Treating cauda equina syndrome

Miss Suneeta Kochhar and Mr Sudhir Rao discuss how to identify and manage cauda equina syndrome.

Cauda equina syndrome (CES) is a neurological disorder characterised by low back pain, saddle paraesthesia, bladder and/or bowel dysfunction, with motor and sensory deficits in the lower limbs.

It is the result of compression or inflammation of the bundle of nerve roots at the base of the spine, known as the cauda equina. This contains nerves that travel to the feet and lower body.

Any lesion that compresses these nerves can cause CES. The lesion may be malignant, infective or related to trauma, sarcoidosis or disease of the intervertebral discs.

CES is an uncommon syndrome that affects all races and both sexes equally. It is associated with high levels of morbidity including pressure sores, UTIs and DVT.

CES may be caused by trauma resulting in fracture, subluxation or penetrating injury. It is sometimes an early sign of lumbar disc herniation, usually at L4/5 or L5/S1.

However, in cases of herniation there is typically chronic lower back pain first.

Compression of the spinal cord producing CES may be caused by primary or metastatic neoplasms. Primary tumours include neoplasms of the marrow, especially multiple myeloma, or tumours of the bone or spinal cartilage.

These neoplasms usually produce progressive back pain that is most severe at night.

Multiple myeloma is the most common primary malignancy of the bone in adults. The condition is very rare in people younger than 40 years, and back pain is the presenting symptom in 35 per cent of cases.

Metastatic spinal disease is 25 times more common than primary tumours. The most common cancers to metastasise to the spine include cancers of the breasts, lungs and kidneys.

Back pain is the presenting symptom in 90 per cent of patients who have spinal metastasis and new back pain should be assumed to have neoplastic origin in any patient who has a history of cancer or unexplained weight loss.

Frequently, early metastasis is not visualised on plain radiographs, although bone scan findings are positive in 85 per cent of patients.

A detailed history of back pain should be taken from any patient with symptoms of CES.

New onset of back pain in an older patient may be significant, and it is important to enquire about weight loss, previous malignancy, metabolic bone disease and any susceptibility to infection. Night pain should be considered and a history of abnormalities in sensation including saddle anaesthesia and motor function should be elicited.

Faecal or urinary incontinence should be established. The patient may report a difference in feeling when wiping after a bowel movement. Clinical examination may reveal tenderness over the back and legs.

Sensory disturbances should be looked for, this includes loss of perianal sensation. Muscle weakness may be elicited and this would correspond to affected nerve roots. Anal sphincter tone should be checked. Usually there is a loss or reduction of reflexes. Hyperreflexia may suggest spinal cord involvement.

Bladder function may be assessed by urinary catheterisation. If a significant volume is measured with no urge to void this may be suggestive of bladder dysfunction.

It is important to exclude a pulsatile abdominal mass, establish whether the patient is febrile and test for any neurological deficit that cannot be explained by nerve compression.

In many cases of CES, blood tests will not identify any abnormality. ESR is usually elevated in metastatic disease and also in infectious disorders of the spine such as osteomyelitis, discitis and epidural abscess.

The ESR may also provide a clue as to the inflammatory nature of the complaint in auto-inflammatory diseases, for example ankylosing spondylitis.

MRI is the gold standard for the initial evaluation of patients with CES. CT scanning should be used in patients with contraindications to MRI.

If CES is suspected an urgent orthopaedic or neurosurgical opinion should be sought. If treatment is delayed motor and sensory deficits, incontinence and impotence may become permanent.

Treatment is related to the underlying aetiology, for example radiotherapy may be appropriate for neoplastic lesions. Some advocate the use of steroids to potentially reduce oedema around nerve root segments.

Miss Kochhar is an SHO and Mr Rao is consultant orthopaedic surgeon at Queen Mary's Hospital, Sidcup, Kent.

  • Low back pain
  • Sciatica
  • Saddle paraesthesia
  • Bowel and bladder disturbances
  • Lower extremity muscle weakness and loss of sensation
  • Reduced or absent lower extremity reflexes

Further reading
- Ahn U, Ahn N, Buchowski J, Garrett E, Sieber A, Kostuik J. Cauda equina syndrome secondary to lumbar disc herniation, meta-analysis of surgical outcomes. Spine 2000; 25: 1,515-22.

- Cohen D. Infectious origins of cauda equina syndrome. Neurosurg Focus 2004; 16 (6): e2.

- Harrop J, Hunt G, Vaccaro A. Conus medullaris and cauda equina syndrome as a result of traumatic injuries: management principles. Neurosurg Focus 2004; 16 (6): e4.

- McCarthy M, Aylott C, Grevitt M, Hegarty J. Cauda equina syndrome: factors affecting long-term functional and sphincteric outcome. Spine 2007; 32(2): 207-16.

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