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Causes and Presentation of Cauda Equina Damage

Severe damage to the cauda equina can occur following high velocity impacts to the lumbosacral spine, as seen following road traffic accidents, falls from great height or from penetrating injuries from gunshot, shrapnel or stabbing. These injuries are likely to be associated with other local and more distant damage to soft tissue and bony structures. In one report it was shown that 85% of the spinal cord damage occurs pre-operatively (all too often at the time of the injury), about 10% in the early post-operative period and the remainder as a late complication. Although these incidents are relatively rare, with increasing numbers and higher velocity of road traffic accidents, together with better emergency treatment, cases of cauda equina injuries are more likely to survive and require long-term care and rehabilitation.

Abnormalities of the cauda equina may be developmental and be evident at birth or even ante-natally. The commonest dysrhaphic anomaly of the lower cord is a tethered conus. The diagnosis is not invariably straightforward although in about 45% of patients there are associated external signs such as a skin dimple, angioma or a hairy patch6. Bladder dysfunction is common. A meningocoele is an extension of the dural sac outside the spinal canal (usually through a posterior defect) and on foetal ultrasound scanning such an abnormality may be seen. Although the diagnosis may be clear there may be very difficult management decisions including the possibility of terminating the pregnancy. Fortunately, these and other congenital causes of cauda equina damage (see Table 1) are rare and their management tends to be referred to dedicated paediatric centres.

Causes of cauda equina damage:

  • Congenital
  • Meningomyelocoele
  • Congenital Dermoid sinus
  • Congenital Midline Tumours: dermoid, epidermoid, teratoma, lipoma
  • Acquired
  • Infectious: Neurosarcoidosis, Schistosomiasis, Abscess formation
  • Traumatic: Road traffic accident, Fall from height, Penetrating injuries – gunshot, stabbing
  • Degenerative: Central disc prolapse
  • Neoplastic: Primary – Ependymoma, Neurofibroma, Meningioma, Secondary metastasis
  • Vascular: Arteriovenous malformations
  • Iatrogenic: Anaesthetic, Orthopaedic and Neurosurgical procedures, Lumbar arachnoiditis following radiculogram

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  • Investigation of Cauda Equina Damage

    Investigations are carried out to make a diagnosis, plan therapeutic intervention or follow progression and allow a prognosis to be made. Cauda equina lesions give rise to bladder, bowel, sexual and somatic dysfunction and the investigation of these is best carried out in a combined pelvic function laboratory.

  • Radiological Investigations

    A plain X-ray of the spine is almost invariably carried out in the initial investigation of cauda equina lesions although most useful information is obtained from computed tomography (CT) or magnetic resonance imaging (MRI). Excellent images of tissue contrast and discrete spatial resolution can be rapidly obtained non-invasively and it is possible to carry out three-dimensional reconstructions. Where AVMs are suspected, selective spinal angiography is helpful both in confirming the diagnosis and planning interventional radiological therapeutic strategies such as embolisation of fistulae. The features of relevance is to know the origin of the AVM, the number of feeding vessels and to find the exact location of the AVM with respect to the spinal cord. Successful selective embolisation has avoided open surgical intervention in some cases of spinal AVMs presenting with Cauda Equina Syndrome.

  • Urological Investigations

    The predominant urological symptom in patients with cauda equina lesions is of voiding difficulty. Patients report reduced flow, double and incomplete voiding and in severe cases complete retention with overflow incontinence. These symptoms can be investigated by a flow rate, measure of residual volume and cystometry. Patients with solitary cauda equina damage commonly demonstrate reduced urinary flowrate and incomplete voiding.

    Assessment of the detrusor muscle by cystometry may show a trace typical of the areflexic bladder which has previously been reported in cauda equina lesions. There are, however, also reports of hyperreflexic cystometric findings following cauda equina damage. Possible mechanisms for this might include a direct and additional higher cord pathology such that a large tumour of the cauda may extend upwards to cause unexpected cystometric findings or there may be secondary ischaemic damage to the cord at a higher level following a primary lesion affecting the cauda.

    Additional information about the sphincter mechanism may be obtained if cystometry is combined with fluoroscopic examination of the bladder. Most studies confirm an incompetent bladder neck although it is not an universal finding in cauda equina lesions and the degree of incompetence may not correlate with the level of nerve injury. Stress incontinence from bladder neck incompetence is a particularly troublesome symptom and when it occurs in men is almost always associated with a lower motor neurone injury.

  • Colo-rectal Investigations

    Colo-rectal Investigations Patients with cauda equina lesions may have troublesome bowel symptoms. Typically they have an atonic bowel and are liable to severe and chronic constipation although they may get occasional overflow faecal incontinence. It is thought this may be as a result of parasympathetic denervation of the sigmoid and rectum. Incontinence to faeces and flatus may also result from a denervated anal sphincter. Anatomical and functional investigations of colo-rectal disturbances may be helpful. Barium studies and colonoscopy can provide useful anatomical information. Functional studies include anorectal manometry and defecography, which may be performed in specialised combined pelvic function laboratories.

  • Investigation of Sexual Dysfunction

    In cases of cauda equina damage there is rarely a need to perform specific tests of sexual function. However, it is important to clearly document all symptoms reported by the patient. Men may volunteer their loss of erectile function while women may be more reluctant to report their symptoms. At a later date this documentation may be required for medico-legal purposes.

    In men, it is important to demonstrate that pharmacologically induced erection is possible (with intracavernous injection or transurethral application of prostaglandin E1). This rules out a vascular cause for the underlying pathology and can also be used as a useful therapeutic intervention. The introduction of sildenafil citrate (Viagra) has been a significant advance not only in developing a new pharmacological agent to aid male erectile dysfunction but also to publicise sexual dysfunction in general. This is helping initiate studies of the management of female sexual disorders and there are clinical trials being carried out to establish if Viagra may be of benefit to women. The impact of sexual dysfunction on the quality of everyday life is unknown. Questionnaires are being validated that may become important tools in the assessment of sexual dysfunction in the future. As the therapeutic options increase with the development of safe and efficacious oral treatment, there is clearly an urgent need for tools which may help the clinician establish the burden of sexual dysfunction in both men and women.

    Neurophysiological Investigations Various neurophysiological techniques may be used to demonstrate the root damage that occurs with a cauda equina lesion.

  • Management of Cauda Equina Damage

    A wide range of conditions can give rise to cauda equina damage and the management reflects the underlying pathology. However, there are general principles that can be followed. An accurate assessment, reliant on history, examination, investigation and special reports from personnel involved in the continuing care of the patient are very necessary. The immediate management of acutely injured distal spinal cord will often require orthopaedic or neurosurgical intervention. Instability of the spine must be accurately identified and promptly stabilised. Root compression must be relieved and there is considerable debate (and medico-legal interest) about the expediency with which such surgical decompression is carried out. During the period of spinal shock an indwelling catheter should drain the bladder and clean intermittent self-catheterisation can be introduced later.

    Cauda equina damage from an acute compressive lesion raises two important issues – is it the degree or duration of compression that is clinically important? The classical teaching has always maintained that immediate decompression is vital for recovery. There have been two important animal studies that have examined the problem. In female beagle hounds, Bodner demonstrated that neurological function evaluated by cystometry (CMG), cortical evoked potentials (CEP) and histology was dependent on the degree of compression of the cauda equina. 25% compression resulted in minimal change to the CMG and an increase in the CEP mean latency of only 3.2%. However with 75% compression, the CMG trace was a flat line, hallmark of an atonic bladder from lower motor neurone damage, and there was a 17.2% increase in the mean CEP latency.

    Delamarter, using a similar animal model for Cauda Equina Syndrome, studied neurological recovery following immediate, early and late decompression following 75% compression to the cauda equina. Following compression, all the animals had significant lower extremity weakness, tail paralysis and urinary incontinence. However, there was no statistically significant difference in recovery between the immediate, early or late decompression groups. This information may be helpful in the consent of the patient prior to surgical intervention and may explain the residual neurological deficit following early decompression.

    Delamarter, using a similar animal model for Cauda Equina Syndrome, studied neurological recovery following immediate, early and late decompression following 75% compression to the cauda equina. Following compression, all the animals had significant lower extremity weakness, tail paralysis and urinary incontinence. However, there was no statistically significant difference in recovery between the immediate, early or late decompression groups. This information may be helpful in the consent of the patient prior to surgical intervention and may explain the residual neurological deficit following early decompression.