Recurrence of synostosis following surgery for isolated sagittal craniosynostosis
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1) The document discusses a study finding a high rate of resynostosis (83.3%) of the sagittal suture following surgery for isolated sagittal craniosynostosis, contrary to animal experiments. 2) It hypothesizes that limiting coagulation of the dura and replacing the removed pericranium could potentially result in reformation of a normal suture and consistent bone regeneration. 3) Other potential factors for the discrepancy include genetic predisposition and inclusion of undiagnosed syndromic patients in the study.
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Recurrence of synostosis following surgery for isolated sagittal craniosynostosis
- 1. Recurrence of Synostosis Following Surgery for Isolated Sagittal Craniosynostosis Deepak Agrawal, P Steinbok, D Cochrane Division of Pediatric Neurosurgery, UBC and BC Children’s Hospital, Vancouver, BC
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Editor's Notes
- The current basis of the management of isolated sagittal craniosynostosis is that it typically occurs as an isolated entity in an otherwise normal child (Albright and Byrd 1981), with operative intervention usually being offered to improve cosmesis. It has been recognized that about 10-15% of children with sagittal synostosis have increased intracranial pressure (ICP), and some have recommended surgery in the hope that it might prevent the adverse effects of raised ICP (Thompson, Malcolm et al. 1995; Cohen and Persing 1998).
- The debate regarding the etiology of craniosynostosis has primarily revolved around Moss’s & Babler’s hypothesis. Moss’s hypothesis is of a primary abnormality at the cranial base (Moss 1958; Moss 1959; Moss 1972; Moss 1975),With syndromic craniosynostosis, it has become reasonably clear that the primary abnormality does involves the cranial base, and that cranial base alterations affect the dural reflections, which somehow predisposes to premature closure of the sutures. As surgery does not correct the underlying pathology, it is not surprising to have recurrent synostosis in these cases.
- In contrast, Babler contends that the abnormality is in the affected calvarial sutures (Babler, Persing et al. 1982). This is gene rally believed to be the case in nonsyndromic, single suture synostosis where the etiology is usually ascribed to compressive intrauterine forces that act on individual sutures. Recurrent synostosis is less likely, since the surgery usually removes the pathological suture (Hudgins, Cohen et al. 1998). Support for this hypothesis comes from animal experiments which have shown that when the calvaria is excised and discarded, a new calvaria forms with time and sutures redevelop in their normal anatomic positions (Mabbutt and Kokich 1979; Mabbutt, Kokich et al. 1979)