Rapid Amplification of Cerebrospinal Fluid Pressure as a Possible Mechanism for Optic Nerve Sheath Bleeding in Infants with Non-Accidental Head Injury

Peter S. Stewart, Bindi S. Brook, Oliver Jensen, Tamsin A. Spelman, Robert J Whittaker, Moussa A. Zouache

Research output: Contribution to journalArticlepeer-review

Abstract

Purpose Subdural haemorrhage along the optic nerve (ON) is a histopathological indicator of abusive head trauma (AHT) in infants. We sought to determine if this bleeding could be caused by an abrupt increase in intracranial pressure (ICP) transmitted to cerebrospinal fluid (CSF) at the optic foramen (OF).

Methods A theoretical model is developed to simulate the effect of a pressure perturbation of maximal amplitude P applied at the OF for a short duration T on the CSF-filled ON subarachnoid space (ONSAS). The ONSAS is modelled as a fluid-filled channel with an elastic wall representing the flexible ONSAS-arachnoid/dura interface. A constitutive law describing the relationship between SF pressure and ONSAS deformation is inferred from published measurements. CSF pressure profiles along the ONSAS are systematically examined over a broad range of P and T.

Results The pressure perturbation initiated at the OF produces a pressure wave that stretches the ONSAS. This wave propagates rapidly along the ONSAS towards the scleral end of the ON, where it is reflected back towards the brain. For sufficiently small T a shock wave with amplification up to six times larger than P over a timescale of tens of milliseconds is observed at the scleral end of the ON. Comparatively smaller amplifications are observed for slower perturbations.

Conclusions A sudden increase in CSF pressure in the cranial cavity can cause a rapid expansion of the ONSAS, which may lead to rupture of the bridging blood vessels. Our study predicts a plausible mechanism for subdural haemorrhage that occurs in AHT in infants.
Original languageEnglish
JournalInvestigative Ophthalmology and Visual Science
Volume65
Issue number12
DOIs
Publication statusPublished - 1 Oct 2024

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