A MODEL FOR THE MECHANISM OF OPTIC-NERVE SHEATH FENESTRATION

The mechanism by which optic nerve sheath fenestration relieves papilledema associated with increased intracranial pressure has not been clearly defined. A model was constructed to determine if the induction of fluid flow along the nerve sheath and through the fenestration could account for a reduction in pressure around the optic nerve, as might be expected according to Bernoulli's equation of fluid dynamics. The model states that as the velocity of a fluid increases, the pressure it exerts decreases. The model simulated fluid spaces corresponding to the intracranial vault, chiasm, and optic nerves. The unfenestrated model showed direct transmission of elevated intracranial pressure to the nerves, consistent with the production of papilledema. When one nerve was fenestrated, fluid flow along the nerve was initiated and pressure in that nerve sheath dropped substantially. In addition, pressure in the unfenestrated sheath dropped due to fluid communication across the chiasm. These lower intrasheath pressures were consistent with the bilateral resolution of papilledema after unilateral fenestration. The reduced intrasheath pressures persisted even when the intracranial pressure was again elevated to pathologic levels as long as active fluid flow continued along the nerve sheaths. Thus, induction of cerebrospinal fluid flow along the optic nerve sheath by fenestration appears to locally reduce the pressure around the optic nerve, in spite of persistently elevated intracranial pressure. This is in accordance with what would be predicted by Bernoulli's equation. © 1990, American Medical Association. All rights reserved.