A wide variety of pathological lesions may cause spinal cord compression. The clinical presentation sometimes indicates the nature of the causal lesion and usually indicates its anatomical location. With modern imaging techniques, the relevance of making a clinical diagnosis of pathology has diminished but the importance of the anatomical diagnosis to guide the choice of imaging site and modality remains fundamental to management. The important diagnostic aspect of acute spinal cord compression is that it should be recognised as early as possible and be referred with the urgency that the particular case merits. Prompt referral enhances the likelihood of reversing neurological deficits by appropriate decompressive surgery. The prognosis for recovery depends mainly on the severity of the deficit before decompression, but the duration of the deficit and rapidity of its onset may also play a role. Trauma results in a virtually instantaneous onset of compression and in this setting, the benefit of urgent decompressive surgery has not been demonstrated. By contrast, compression of a more gradual onset, for example in infectious or neoplastic cord compression, allows an opportunity for intervention before spinal cord function is lost completely. This window of opportunity may be brief and so deteriorating spinal cord function on serial neurological examinations demands immediate consultation with a specialist unit.

Successful spinal cord decompression means return of normal function in affected limbs and a stable, painless spine.

Generally, this means restoring independent walking, although both patient and surgeon may have to settle for lesser degrees of functional recovery.

Spinal cord compression implies a "structural" lesion of the vertebral column compromising the spinal canal and producing a myelopathy. The signs and symptoms of any spinal cord dysfunction are motor and sensory deficit and reflex changes, but a common feature of "structural" lesions is pain. Spinal pain or nerve root pain, occurring in the presence of myelopathic symptoms, strongly implies a surgically remediable aetiology. Most patients presenting with spinal cord compression reach hospital by referral through their general practitioner or through an accident and emergency department and are usually admitted to general medical or surgical wards. In the early stages abnormal neurological signs may be difficult to detect, especially if these are subtle and the pain is severe. For a variety of reasons, including late self-referral to any medical practitioner, delays can and do occur in the transfer of such a patient to a specialist spinal unit. This was the subject of a candid and disturbing report by Maurice-Williams and Richardson illustrating the diverse causes for delayed referral and its consequences.1

Any surgeon who carries out spinal decompression has experience of patients who are referred having been paraplegic for several days. Surgical treatment is very unlikely to result in a functional recovery when motor power has deteriorated below MRC grade 3 (active movement against gravity). Recognition of signs and symptoms of spinal cord compression may be difficult outside a neuroscience environment and it is important that neurosurgeons, spinal orthopaedic surgeons, and neurologists take the trouble to facilitate referral from physicians and general surgeons at an early stage. This includes an ongoing educational element, of which a most important aspect is to encourage colleagues to recognise the early signs of myelopathy. Easier access to spinal imaging should help.

Diverse factors are taken into consideration when planning surgical management of spinal cord compression including general fitness, life expectancy, tumour pathology, and the extent of any metastatic spread if the lesion is neoplastic. Details of past medical history are thus important information to relay to the specialist unit.

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