Rapid Amplification of Cerebrospinal Fluid Pressure as a Possible Mechanism for Optic Nerve Sheath Bleeding in Infants With Nonaccidental Head Injury

• Published in: Investigative ophthalmology & visual science Vol. 65; no. 12; p. 9
• Main Authors: Stewart, Peter S, Brook, Bindi S, Jensen, Oliver E, Spelman, Tamsin A, Whittaker, Robert J, Zouache, Moussa A
• Format: Journal Article
• Language: English
• Published: United States The Association for Research in Vision and Ophthalmology 07.10.2024
• Subjects: Cerebrospinal Fluid Pressure - physiology; Child Abuse - diagnosis; Craniocerebral Trauma - complications; Craniocerebral Trauma - physiopathology; Eye Movements, Strabismus, Amblyopia and Neuro-Ophthalmology; Hematoma, Subdural - diagnosis; Hematoma, Subdural - etiology; Hematoma, Subdural - physiopathology; Humans; Infant; Intracranial Pressure - physiology; Optic Nerve; Subarachnoid Space - physiopathology
• ISSN: 1552-5783; 0146-0404; 1552-5783
• DOI: 10.1167/iovs.65.12.9

Subdural hemorrhage 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 transmitted to cerebrospinal fluid (CSF) at the optic foramen (OF). A theoretical model is developed to simulate the effect of a pressure perturbation of maximal amplitude P applied at the optic foramen 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 CSF pressure and ONSAS deformation is inferred from published measurements. CSF pressure profiles along the ONSAS are examined systematically over a broad range of P and T. The pressure perturbation initiated at the OF produces a pressure wave that stretches the ONSAS. This wave propagates rapidly along the ONSAS toward the scleral end of the ON, where it is reflected back toward 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. 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 hemorrhage that occurs in abusive head trauma in infants.