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Spinal Surgery
Cauda Equina Syndrome: A review of the current position
RB Dhokia 1*, NW Eames 1
Abstract
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.
Introduction
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, 16001. In 1934, Mixter and Barr2
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.
Discussion
Anatomy
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).
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 equine3 (Figure 2).
Orientation of these nerve roots within the vertebral canal
is specific and unqiue4. The neural elements are contained
within the dural sac and are orientated in a symmetrical
*Corresponding author
Email: rakesh@dhokia.com
1
Musgrave Park Hospital, Stockman's La, Belfast BT9 7JB,Ireland
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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 element4 (Figure 3).
All authors contributed to conception and design, manuscript preparation, read and approved the final manuscript.
Pathophysiology
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
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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.
Competing interests: None declared. Conflict of interests: None declared.
Delamarter et al6 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
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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.

All authors contributed to conception and design, manuscript preparation, read and approved the final manuscript.
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
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 CES11,12,13. There are
however no reliable negative markers (Figure 4).
In 1967, Tandon and Sankaran14 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 Macfarlane15 proposed the description
of CES into 2 stages.
Figure 2: Posterior view of cauda equina from (BMJ 2009;
338 doi: 10.1136/bmj.b936).
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 outcome16.
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

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Review

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

All authors contributed to conception and design, manuscript preparation, read and approved the final manuscript.
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 5: Sagittal T2 showing CES from large
central disc prolapse at L5/S1.
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.
One patient was treated via a unilateral microdiscectomy
approach. They also reported reasonable results.

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Table: 1 Causes of CES Lesions.
Causes Lesions
Congenital Spinal dysraphism
Vertebral body malformations
Dwarfing syndromes
Congenital tumours
Acquired Trauma Spinal fracture or
dislocation
Infective Bacterial abscess
Tuberculosis
Neoplastic Primary tumour
Secondary metastases
Degenerative Spondylolisthesis
Spinal stenosis
Disc Prolapse
Inflammatory Rheumatoid arthritis
Ankyolsing spondylitis
Vascular AV malformation
Epidural or subdural
haematoma
Iatrogenic Secondary to surgery
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 Shepard23 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
colleagues21 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 Shapiro25
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 potency22. In 2000 Ahn et al26
published a landmark meta-analysis of 322 patients. They
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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 al27 challenged the
All authors contributed to conception and design, manuscript preparation, read and approved the final manuscript.
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 Todd28 specifically examined 1
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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 al29 performed a systematic review of the
Competing interests: None declared. Conflict of interests: None declared.
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.
Prognosis
The evidence also remains weak for symptom duration
before surgery and functional recovery.
McCarthy et al30 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 Macfarlane15,31 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 Sell32 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.
Conclusion
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
dysfunction23. 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
al9 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.
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Competing interests: None declared. Conflict of interests: None declared.

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