For citation purposes: Dhokia R, Eames N. Cauda Equina Syndrome: A review of the current position. Hard Tissue 2014 Apr 18;3(1):7.


Spinal Surgery

Cauda Equina Syndrome: A review of the current position.

R Dhokia 1*, N Eames 1

Authors affiliations

(1) Musgrave Park Hospital, Stockman's La, Belfast BT9 7JB,Ireland

(2) Musgrave Park Hospital, Stockman's La, Belfast BT9 7JB,Ireland

* Corresponding author Email:


Cauda Equina Syndrome is a rare but serious neurologic condition. It is deemed a surgical emergency. In this article we provide a comprehensive review of the current literature and key concepts to understanding the pathology. There are also medico legal consequences of the residual impairment.


Cauda equina syndrome (CES) is a serious neurologic condition in which neurological dysfunction affects the lumbar and sacral nerve roots within the vertebral canal.

The term “cauda equina” was first applied by the French anatomist Lazarius,1600[1]. In 1934, Mixter and Barr[2] published the first definition of CES in English literature. They reported a spectrum of neurological and autonomic dysfunction in patients with a lumbar disc prolapse, which resulted in a severe compression of the cauda equina requiring emergency decompression.

Recognition of CES is not only important to orthopaedic and neurosurgeons, but also to primary care practitioners, emergency room physicians, physiotherapists and allied health care professionals involved in management of back pain. It is an important diagnosis from a clinical and medico legal perspective. Undiagnosed delays to diagnosis or a delay in treatment can have a disproportionate medico legal impact.

In this review we discuss the anatomy, clinical diagnosis and management of CES.



The vertebral column consists of 7 cervical, 12 thoracic, 5 lumbar, 5 fused sacral and coccyx bony vertebrae. There are 31 pairs of spinal nerves and roots. In particular, below the level of the spinal cord there are 5 pairs of lumbar nerve roots, 5 pairs of sacral nerve roots and 1 pair of coccygeal nerve roots (Figure 1).

Cross Section of vertebral canal (plate 170 Atlas of Human Anatomy, 4th Edition, 2006, Frank H. Netter, Saunders Elsevier)

The spinal cord runs within the vertebral canal of the cervical, thoracic and lumbar vertebrae. In adults this normally terminates at the lower border of the L1 vertebra and continues to descend from the conus medularis as a bundle of lumbar and sacral nerve roots. This bundle is collectively termed the cauda equine[3] (Figure 2).

Posterior view of cauda equina from (BMJ 2009; 338 doi: 10.1136/bmj.b936)

Orientation of these nerve roots within the vertebral canal is specific and unqiue[4]. The neural elements are contained within the dural sac and are orientated in a symmetrical pattern, with respect to each pair. The most inferior neural element is S5. This sits most posterior and lateral within the vertebral canal. Then the next element, S4 sits in a more medial position. Each element progressively lies adjacent medially and anteriorly to its lower neural element. At the corresponding vertebral level the neural element would exit the sac and form the nerve root respective for that level. The motor fibre components (ventral root) are anteromedial, and the larger sensory components (dorsal root) are posterolateral within each neural element[4] (Figure 3).

Axial MRI T2 at L3/L4 disc level depicting the exiting L3 nerve root with sacral roots lying posterior in canal



The pathophysiological mechanisms of CES are not completely understood. It may result from any lesion affecting the 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. They are autonomic nerves and have nor schwann cell covering. Parke et al[5] suggest there is an area of relative hypovascularity at the proximal portion of the root which is sensitive to neuroischemic manifestations concurrent with degenerative changes.

Delamarter et al[6] analyzed evoked potentials and the pathology of cauda equina nerve root compression. They discovered that mild compression (25%) may not show signs of neurologic dysfunction, moderate compression (50%) may show signs of mild motor weakness with major changes in cortical evoked potentials and severe constriction (75%) may show signs of significant weakness, urinary incontinence and signs of complete nerve root atrophy at the level of the constriction. They found that chronic severe constriction blocked the axoplasmic flow, leading to distal motor Wallerian degeneration and proximal sensory Wallerian degeneration.

Aetiology and epidemiology

Any compressive lesion, can lead to CES. The most common cause is disc prolapse. In our practice this is commonly a central disc protrusion at the L5/S1 and L4/5 level. However disc prolapse at any lumbar level can cause CES.

Patients may be predisposed to CES if they have a congenitally narrow spinal canal or have acquired spinal stenosis.

Various other less common causes of cauda equina syndrome have been reported. We outline in Table 1 the causes. Examples include spinal injury with fractures or subluxation. Spinal neoplasms of metastatic or primary origin can cause compression, usually accompanied by non-mechanical pain and pronounced neurological. Infective causes with abscess formation or bony involvement, either within the spinal canal or impinging on it, may also cause cauda equina syndrome. The spine is the most commonly affected skeletal site for tuberculosis, and Pott’s paralysis is documented.

A wide range of iatrogenic causes are reported, including manipulation, spinal anaesthesia, postoperative complications such as haematoma or recurrent disc protrusions. Other space-occupying lesions, such as nerve derived tumours, schwannomas, ependymomas and facet joint cysts are also recognized (Table 1).

Table 1

Causes of CES Lesions


Following a lumbar disc prolapse Kostuik et al7 report an incidence of between 2-6%. Podnar et al[8] reports an annual incidence rate of 3.4/1.5 million and period prevalence of 8.9/4.5 per 100,000 population calculated.

Diagnosis: History and Clinical Examination

There are no accepted criteria in the literature defining CES. Timely diagnosis and prompt treatment are however widely accepted. CES is a clinical diagnosis from the patient history and physical examination. Radiographic studies serve to confirm the diagnosis and define the pathological level of the lesion.

Fraser et al[9] reviewed 105 articles and proposed a single definition. For a diagnosis of CES, one or more of the following must be present:

(1) bladder and/or bowel dysfunction,

(2) reduced sensation in the saddle area, and

(3) sexual dysfunction, with possible neurologic deficit in the lower limb (motor/sensory loss, reflex change).

There is no clear documented evidence about the long term sequelae of these dysfunctions. This remains a problem for the surgeon who needs to provide the patient with an accurate prognosis and obtain true informed consent.

The autonomic dysfunctions may be present in various combinations. The psychosocial aspect or presence of back pain and other urological dysfunction may inhibit the patient to volunteer sexual dysfunction. Micturition dysfunction is generally required [10]. Saddle anesthesia and urinary retention greater than 500 mL may be the best positive predictive indicators for CES[11,12,13]. There are however no reliable negative markers (Figure 4).

axial T2 showing CES from large central disc prolapse.

In 1967, Tandon and Sankaran[14] described 3 clinical scenarios for CES:

1.Rapid onset without a previous history of back problems.

2.Acute bladder dysfunction with a history of low back pain and sciatica.

3.Chronic backache and sciatica with gradually progressing CES often with canal stenosis.

In 2002, Gleave and Macfarlane[15] proposed the description of CES into 2 stages.

CESI - When the syndrome is incomplete the patient has urinary difficulties of neurogenic origin including altered urinary sensation, loss of desire to void, poor urinary stream and the need to strain in order to micturate.

CESR - The complete syndrome is characterized by painless urinary retention and overflow incontinence, when the bladder is no longer under executive control. There is usually extensive or complete saddle and genital sensory deficit with deficient trigone sensation.

It is well established that the outcome for patients with CESI at the time of surgery is generally favourable, whereas those who have deteriorated to CESR when the compression is relieved have a poorer prognosis, although around 70% of CESR patients have a socially acceptable long term outcome[16].

Although the above description is clinically useful, in medico-legal and also clinical terms the important distinction is whether, at any given time, CES is complete or incomplete in relation to urinary function and perineal sensation[14]. A useful test, not generally described, is to test the bulbocavernous reflex. In this test for trigone sensitivity an inflated Foley catheter is gently pulled with the patient unaware [17]. This should produce the urge to micturate. This will help to distinguish patients with a genuine neurological deficit from those who have purely pain related retention, which is not uncommon as is retention as a result of constipation or medication[18].


Plain radiography has limited role in confirming CES. The accepted gold standard is Magnetic Resonance Imaging (MRI). This clearly depicts the patients soft tissue pathology and delineates the level. Disadvantages include difficulties accessing availability and contraindications such as pacemakers and poor patient tolerance due to claustrophobia[19].

Myelography and CT Myelography can be used as an alternative for patients not suitable for MRI but have the disadvantage of being invasive techniques. High resolution fine slice CT maybe used as a non-invasive tool in where MRI is not possible[20]. Inflammatory markers and CSF studies should be performed when an inflammatory or infectious aetiology is being considered (Figure 5).

Sagittal T2 showing CES from large central disc prolapse at L5/S1.


A variety of techniques have been described for decompression in CES. Most procedures for lumbar disc prolapse will entail posterior decompression but in cases where tumour or infection causes anterior spinal column pathology anterior surgery may be required.

Posterior approaches available to the surgeon are unilateral, bilateral or wide central flavotomy. These can be performed open, mini or microscopically. The surgeon can remain in the interlaminar space. However for greater exposure, particularly at higher lumbar levels, the addition of laminotomy or laminectomy are used to access the vertebral canal.

There is not sufficient evidence comparing one approach to the other. Kostuik et al[21] 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. Shapiro et al[22] performed 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. They also reported reasonable results.

The aim of surgery is to safely decompress the nerve roots and cauda equina and should be performed by the surgeon in the way they are most comfortable with.

Timing of surgery

The time of decompression for CES is a contentious issue. For more than 50 years authors have attempted to make recommendations for critical duration of symptoms and time to surgery. The evidence is weak however the majority of authors agree that urgent decompression can improve the outcome of CES. We discuss the evolution of published studies and their relative merits for timing on decompressive surgery.

In 1959 Shepard[23] first presented the notion of early decompression for CES in 13 patients, but provided no real patient outcomes. In 1979 Tay and Chacha[24] found no difference in 8 CES patients who were decompressed before and after 48 hours. In 1986 Kostuik and colleagues[21] proposed the first perception that CESR was worse than CESI. They reviewed two groups CESI and CESR and found residual bladder dysfunction in 10% of CESI groups and 50% in CESR group. In 1993 Shapiro[25] published the first study that supported surgery before the 48 hours time mark having improved outcome. This retrospective review demonstrated all patients that had decompression within 48 hours regained bladder control and returned to unassisted ambulation, with 1 patient having chronic sciatica. Those decompressed after 48 hours 67% had residual bladder function and 33% returned to unassisted ambulation. This gave rise to the 48 hour mark. A further study by the same author in 2000 looked at outcome at one year and showed that those patients decompressed within 48 hours had reduced late bladder dysfunction and also reduced chronic sciatica with resultant good sexual potency[22].

In 2000 Ahn et al[26] published a landmark meta-analysis of 322 patients. They excluded non-lumbar disc causes of CES. They demonstrated no difference between those surgically decompressed at 24 and 48 hours. Preoperative chronic back pain was associated with poorer outcomes in urinary and rectal function, and preoperative rectal dysfunction was associated with worsened outcome in urinary continence. In addition, increasing age was associated with poorer postoperative sexual function. No significant improvement in surgical outcome was identified with intervention less than 24 hours from the onset of cauda equina syndrome compared with patients treated within 24-48 hours. Similarly, no difference in outcome occurred in patients treated more than 48 hours after the onset of symptoms. Significant differences, however, were found in resolution of sensory and motor deficits as well as urinary and rectal function in patients treated within 48 hours compared with those treated more than 48 hours after onset of symptoms. In 2004 Kohles et al[27] challenged the meta analysis published by Ahn et al. 2000. The performed a critical evaluation of the original data provided. They highlighted flaws in the study and cited the small sample size, lacking controls, low statistical power and methodology with an inability to replicate some results. They concluded that an increased risk existed in delaying surgery from 24 to 48 hours and poorer outcomes were associated with increasing time.

In 2005, a meta-analysis by Todd[28] specifically examined 1 variable and included studies with their own controls. This study concluded that bladder function was more likely to be recovered if decompression was performed before 24 hours instead of the 48 hour time mark.

In 2014 Chau et al[29] performed a systematic review of the clinical literature. They examined the evidence for urgent surgical decompression in CES and the much-quoted 48-hour rule. The authors concluded there is significant discordance in the literature regarding whether emergency surgery improves outcomes. There is no strong basis to support 48 hours as a blanket safe time point to delay surgery. However, it is likely that the earlier the surgical intervention, the more beneficial the effects for compressed nerves, especially with acute neurological compromise.


The evidence also remains weak for symptom duration before surgery and functional recovery.

McCarthy et al[30] 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 Macfarlane[15,31] retrospectively reviewed 33 CES cases and found that the duration of bladder paralysis prior to surgery did not influence the outcome.

In 2007 Qureshi and Sell[32] supported this. They performed a prospective longitudinal inception cohort study of 33 patients. There was no statistically significant difference in outcome between three groups of patients with respect to length of time from symptom onset to surgery- Less than 24, 24–48 and greater than 48h. A significantly better outcome was found in patients who were continent of urine at presentation compared with those who were incontinent. The duration of symptoms prior to surgery does not appear to influence the outcome. This finding has significant implications for the medico-legal sequelae of this condition. The data suggests that the severity of bladder dysfunction at the time of surgery is the dominant factor in recovery of bladder function.


The timing of surgery remains a contentious issue and it is agreed that early decompressive surgery should be performed to reduce the risk of long term neurological dysfunction[23]. The limitations of reviews being retrospective remain a potential weakness. We accept that a level 1 study in this area would not be ethically approved given the trend of poorer outcomes with delayed surgery. We also note the practical limitations of performing urgent surgery out of hours with unfamiliar staff. This may potentially increase the risk of morbidity to the patient, which would otherwise be avoided if performed at the next available session.

We would recommend the definition provided by Fraser et al[9] for diagnosis of CES. Here one or more of the following must be present:

(1) bladder and/or bowel dysfunction,

(2) reduced sensation in the saddle area, and

(3) sexual dysfunction, with possible neurologic deficit in the lower limb (motor/sensory loss, reflex change).

We would recommend the definition provided

We accept there are numerous causes of CES, however degenerative disc disease with resultant prolapse remains the most common cause.

Clear documentation of onset of symptoms is imperative. There should be particular attention to CESI or CESR. This is likely to be the dependent factor with respect to the patient’s recovery from dysfunction.

Whilst there remains weak evidence for the time of decompression we would advocate surgery as early as possible, at a reasonable time (NCEPOD), for improved chance of recovery.

Conflict of interests

None declared.

Competing interests

None declared


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    Causes of CES Lesions




    Spinal dysraphism

    Vertebral body malformations

    Dwarfing syndromes

    Congenital tumours



    Spinal fracture or dislocation


    Bacterial abscess



    Primary tumour

    Secondary metastases



    Spinal stenosis

    Disc Prolapse


    Rheumatoid arthritis

    Ankyolsing spondylitis


    AV malformation

    Epidural or subdural haematoma


    Secondary to surgery