion such as vertebrae destruction. a few authors argued that no benefit could be obtained from urgent decompression. Ahn et al68 recommended either lumboperitoneal shunting or laminectomy to improve neurologic dysfunction or halt the progression of neurologic deficit.1. It was estimated about 80% of CES patients could make either a complete or a delayed partial recovery. Kennedy et al78 found that no correlation existed between presence of initial motor dysfunction. neurolysis of CE.118 There is much controversy within the literature regarding the urgency of depression and the prognosis. hemisemilaminotomy. neoplasm or large abscess in the anterior spine as well. 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