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Review
Spinal Surgery

Cauda Equina Syndrome: A review of the current position


RB Dhokia 1*, NW Eames 1

Abstract pattern, with respect to each pair. The most inferior neural
Cauda Equina Syndrome is a rare but serious neurologic element is S5. This sits most posterior and lateral within
condition. It is deemed a surgical emergency. In this article the vertebral canal. Then the next element, S4 sits in a
we provide a comprehensive review of the current more medial position. Each element progressively lies
literature and key concepts to understanding the adjacent medially and anteriorly to its lower neural
pathology. There are also medico legal consequences of the element. At the corresponding vertebral level the neural
residual impairment. element would exit the sac and form the nerve root
respective for that level. The motor fibre components
Introduction (ventral root) are anteromedial, and the larger sensory
Cauda equina syndrome (CES) is a serious neurologic components (dorsal root) are posterolateral within each
condition in which neurological dysfunction affects the neural element4 (Figure 3).

All authors contributed to conception and design, manuscript preparation, read and approved the final manuscript.
lumbar and sacral nerve roots within the vertebral canal.
The term “cauda equina” was first applied by the French Pathophysiology
anatomist Lazarius, 16001. In 1934, Mixter and Barr2 The pathophysiological mechanisms of CES are not
published the first definition of CES in English literature. completely understood. It may result from any lesion
They reported a spectrum of neurological and autonomic affecting the CE nerve roots such as direct mechanical
dysfunction in patients with a lumbar disc prolapse, which compression, inflammation, and venous congestion or
resulted in a severe compression of the cauda equina ischemia.
requiring emergency decompression. CE nerve roots are especially vulnerable to injury of
Recognition of CES is not only important to orthopaedic compressive and tensile stresses. They are autonomic

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and neurosurgeons, but also to primary care practitioners, nerves and have nor schwann cell covering. Parke et al 5
emergency room physicians, physiotherapists and allied suggest there is an area of relative hypovascularity at the
health care professionals involved in management of back proximal portion of the root which is sensitive to
pain. It is an important diagnosis from a clinical and neuroischemic manifestations concurrent with
medico legal perspective. Undiagnosed delays to diagnosis degenerative changes.

Competing interests: None declared. Conflict of interests: None declared.


or a delay in treatment can have a disproportionate medico Delamarter et al6 analyzed evoked potentials and the
legal impact. In this review we discuss the anatomy, clinical pathology of cauda equina nerve root compression. They
diagnosis and management of CES. discovered that mild compression (25%) may not show
signs of neurologic dysfunction, moderate compression
Discussion (50%) may show signs of mild motor weakness with major
Anatomy changes in cortical evoked potentials and severe
The vertebral column consists of 7 cervical, 12 thoracic, 5 constriction (75%) may show signs of significant
lumbar, 5 fused sacral and coccyx bony vertebrae. There weakness, urinary incontinence and signs of complete
are 31 pairs of spinal nerves and roots. In particular, below nerve root atrophy at the level of the constriction. They
the level of the spinal cord there are 5 pairs of lumbar found that chronic severe constriction blocked the
nerve roots, 5 pairs of sacral nerve roots and 1 pair of axoplasmic flow, leading to distal motor Wallerian
coccygeal nerve roots (Figure 1). degeneration and proximal sensory Wallerian
The spinal cord runs within the vertebral canal of the degeneration.
cervical, thoracic and lumbar vertebrae. In adults this
normally terminates at the lower border of the L1 vertebra Aetiology and epidemiology
and continues to descend from the conus medularis as a Any compressive lesion, can lead to CES. The most common
bundle of lumbar and sacral nerve roots. This bundle is cause is disc prolapse. In our practice this is commonly a
collectively termed the cauda equine3 (Figure 2). central disc protrusion at the L5/S1 and L4/5 level.
Orientation of these nerve roots within the vertebral canal However disc prolapse at any lumbar level can cause CES.
is specific and unqiue4. The neural elements are contained Patients may be predisposed to CES if they have a
within the dural sac and are orientated in a symmetrical congenitally narrow spinal canal or have acquired spinal
stenosis.
Various other less common causes of cauda equina
*Corresponding author
syndrome have been reported. We outline in Table 1 the
Email: rakesh@dhokia.com
causes. Examples include spinal injury with fractures or
1
Musgrave Park Hospital, Stockman's La, Belfast BT9 7JB,Ireland subluxation. Spinal neoplasms of metastatic or primary
origin can cause compression, usually accompanied by

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Review

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).

Incidence Figure 1: Cross Section of vertebral canal (plate 170 Atlas of


Following a lumbar disc prolapse Kostuik et al7 report an Human Anatomy, 4th Edition, 2006, Frank H. Netter, Saunders
incidence of between 2-6%. Podnar et al8 reports an Elsevier).
annual incidence rate of 3.4/1.5 million and period
prevalence of 8.9/4.5 per 100,000 population calculated.

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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 al9 reviewed 105 articles and proposed a single

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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

Competing interests: None declared. Conflict of interests: None declared.


deficit in the lower limb (motor/sensory loss,
reflex change).

There is no clear documented evidence about the long Figure 2: Posterior view of cauda equina from (BMJ 2009;
term sequelae of these dysfunctions. This remains a 338 doi: 10.1136/bmj.b936).
problem for the surgeon who needs to provide the patient
with an accurate prognosis and obtain true informed CESI - When the syndrome is incomplete the patient has
consent. urinary difficulties of neurogenic origin including altered
The autonomic dysfunctions may be present in various urinary sensation, loss of desire to void, poor urinary
combinations. The psychosocial aspect or presence of back stream and the need to strain in order to micturate.
pain and other urological dysfunction may inhibit the CESR - The complete syndrome is characterized by
patient to volunteer sexual dysfunction. Micturition painless urinary retention and overflow incontinence,
dysfunction is generally required 10. Saddle anesthesia and when the bladder is no longer under executive control.
urinary retention greater than 500 mL may be the best There is usually extensive or complete saddle and genital
positive predictive indicators for CES11,12,13. There are sensory deficit with deficient trigone sensation.
however no reliable negative markers (Figure 4). It is well established that the outcome for patients with
In 1967, Tandon and Sankaran14 described 3 clinical CESI at the time of surgery is generally favourable,
scenarios for CES: whereas those who have deteriorated to CESR when the
1. Rapid onset without a previous history of back compression is relieved have a poorer prognosis, although
problems. around 70% of CESR patients have a socially acceptable
2. Acute bladder dysfunction with a history of low long term outcome16.
back pain and sciatica. Although the above description is clinically useful, in
3. Chronic backache and sciatica with gradually medico-legal and also clinical terms the important
progressing CES often with canal stenosis. distinction is whether, at any given time, CES is complete
In 2002, Gleave and Macfarlane15 proposed the description or incomplete in relation to urinary function and perineal
of CES into 2 stages.

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sensation14. 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 medication18.

Investigation
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
claustrophobia19. Figure 3: Axial MRI T2 at L3/L4 disc level depicting
Myelography and CT Myelography can be used as an the exiting L3 nerve root with sacral roots lying

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alternative for patients not suitable for MRI but have the posterior in canal.
disadvantage of being invasive techniques. High resolution
fine slice CT maybe used as a non-invasive tool in where
MRI is not possible20. Inflammatory markers and CSF
studies should be performed when an inflammatory or
infectious aetiology is being considered (Figure 5).

Surgery
A variety of techniques have been described for

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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.

Competing interests: None declared. Conflict of interests: None declared.


Figure 4: axial T2 showing CES from large central
disc prolapse.
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 al21 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.
Figure 5: Sagittal T2 showing CES from large One patient was treated via a unilateral microdiscectomy
central disc prolapse at L5/S1. approach. They also reported reasonable results.

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Table: 1 Causes of CES Lesions. excluded non-lumbar disc causes of CES. They
demonstrated no difference between those surgically
Causes Lesions decompressed at 24 and 48 hours. Preoperative chronic
Congenital Spinal dysraphism back pain was associated with poorer outcomes in urinary
Vertebral body malformations and rectal function, and preoperative rectal dysfunction
Dwarfing syndromes
was associated with worsened outcome in urinary
Congenital tumours
continence. In addition, increasing age was associated with
Acquired Trauma Spinal fracture or
dislocation poorer postoperative sexual function. No significant
Infective Bacterial abscess improvement in surgical outcome was identified with
Tuberculosis intervention less than 24 hours from the onset of cauda
Neoplastic Primary tumour equina syndrome compared with patients treated within
Secondary metastases 24-48 hours. Similarly, no difference in outcome occurred
Degenerative Spondylolisthesis in patients treated more than 48 hours after the onset of
Spinal stenosis symptoms. Significant differences, however, were found in
Disc Prolapse resolution of sensory and motor deficits as well as urinary
Inflammatory Rheumatoid arthritis and rectal function in patients treated within 48 hours
Ankyolsing spondylitis compared with those treated more than 48 hours after
onset of symptoms. In 2004 Kohles et al27 challenged the

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Vascular AV malformation
Epidural or subdural meta analysis published by Ahn et al. 2000. The performed
haematoma a critical evaluation of the original data provided. They
Iatrogenic Secondary to surgery highlighted flaws in the study and cited the small sample
size, lacking controls, low statistical power and
The aim of surgery is to safely decompress the nerve roots methodology with an inability to replicate some results.
and cauda equina and should be performed by the surgeon They concluded that an increased risk existed in delaying
in the way they are most comfortable with. surgery from 24 to 48 hours and poorer outcomes were
associated with increasing time.
Timing of surgery In 2005, a meta-analysis by Todd28 specifically examined 1

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The time of decompression for CES is a contentious issue. variable and included studies with their own controls. This
For more than 50 years authors have attempted to make study concluded that bladder function was more likely to
recommendations for critical duration of symptoms and be recovered if decompression was performed before 24
time to surgery. The evidence is weak however the hours instead of the 48 hour time mark.
majority of authors agree that urgent decompression can In 2014 Chau et al29 performed a systematic review of the

Competing interests: None declared. Conflict of interests: None declared.


improve the outcome of CES. We discuss the evolution of clinical literature. They examined the evidence for urgent
published studies and their relative merits for timing on surgical decompression in CES and the much-quoted 48-
decompressive surgery. hour rule. The authors concluded there is significant
In 1959 Shepard23 first presented the notion of early discordance in the literature regarding whether emergency
decompression for CES in 13 patients, but provided no real surgery improves outcomes. There is no strong basis to
patient outcomes. In 1979 Tay and Chacha 24 found no support 48 hours as a blanket safe time point to delay
difference in 8 CES patients who were decompressed surgery. However, it is likely that the earlier the surgical
before and after 48 hours. In 1986 Kostuik and intervention, the more beneficial the effects for
colleagues21 proposed the first perception that CESR was compressed nerves, especially with acute neurological
worse than CESI. They reviewed two groups CESI and CESR compromise.
and found residual bladder dysfunction in 10% of CESI
groups and 50% in CESR group. In 1993 Shapiro25 Prognosis
published the first study that supported surgery before the The evidence also remains weak for symptom duration
48 hours’ time mark having improved outcome. This before surgery and functional recovery.
retrospective review demonstrated all patients that had McCarthy et al30 performed a retrospective cohort study
decompression within 48 hours regained bladder control and found that the symptom duration before operation and
and returned to unassisted ambulation, with 1 patient the speed of onset do not affect the outcome more than 2
having chronic sciatica. Those decompressed after 48 years after surgery.
hours 67% had residual bladder function and 33% Gleave and Macfarlane15,31 retrospectively reviewed 33
returned to unassisted ambulation. This gave rise to the 48 CES cases and found that the duration of bladder paralysis
hour mark. A further study by the same author in 2000 prior to surgery did not influence the outcome.
looked at outcome at one year and showed that those In 2007 Qureshi and Sell32 supported this. They performed
patients decompressed within 48 hours had reduced late a prospective longitudinal inception cohort study of 33
bladder dysfunction and also reduced chronic sciatica with patients. There was no statistically significant difference in
resultant good sexual potency22. In 2000 Ahn et al26 outcome between three groups of patients with respect to
published a landmark meta-analysis of 322 patients. They length of time from symptom onset to surgery- Less than

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24, 24–48 and greater than 48h. A significantly better 5.Parke WW, Gammell K, Rothman RH. Arterial 

outcome was found in patients who were continent of vascularization of the cauda equina. J Bone Joint Surg Am 

urine at presentation compared with those who were 1981; 63: 53-62.
incontinent. The duration of symptoms prior to surgery 6.Delamarter R, Bohlman H, Dodge L, Biro C. Experimental
does not appear to influence the outcome. This finding has lumbar spinal stenosis. Analysis of the cortical evoked
significant implications for the medico-legal sequelae of potentials, microvasculature, and histopathology. The
this condition. The data suggests that the severity of Journal of Bone \& Joint Surgery. 1990;72(1):110--120.
bladder dysfunction at the time of surgery is the dominant 7.Kostuik J. Medicolegal consequences of cauda equina
factor in recovery of bladder function. syndrome: an overview. Neurosurgical focus.
2004;16(6):39--41
Conclusion 8.Podnar S. Epidemiology of cauda equina and conus
The timing of surgery remains a contentious issue and it is medullaris lesions. Muscle Nerve 2007;35:529-31
agreed that early decompressive surgery should be 9.Fraser S, Roberts L, Murphy E. Cauda equina syndrome: a
performed to reduce the risk of long term neurological literature review of its definition and clinical presentation.
dysfunction23. The limitations of reviews being Archives of physical medicine and rehabilitation.
retrospective remain a potential weakness. We accept that 2009;90(11):1964--1968.
a level 1 study in this area would not be ethically approved

All authors contributed to conception and design, manuscript preparation, read and approved the final manuscript.
given the trend of poorer outcomes with delayed surgery. 10.Korse NS, Jacobs WCH, Elzevier HW, Vleggeert-
We also note the practical limitations of performing urgent Lankamp CLAM: Complaints of micturition, defacation and
surgery out of hours with unfamiliar staff. This may sexual function in cauda equina syndrome due to lumbar
potentially increase the risk of morbidity to the patient, disk herniation: a systematic review. Eur Spine J 22:1019-
which would otherwise be avoided if performed at the next 1029, 2013.
available session. 11.Balasubramanian K, Kalsi P, Greenough CG: Kus- koor
We would recommend the definition provided by Fraser et Seetharam MP: Reliability of clinical assess- ment in
al9 for diagnosis of CES. Here one or more of the following diagnosing cauda equina syndrome. Br J Neurosurg
must be present: 24:383-386, 2010.
1. Bladder and/or bowel dysfunction, 12.Domen PM, Hofman PA, van Santbrink H, Weber WE:

All authors abide by the Association for Medical Ethics (AME) ethical rules of disclosure.
2. Reduced sensation in the saddle area, and Predictive value of clinical characteristics in patients with
3. Sexual dysfunction, with possible neurologic suspected cauda equina syndrome. Eur J Neurol 16:416-
deficit in the lower limb (motor/sensory loss, 419, 2009.
reflex change). 13.Shi J, Jia L, Yuan W, Shi G, Ma B, Wang B et al. Clinical
We would recommend the definition provided. We accept classification of cauda equina syndrome for proper

Competing interests: None declared. Conflict of interests: None declared.


there are numerous causes of CES, however degenerative treatment: A retrospective analysis of 39 patients. Acta
disc disease with resultant prolapse remains the most orthopaedica. 2010;81(3):391--395
common cause. 14.Tandon PN, Sankaran B (1967) Cauda equina syndrome
Clear documentation of onset of symptoms is imperative. due to lumbar disc prolapse. Indian J Orthop 1:112–119
There should be particular attention to CESI or CESR. This 15.Gleave JR, Macfarlane R: Cauda equina syndrome: what
is likely to be the dependent factor with respect to the is the relationship between timing of surgery and
patient’s recovery from dysfunction. outcome? Br J Neurosurg 16:325-328, 2002.
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Competing interests: None declared. Conflict of interests: None declared.


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FOR CITATION PURPOSES: Dhokia R, Eames N. Cauda Equina Syndrome: A review of the current position. Hard
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