EXPERIMENTAL PATHOLOGY OF THE OPTIC NERVE

  • Anderson, Douglas, (PI)

Project: Research project

Description

The basic goal of this project has been to understand better the
underlying pathogenic mechanisms involved in papilledema, optic
atrophy, and glaucoma. The emphasis has been on glaucoma, and
essentially is now the exlcusive subject of investigation. The
long-term aim is to understand how elevation of intraocular
pressure--together with any other factors that might be involved-
-destroys axons, causes loss of redistribution of astroglia, and
changes the configuration of the lamina cribrosa. The axon
damage is the main feature relevant to visual loss. The hope is
that by identifying the mechanism of pressure-induced damage and
the factors involved we can (1) identify those at risk, in order to
guide us when deciding who needs to have their intraocular
pressure lowered, and (2) perhaps also to be able to devise rational
and effective therapy directed at the optic nerve pathophysiology
in place of or in addition to lowering the intraocular pressure.
Therapy directed at the pathophysiology is the optic nerve is
needed especially when faced with a case in which the optic nerve
continues to be damaged despite a normal intraocular pressure
("low tension glaucoma") or in ordinary glaucoma despite the
maximal pressure lowering that can be achieved with safe current
therapy. It is now proposed specifically to explore the hypothesis that
special sensitivity of the optic disc is an indirect consequence of
the fact that certain blood components that are retained by the
blood-brain-barrier leak into the choroid (which has no such
barrier), and from there they diffuse into the optic nerve head,
circumventing the barriar of the wall of the optic disc vessels.
Vasoconstrictors are among the substances circulating in the
blood stream, and they presumably participate in the body's
vascular homeostasis by controlling vascular tone in peripheral
tissues. They do not affect CNS vessels (where flow is controlled
by autoregulation according to local tissue needs), because they
are prevented from reaching the muscular walls of the vessels by
the tightly joined endothelial cells that contribute the blood-
brain-barrier. However, when these circulating vasoconstrictors
reach the muscular coat of the optic nerve vessel by diffusing
from the choroid, resulting vascular tone may impair the dilation
required as an autoregulatory response when the circulating is
challenged by elevation of intraocular pressure.
StatusFinished
Effective start/end date11/1/774/30/91

Funding

  • National Institutes of Health
  • National Institutes of Health
  • National Institutes of Health
  • National Institutes of Health
  • National Institutes of Health
  • National Institutes of Health
  • National Institutes of Health: $65,995.00
  • National Institutes of Health

Fingerprint

Optic Disk
Optic Nerve
Intraocular Pressure
Papilledema
Blood Vessels
Pathology
Glaucoma
Choroid
Optic Atrophy
Optic Nerve Diseases
Intracranial Pressure
Nerve Fibers
Neuroglia
Primates
Homeostasis
Low Tension Glaucoma
Pressure
Vasoconstrictor Agents
Blood-Brain Barrier
Astrocytes

ASJC

  • Medicine(all)