Etiology

Syndromic craniosynostosis arises from a known disorder and is well discussed elsewhere [23]. As is evident in Table 25.2, a myriad of conditions may lead to secondary craniosynos-tosis. For example, in malformations such as microcephaly, lack of growth stretch is postulated to cause secondary craniosynostosis. In infants with hyperthyroidism, premature osseous fusion is thought to result in premature suture closure.

Study of syndromic craniosynostoses has been invaluable in advancing contemporary insight into the molecular pathophysiology of craniosynostosis. For many of the craniosyn-ostosis syndromes, the underlying genetic defects have already been identified. For example, mutation in a member of the home-obox gene, MSX2, has been identified in Boston craniosynostosis and studies in transgenic mice reveal that this mutation also causes craniosyn-ostosis in this model. In addition, mutations in the TWIST gene have been discovered in

Table 25.2. Disorders with secondary craniosynostosis.

Hematological disorders

Polycythemia Sickle cell anemia Thalassemias Iatrogenic disorders Shunted hydrocephalus Malformations Encephalocele Holoprosencephaly Microcephaly Metabolic disorders Hyperthyroidism Rickets

Mucopolysaccharidoses and related disorders a-D-mannosidase deficiency

^-glucuronidase deficiency

Hurler syndrome

Morquio syndrome

Mucolipidosis III

Teratogens

Aminopterin

Cyclophosphamide

Diphenylhydantoin

Fluconazole

Retinoids

Valproate

Table 25.1. Classification of craniosynostosis.

Type

Deformity

Syndromic

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