Schwannosis: Role of gliosis and proteoglycan in human spinal cord injury

Schwannosis (aberrant proliferation of Schwann cells and nerve fibers) has been reported following spinal cord injury (SCI). In this study, we examine d the incidence of schwannosis following human SCI, and investigated its re lationship to gliosis. We found evidence of schwannosis in 32 out of 65 cas es (48%) of human SCI that survived 24 h to 24 years after injury; this inc idence rose to 82% in those patients who survived for more than 4 months. S chwannosis was not observed in cases that survived less than 4 months after injury. In affected cases, it was generally noted in areas that had low im munoreactivity for glial fibrillary acidic protein (GFAP), suggesting that reduced gliosis might have contributed to the aberrant proliferation of Sch wann cells following SCI. Since chondroitin sulfate proteoglycan (CSPG) has been proposed to play a role in Schwann cell/glial interaction, we perform ed immunohistochemical staining for CSPG to investigate its potential relat ionship with schwannosis. CSPG in the injured cord was generally associated with the blood vessel walls, but was also sometimes noted in reactive astr ocytes. In SCI with schwannosis, CSPG staining was more prominent and confi ned largely to the extracellular matrix and basal lamina of proliferating S chwann cells. Our study suggests that Schwann cells, which may have been di splaced from spinal roots and introduced into the injured cord through a br eak in the pial surface, are capable of proliferating and producing CSPG, p articularly in the setting of reduced gliosis. Since CSPG has been associat ed with inhibition of neurite outgrowth, its increased production by aberra nt Schwann cells may impair spinal cord regeneration after injury.