A Spinal Cord Injury (SCI) is trauma to the spinal cord and a significant cause of disability. In the western world the yearly incidence of disability related to SCI can be estimated at about 5 per 100,000 people.
The causes of spinal cord injury are vehicular (44,8%), falls (21,7%), acts of violence (16%) and sports injuries (13%). The most frequent neurological deficit is incomplete tetraplegia (30,6%), followed by complete paraplegia (25,8%), complete tetraplegia (22,1%), and incomplete paraplegia (19,3%). Since nearly 60% of cases occur in young adults between the ages of 16 to 30 years spinal injury carries a significant cost in terms of lifetime care and loss of productivity.
The cord lesion may result from anatomical disruption, compression, ischaemia, or any combination of these factors. From a practical point of view active compression requiring acute surgery are to be distinguished from spinal injury secondary to contusion or concussion with "restitutio ad integrum" of the spinal axis.
Several clinical syndromes have been described following spinal cord injury: the most severe and the most common is a complete transverse myelopathy with total loss of all motor and sensory functions below the level of injury. Above the C4 level this lesion results in paralysis of the muscles of respiration in addition to quadraplegia.
Incomplete syndromes may be seen less frequently including anterior and central cord syndromes and the Brown-Séquard syndrome. The anterior cord lesion is more prone to develop in the setting of a vascular mediated injujry, the central cord syndrome following hyperextension trauma and the Brown-Séquard syndrome as a result of penetrating injury.
MRI (Fig.1) is advocated as the method of choice in the evaluation of any patient who has a persistent neurological deficit following spinal trauma since it allows direct visualization of the injured cord, bony intervertebral and ligamentous structures, and paraspinal soft tissues. MR has replaced myelography and CT myelography as the primary imaging option available to assess compression of the spinal cord and is also an essential diagnostic modality in cases of SCI without radiographic abnormality.
The depiction of SCI on MRI not only correlates well with the degree of neurological deficit, but also carries significant implications with regard to the prognosis and the potential for neurological recovery. Conventional radiological imaging, supplemented by CT, remains essential in the initial assessment of the damage to the spinal axis.
Spinal cord injuries range from spinal cord simple contusions to contusion with haemorrhagic necrosis. Simple contusions are visible on MRI as a focus of abnormal high signal intensity on T2-weighted images within the substance of the cord. This signal abnormality presumably reflects a focal accumulation of intracellular and interstitial fluid in response to the injury. Definition of this abnormality is usually optimal on the midsagittal long TR image. Axial T2-weighted images offer supplementary information with regard to the involvement of structures in cross-section. Oedema involves a variable length of spinal cord above and below the level of injury, with discrete boundaries adjacent to uninvolved parenchyma. Spinal cord oedema on MRI is invariably associated with some degree of spinal cord swelling. A haemorrhagic contusion is composed of an epicentre of haemorrhage surrounded by a halo of oedema; the latter has a greater rostrocaudal extent than the central haemorrhage. Spinal cord swelling usually involves a slightly larger length of spinal cord than oedema or haemorrhage alone. On MR blood degradation products produce typical paramagnetic signal abnormalities. The detection of a sizable focus of blood (10 mm in length on sagittal images) in the cord is usually indicative of a complete neurological injury at the anatomical location of the haemorrhage and it often implies that there is poor potential for neurological recovery.
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