Age related changes in intracranial volume in rabbits with craniosynostosis.

Neurocapsular growth is highly heritable and determines neurocranial form. Although craniosynostosis alters brain growth direction, resulting in compensatory changes in the neurocranium, it is believed that such compensations occur without reduction in intracranial volume. This hypothesis was tested in a rabbit model with nonsyndromic, familial coronal suture synostosis. Skulls of 56 rabbits (20 normals, 20 with delayed onset synostosis, and 16 with complete synostosis) were scanned using three-dimensional computed tomography at 6 and 18 weeks of age. Intracranial contents were reconstructed, and indirect intracranial volume was calculated. Qualitatively, re-formations of intracranial contents from completely synostosed rabbit skulls exhibited the typical "copper beaten" morphology. Quantitatively, intracranial volume was significantly (p < 0.05) reduced in rabbit skulls with complete synostosis compared with both control rabbit skulls and rabbit skulls with delayed onset synostosis at 6 weeks by 11 percent and 14 percent, respectively). By 18 weeks, intracranial volume in rabbit skulls with synostosis was significantly (p < 0.05) reduced (by 12 percent in complete synostosis and 8 percent in delayed onset synostosis) compared with normal rabbits. Results suggest that in rabbits with uncorrected craniosynostosis, compensatory changes in the neurocranium were not adequate to allow normal expansion of the neurocapsular matrix. Further research is needed to determine whether reduction in intracranial volume was a result of neural tissue deficiency or cerebrospinal fluid (i.e., ventricular or subarachnoid) space compression in this model.