A model for the mechanism of optic nerve sheath fenestration
S. R. Seiff and L. Shah
Department of Ophthalmology, University of California, San Francisco 94143.
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.
