Dural sinus volume in children with syndromic craniosynostosis and intracranial hypertension

Author:

de Goederen Robbin1,Cuperus Iris E.1,Tasker Robert C.2,den Ottelander Bianca K.1,Dremmen Marjolein H. G.3,van Veelen Marie-Lise C.4,Spoor Jochem K. H.4,Joosten Koen F. M.5,Mathijssen Irene M. J.1

Affiliation:

1. Departments of Plastic and Reconstructive Surgery, and Hand Surgery,

2. Departments of Neurology and Anesthesia (Pediatrics), Harvard Medical School and Boston Children’s Hospital, Boston, Massachusetts

3. Radiology,

4. Neurosurgery, and

5. Pediatrics, Intensive Care Unit, Erasmus MC, Rotterdam, The Netherlands; and

Abstract

OBJECTIVEIntracranial hypertension is a major concern in children with syndromic craniosynostosis (sCS). Cerebral venous hypertension caused by cerebral venous outflow obstruction is believed to contribute to intracranial hypertension. The authors therefore hypothesized that cerebral venous volume would be increased in those children with sCS and intracranial hypertension.METHODSIn a case series of 105 children with sCS, of whom 32 had intracranial hypertension, cerebral MRI techniques were used to quantify the volume of the superior sagittal sinus, straight sinus (StrS), and both transverse sinuses.RESULTSLinear regression showed that total cerebral venous volume increased by 580.8 mm3 per cm increase in occipitofrontal head circumference (p < 0.001). No significant difference was found between the intracranial hypertension group and the nonintracranial hypertension group (p = 0.470). Multivariate ANOVA showed increased StrS volume (as a proportion of total volume) in the intracranial hypertension group (8.5% vs 5.1% in the nonintracranial hypertension group, p < 0.001). Multivariate logistic regression showed that a 100-mm3 increase in StrS volume is associated with increased odds of having intracranial hypertension by 60% (OR 1.60, 95% CI 1.24–2.08).CONCLUSIONSAlthough intracranial hypertension was not associated with total cerebral venous volume increase, it was associated with an isolated increase in StrS volume. Hence, it is unlikely that general cerebral venous outflow obstruction is the mechanism of intracranial hypertension in sCS. Rather, these findings indicate either a central cerebral vulnerability to intracranial hypertension or a mechanism involving venous blood redistribution.

Publisher

Journal of Neurosurgery Publishing Group (JNSPG)

Subject

General Medicine

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