Glaucoma patients have on the average a reduced ocular
perfusion. .
The reduction of ocular blood flow is even more
pronounced in normal tension glaucoma than in high tension glaucoma, indicating
that the reduction cannot simply be due to intraocular pressure (IOP). The fact that the vascular
insufficiency often precedes glaucomatous damage and is often not confined to
the eye indicates that it is also not simply a consequence of glaucoma, but
rather a primary risk factor. The
major cause for this insufficency is not arteriosclereosis, but rather a
vascular dysregulation. The vascular dysregulation interferes with the
autoregulation of ocular perfusion rendering the eye more sensitive towards IOP
increase and blood pressure decrease.
What are the therapeutical consequences? Even in cases with major vascular risk
factors, an IOP reduction is meaningful.
In many cases, however, this may not be sufficient to stop further
progression. An improvement of circulation, especially an improvement of
autoregulation, is desired.
Several studies indicate that carboanhydrase inhibitors have such a
beneficial influence. A
combination of a betablocker with a carboanhydrase inhibitor induces a marked
IOP reduction in most cases and has a beneficial influence on ocular perfusion
at the same time.