GLAUCOMA. Harold E. Cross M.D., Ph.D. 1-17-12 v. 8.0. (With contributions by T. Altenbernd, MD, and P. Tsai, MD). What is it? A disease of progressive optic neuropathy with loss of retinal neurons and their axons (nerve fiber layer) resulting in blindness if left untreated.
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Harold E. Cross M.D., Ph.D.
1-17-12 v. 8.0
(With contributions by T. Altenbernd, MD, and P. Tsai, MD)
“Glaucoma describes a group of diseases that kill retinal ganglion cells.”
“High IOP is the strongest known risk factor for glaucoma but it is neither necessary nor sufficient to induce the neuropathy.”
Libby, RT, et al: Annu Rev Genomics Hum Genet 6: 15, 2005
What causes it?
There is a dose-response relationship between intraocular pressure and the risk of damage to the visual field.
How do we diagnose it?
approximately 40 mm Hg at which level the
likelihood of damage is significant.
of diagnosis because a considerable number of neurons must be lost before VF changes can be
or impossible to recognize.
Intraocular pressure is not the only factor
responsible for glaucoma!
with glaucoma also occur in people without glaucoma.
have IOP <22 mmHg
Population distribution of IOP
Normal vs glaucoma:
How do we measure IOP?
Glaucoma visual fields
The normal visual field: an island of vision in a sea of darkness:
Humphrey automated perimetry
Visual fields in glaucoma
The histology of glaucomatous optic nerve cupping:
Optic nerve signs of glaucoma progression
visual field damage)
Ocular hypertension treatment study
medications in preventing or delaying visual field loss
and/or optic nerve damage in subjects with ocular hyper-
tension at moderate risk for developing open-angle
mm HG in one eye, and 21-32 in the other, randomly
assigned to observation and treatment groups.
prostaglandin analogues, topical carbonic anhydrase inhibitors, alpha-2 agonists, parasympathomimetic agents, and epinephrine.
At 60 months, the probability of developing glaucoma was:
9.5% in observation group
4.4% in treatment group
OHTS parameters that influence the risk of developing POAG
Central corneal thickness
Percentage of OHTS participants in observation group who developed POAG (mean follow-up = 72 mo)
IOP vs central corneal thickness
Normal central corneal thickness: 545 – 550 u
Add or subtract 2.5 mmHg for each 50 u change in central corneal thickness
Onset: antenatally to 2 years old
Buphthalmos and cloudy corneas
Onset: 50+ years of age
Nausea and vomiting
Halos around lights
Intermittent eye ache
Red, teary eye
Grade I Grade 0 Grade III Grade II
Anatomy of Angle Closure Glaucoma
Mid-dilated, fixed pupil
Treatment: Peripheral Iridotomy
Family history Cardiovascular
Central corneal disease
Onset: 50+ years of age
Visual field loss
Glaucomatous disk changes
May have loss of central
and peripheral vision
blood dyscrasias, autoimmune diseases
elongation of disc
Surgical treatment of glaucoma