INTRODUCTION

Louis-Antoine Ranvier first described myelin in 1878 (Ranvier, 1878); however it was not until 1928 that del Rio Hortega described the oligodendrocyte – the myelin-forming cell of the CNS (Hortega, 1928). Myelin pathology present in spinal cord injury was first mentioned in 1907 (Holmes, 1907) and had become more widely recognized by the 1960s (Bunge et al., 1960). Today the oligodendrocyte with its compact and non-compact myelin components has become an avidly pursued therapeutic target, yet our understanding of the physical and functional changes in the oligodendrocyte myelin with injury are relatively understudied and misunderstood.

Spinal cord injury (SCI) is a devastating condition currently affecting 250 000 people in the United States, with 11 000 new cases recorded each year (2005). SCI is a complex neurological disorder with varied pathological patterns. The majority of injuries result in permanent anatomical and functional deficits. The most frequent type of injury – contusion injuries in the cervical and thoracic regions – is caused by a bone or disk displacement into the spinal cord due to bone dislodgement or fracture of the spinal column (Rothman and Simeone, 1992). Few injuries are caused by laceration or transection of the spinal cord. Contusion injury is typified by a necrotic core or cavity, which is partly surrounded by a rim of remaining white matter containing spared descending and ascending axons (Balentine, 1978a; Blight, 1983). SCI results in a loss of function due to the disruption of sensory and motor pathways and glial cell support.