DEFECTS in the dura mater can result from craniocerebral trauma, neoplastic or inflammatory destruction, surgical removal, and congenital absence. The experimental work of Trotter,1 Sayad and Harvey,2 Cone,3 Penfield,4 and Keener,5 indicates that if these dural defects are adjacent to soft tissue, adequate dural regeneration can occur in several weeks. Fibroblasts derived from surrounding mesenchymal tissue move into the defect restoring the continuity of the dura. However, if the defect is adjacent to bone, poor dural regeneration results, since the mesenchymal source for fibroblasts is not readily available. The advantages of closing such a dural defect are multiple. Closure prevents cerebral herniation with subsequent cerebritis, cerebrospinal fluid fistula with ensuing meningitis, and corticomeningeal adhesions with a resultant seizure focus.
Materials used for the closure of dural defects have been reviewed by Pudenz,6 Keener,7 Teng,8 and Rosomoff.9 Replacement materials which have appeared