We recorded compound muscle action potentials (CMAPs) from the diaphragm in 15 normal volunteers, nine patients with lesions of the lower cervical cord (C5 to C8), one completely quadriplegic patient (C6) and seven patients with lesions at a higher cervical level (C1 to C4). Transcranial magnetic stimulation and electrical stimulation of the phrenic nerve were carried out. When the centre of the coil was placed on the interauricular line at a point 3 cm lateral to the vertex on the scalp, the CMAPs from the diaphragm had the largest amplitude and the shortest latency. There was no difference in the mean latency of the CMAPs recorded by transcranial magnetic stimulation in the normal volunteers and in the patients with lesions of the lower cervical cord. In the quadriplegic patient, the latency of the CMAPs was not delayed, but was prolonged in the patients with lesions at a higher level. Those evoked by electrical stimulation of the phrenic nerve were not prolonged in the patients with higher lesions. Our findings suggest that the prolongation of the latency by transcranial magnetic stimulation reflects dysfunction of the higher cervical cord. The combination of transcranial magnetic stimulation and electrical stimulation of the phrenic nerve can detect the precise level of the lesion in the motor tract to the diaphragm

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.

Aims

The aim of this study was to investigate the efficacy of coccygectomy in patients with persistent coccydynia and coccygeal instability.

The aim of this study was to evaluate the feasibility of using the intact S1 nerve root as a donor nerve to repair an avulsion of the contralateral lumbosacral plexus. Two cohorts of patients were recruited. In cohort 1, the L4–S4 nerve roots of 15 patients with a unilateral fracture of the sacrum and sacral nerve injury were stimulated during surgery to establish the precise functional distribution of the S1 nerve root and its proportional contribution to individual muscles. In cohort 2, the contralateral uninjured S1 nerve root of six patients with a unilateral lumbosacral plexus avulsion was transected extradurally and used with a 25 cm segment of the common peroneal nerve from the injured leg to reconstruct the avulsed plexus.

The results from cohort 1 showed that the innervation of S1 in each muscle can be compensated for by L4, L5, S2 and S3. Numbness in the toes and a reduction in strength were found after surgery in cohort 2, but these symptoms gradually disappeared and strength recovered. The results of electrophysiological studies of the donor limb were generally normal.

Severing the S1 nerve root does not appear to damage the healthy limb as far as clinical assessment and electrophysiological testing can determine. Consequently, the S1 nerve can be considered to be a suitable donor nerve for reconstruction of an avulsed contralateral lumbosacral plexus.

Cite this article: Bone Joint J 2015; 97-B:358–65.