Age-Related Changes in Intracranial Pressure in Rabbits with Uncorrected Familial Coronal Suture Synostosis

Autor: Annie M. Burrows, H. Wolfgang Losken, Gregory M. Cooper, Timothy D. Smith, Ian F. Pollack, Wendy Fellows-Mayle, Michael I. Siegel, Mark P. Mooney, Jason Dechant
Rok vydání: 2000
Předmět:
Zdroj: The Cleft Palate-Craniofacial Journal. 37:370-378
ISSN: 1545-1569
1055-6656
DOI: 10.1597/1545-1569_2000_037_0370_arciip_2.3.co_2
Popis: Objective Chronic, elevated intracranial pressure (ICP) in craniosynostotic infants may result in ocular and neurocapsular problems; however, not all infants exhibit elevated ICP. Clinical ICP studies are further confounded by small and heterogeneic samples, multiple-suture involvement, and varying surgical management protocols. The present study was designed to describe longitudinal changes in ICP in a large, homogenous sample of rabbits with uncorrected familial, nonsyndromic coronal suture synostosis. Methods Ninety-one rabbits were divided into four groups: (1) normal rabbits (n = 28), (2) rabbits with delayed-onset coronal suture synostosis (DOCS; n = 25), (3) rabbits with unilateral coronal suture synostosis (UCS; n = 12), and (4) rabbits with bilateral coronal suture synostosis (BCS; n = 26). ICP was measured at 24 and 42 days of age using a Codman epidural microtransducer. Results Rabbits with BCS had a significantly (p < .05) higher mean ICP at 25 days of age than rabbits in the other three groups by approximately 146%. However, by 42 days of age, mean ICP in normal control rabbits and rabbits with DOCS was significantly (p < .01) increased compared with their mean ICP values seen at 25 days of age, while mean ICP in BCS rabbits significantly (p < .01) decreased (by 32%) over the same time period. ICP in rabbits with UCS was between that seen in normal control rabbits and rabbits with BCS and did not significantly (p > .05) change over time. Conclusions These findings suggest that the degree of suture involvement may be related to early increases in ICP. Possible multifactorial explanations for intracranial decompression and compensation in the craniosynostotic rabbit model are discussed.
Databáze: OpenAIRE