This review provides a concise outline of the advances made in the care of patients and to the quality of life after a traumatic spinal cord injury (SCI) over the last century. Despite these improvements reversal of the neurological injury is not yet possible. Instead, current treatment is limited to providing symptomatic relief, avoiding secondary insults and preventing additional sequelae. However, with an ever-advancing technology and deeper understanding of the damaged spinal cord, this appears increasingly conceivable. A brief synopsis of the most prominent challenges facing both clinicians and research scientists in developing functional treatments for a progressively complex injury are presented. Moreover, the multiple mechanisms by which damage propagates many months after the original injury requires a multifaceted approach to ameliorate the human spinal cord. We discuss potential methods to protect the spinal cord from damage, and to manipulate the inherent inhibition of the spinal cord to regeneration and repair. Although acute and chronic SCI share common final pathways resulting in cell death and neurological deficits, the underlying putative mechanisms of chronic SCI and the treatments are not covered in this review.

Introduction Charcot arthropathy is a well recognised complication in denervated synovial joints. This is a late complication of traumatic spinal cord injury that is rarely reported in the literature. Early recognition is important and can be difficult as the clinical presentation can vary from pain, deformity, autonomic dysreflexia and audible noises with motion. Methods We present 5 cases of Charcot’s arthropathy of the spine in patients with in patients with traumatic paraplegia. All patients had spinal surgery to stabilise the spine shortly after the acute injury. Results The average time from initial injury to presentation with Charcot’s arthropathy was 27 years (range 10–41). A combination of localised and neuropathic pain was the dominant symptom (4 patients) causing re-presentation, but other symptoms included deformity (1 patient). The level of the initial spinal cord injury was at the thoracolumbar junction patients. The Charcot joint level was usually 1 to 2 segments caudal to the spinal fusion. The features noted on plain radiology were destructive changes of the endplate in 4 patients and deformity in 1. With one exception, all patients went on to have MRI to exclude infection and subsequently all were surgically stabilised. All patients were treated surgically. One had an anterior approach, one had posterior approach and one had staged anterior and posterior approaches. The remaining two had anterior and posterior stabilisation through a lateral extra-cavitary approach. At an average follow-up of 36 months all patients reported good relief of their symptoms, and had returned to their best function post-injury. Discussion Surgical stabilisation in this series yielded very good results. We observed a wide variation in presenting symptoms and therefore would indicate that a high index of suspicion is required. We believe that MRI is mandatory to exclude infection and would advocate early stabilisation. The lateral extra-cavitary approach allows posterior and anterior stabilisation in a single procedure and in now the preferred method in our institution. As patients with spinal cord injuries live increasingly active lives, this problem will be seen more frequently

Aims

To report the outcome of spinal deformity correction through anterior spinal fusion in wheelchair-bound patients with myelomeningocele.