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. E-mail:email@example.com)
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).
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).
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 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
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, 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 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.
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