Cooper G M, Mooney M P, Burrows A M, Smith T D, Dechant J, Losken H W, Marsh J L, Siegel M I
Department of Anatomy and Histology, University of Pittsburgh, Pennsylvania 15261, USA.
Cleft Palate Craniofac J. 1999 Jul;36(4):314-21. doi: 10.1597/1545-1569_1999_036_0314_bgricr_2.3.co_2.
It has been suggested that abnormal brain morphology or growth rates may be a primary causal factor of craniosynostosis due, in part, to a lack of normal growth stretch and tension at the sutural margins. The purpose of the present study was to quantify cerebral hemisphere morphology and growth in a rabbit model of nonsyndromic coronal suture synostosis to determine whether cerebral dysmorphology is primary or secondary to synostosis in this model.
Fifty-seven brains (114 hemispheres) were examined from 40 normal control rabbits and 17 rabbits with bilateral coronal suture synostosis ranging in age from 25 to 450 days postconception (synostosis occurs at approximately 23 days postconception in this model). The calvariae were removed, the brains were fixed in 10% paraformaldehyde, and in situ bilateral measurements of cerebral hemisphere length and cerebral hemisphere width were obtained using a Wild microscope with a camera lucida attachment and digital caliper. Regression analysis was used to compare cerebral cortex growth rates by age between the two groups.
Cerebral hemisphere width and cerebral index regression line slopes had similar y intercepts (23 day postconception) with significantly (p < .05) diverging slopes over time. Normal rabbits increased more rapidly than synostosed rabbits. No significant (p > .05) differences were noted in regression line slopes between groups for cerebral hemisphere length by age or length by width.
Cerebral dysmorphologies are probably a compensatory, secondary (postsynostotic) event and not a primary causal factor of craniosynostosis in this rabbit model of human familial, nonsyndromic coronal suture synostosis.