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Dive into the research topics where W. Richard Green is active.

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Featured researches published by W. Richard Green.


American Journal of Ophthalmology | 1989

Retinal Ganglion Cell Atrophy Correlated With Automated Perimetry in Human Eyes With Glaucoma

Harry A. Quigley; Gregory R. Dunkelberger; W. Richard Green

We measured the number and size of retinal ganglion cells from six human eyes with glaucoma. In each, the histologic findings were correlated with visual field results. Five age-matched normal eyes were studied for comparison. In general, there were fewer remaining large ganglion cells in retinal areas with atrophy. In the perifoveal area, however, no consistent pattern of cell loss by size was found. Our estimates suggest that visual field sensitivity in automated testing begins to decline soon after the initial loss of ganglion cells. Throughout the central 30 degrees of the retina, 20% of the normal number of cells were gone in locations with a 5-dB sensitivity loss, and 40% cell loss corresponded to a 10-dB decrease. There were some remaining ganglion cells in areas that had 0-dB sensitivity in the field test.


American Journal of Ophthalmology | 1983

Morphologic Changes in the Lamina Cribrosa Correlated with Neural Loss in Open-Angle Glaucoma

Harry A. Quigley; Rebecca M. Hohman; Earl M. Addicks; Robert W. Massof; W. Richard Green

We divided 25 glaucomatous human eyes into three groups representing mild (Group 1, seven eyes), moderate (Group 2, 11 eyes), and severe (Group 3, six eyes) optic nerve damage, based on visual field testing or remaining number of optic nerve fibers. The optic nerve head of each eye was examined by scanning electron microscopy. Compression of the successive lamina cribrosa sheets was the earliest detected abnormality, occurring in some eyes before the detection of visual field loss. Backward bowing of the entire lamina cribrosa was a later change and involved its upper and lower poles more than the mid-nerve head. The diameter of the scleral opening at the level of Bruchs membrane did not enlarge in these adult glaucomatous eyes. Mechanical compression of the nerve head occurred early enough to be considered a primary pathogenetic event in glaucomatous damage.


Ophthalmology | 1988

Chronic Human Glaucoma Causing Selectively Greater Loss of Large Optic Nerve Fibers

Harry A. Quigley; Gregory R. Dunkelberger; W. Richard Green

Eighteen eyes of 12 persons with chronically elevated intraocular pressure (IOP) were studied histologically to determine the number and diameter of optic nerve fibers. In some eyes, automated perimetry had been performed. Optic nerve fibers larger than the mean diameter were killed more rapidly than smaller fibers, although no fiber size was completely spared at any stage of atrophy. The number of optic nerve fibers varies considerably among normal eyes. The authors confirmed that the death of a substantial proportion of optic nerve fibers precedes detectable visual field loss.


Ophthalmology | 1979

The Histology of Human Glaucoma Cupping and Optic Nerve Damage: Clinicopathologic Correlation in 21 Eyes

Harry A. Quigley; W. Richard Green

We have examined by light and electron microscopy the retina, optic nervehead, and optic nerves of 21 human eyes from glaucoma patients in whom clinical information was available for comparison. In several cases it was possible to correlate the degree and distribution of optic nerve damage with the clinical appearance of the optic disc and visual field studies. There was no selective loss of astrocytes of the optic nervehead in early glaucoma cupping. Acquired increases in optic disc cup size prior to detectable visual field loss probably represent loss of ganglion cell axonal fibers which is not yet significant enough to produce field defects. It is unlikely that the mechanism of axonal damage in chronic human glaucoma involves early loss of astrocytic glial cells at the optic nervehead. At the level of the retrobulbar optic nerve, the ganglion cell axonal fibers of the superior and inferior quadrants seem to be lost earlier than the fibers of the nasal and temporal nerve periphery. Since the superior and inferior poles of the optic nerve may contain the fibers of arcuate area ganglion cells, these data confirm the presumption from visual field testing that arcuate area ganglion cell fibers are selectively more susceptible to damage in chronic glaucoma.


Ophthalmology | 1989

Ocular Manifestations of Acquired Immune Deficiency Syndrome

Douglas A. Jabs; W. Richard Green; Robin Fox; B. Frank Polk; John G. Bartlett

The ocular complications of acquired immune deficiency syndrome (AIDS) include: (1) a noninfectious microangiopathy, most often seen in the retina, consisting of cotton-wool spots with or without intraretinal hemorrhages and other microvascular abnormalities; (2) opportunistic ocular infections, primarily cytomegalovirus (CMV) retinitis; (3) conjunctival, eyelid, or orbital involvement by those neoplasms seen in patients with AIDS (i.e., Kaposis sarcoma and lymphoma); and (4) neuro-ophthalmic lesions. In a series of 200 AIDS patients evaluated clinically, AIDS retinopathy was present in 66.5%. Sixty-four percent had cotton-wool spots, and 12% had intraretinal hemorrhages. Cytomegalovirus retinitis was diagnosed in 28% of AIDS patients. Neuro-ophthalmic lesions were found in 8% of all AIDS patients and were present in 33% of those patients with cryptococcal meningitis. Acquired immune deficiency syndrome retinopathy was present in 40% of 35 patients with the AIDS-related complex (ARC) and in 1.3% of 232 patients with asymptomatic human immunodeficiency virus (HIV) infection, evaluated photographically. These results suggest that the prevalence of AIDS retinopathy increases with increasing severity of HIV infection, and that CMV retinitis presents a significant vision-threatening problem in AIDS patients.


Journal of Cataract and Refractive Surgery | 1999

Provision of anesthesia with single application of lidocaine 2% gel

Irina S. Barequet; Eduardo S. Soriano; W. Richard Green; Terrence P. O’Brien

PURPOSEnTo compare the efficacy of a single application of lidocaine 2% gel with tetracaine 0.5% drops for topical anesthesia in clear corneal cataract surgery.nnnSETTINGnThe Wilmer Eye Institute, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.nnnMETHODSnA preliminary toxicity study applied lidocaine 2% gel in the conjunctival fornices of rabbit eyes (n = 9). Biomicroscopic examination was performed and then enucleation at sequential intervals after the application. Intentional intracameral injection of lidocaine gel was performed (n = 3), followed by enucleation. Histopathological analysis was performed on all eyes. A randomized clinical trial comparing topical anesthesia in clear corneal cataract surgery was performed in 25 eyes of 25 patients (12 eyes randomly assigned to lidocaine gel, 13 eyes to tetracaine drops). Corneal sensation was measured with the Cochet-Bonnet aesthesiometer before application of the topical anesthesia, 5 minutes after application, and at the conclusion of surgery. Additional intraoperative local anesthesia and systemic sedation were recorded. Patients subjective level of comfort was reported 20 minutes after surgery, and the surgeons perception of patients comfort was also noted.nnnRESULTSnIn rabbits, lidocaine gel did not cause clinical or histopathological alteration of the ocular tissues. In the clinical study, median corneal sensitivity before application, after 5 minutes, and postoperatively was 6, 0, 0 (maximum sensitivity = 6), respectively, in the lidocaine gel group and 5, 0, 0, respectively, in the tetracaine drops group. Additional local anesthesia was administered in 17% and 31% of patients, respectively. Satisfactory comfort was reported by 58% in the lidocaine gel group and 62% in the tetracaine drops group.nnnCONCLUSIONSnA single application of lidocaine 2% gel was a safe and effective alternative to multiple topical anesthetic drops for clear corneal cataract surgery. Lidocaine 2% gel was similar to tetracaine drops in provision of corneal anesthesia and patient comfort, while causing no significant toxicity to the ocular surface.


American Journal of Ophthalmology | 1985

The Pattern of Optic Nerve Fiber Loss in Anterior Ischemic Optic Neuropathy

Harry A. Quigley; Neil R. Miller; W. Richard Green

Postmortem quantification of the remaining optic nerve fibers in three eyes with nonarteritic anterior ischemic optic neuropathy showed that the loss of fibers was complete in the superior half of each nerve and included loss of peripheral fibers in the other half. The fibers with the greatest resistance to atrophy were found in the middle of the nerve cross section. The pattern was similar to that found in a previous example of anterior ischemic optic neuropathy and unlike that found in glaucoma or other optic neuropathies studied in similar fashion.


Graefes Archive for Clinical and Experimental Ophthalmology | 1996

Blood-aqueous barrier in pseudoexfoliation syndrome: evaluation by immunohistochemical staining of endogenous albumin

Michael Küchle; Stanley A. Vinores; Jeremy Mahlow; W. Richard Green

Abstract• Background: Alterations of the integrity of the blood-aqueous barrier (BAB) are frequent findings in eyes with pseudoexfoliation syndrome (PSX). • Methods: Immunohistochemical staining for the demonstration of albumin was used to analyze the BAB in 10 eyes with PSX without previous intraocular surgery and in 10 age-matched normal control eyes. • Results: In eyes with PSX, small amounts of albumin were detected along the anterior surface of the iris in 7, in the anterior chamber in 1, along the ciliary epithelium in 4, and in the trabecular meshwork in 9 of 10 eyes. PSX material was also immunoreactive. In the 10 normal control eyes, albumin was detected anterior to the iris stroma in 1 eye, in the anterior chamber in 2 eyes, in the trabecular meshwork in 1 eye, but not internal to the ciliary epithelium. • Conclusions: Our findings indicate that impairment of the BAB in PSX can be localized at the level of the iris and, less frequently or to a lesser extent, at the level of the ciliary body.


Ophthalmology | 1997

Ocular Explosion after Peribulbar Anesthesia: Case Report and Experimental Study

David O. Magnante; John D. Bullock; W. Richard Green

PURPOSEnA peribulbar anesthetic injection for cataract surgery produced a 10.5-mm scleral laceration and lens extrusion. This study sought to recreate this unfortunate clinical situation.nnnMETHODSnTwenty-one human eye bank eyes were ruptured by intraocular injection of saline through Atkinson needles. The hydrostatic pressure required for globe rupture was measured by three different techniques in seven globes.nnnRESULTSnForty-eight percent of the scleral lacerations were equatorial and 52% were perilimbal. Lens extrusion occurred with three of the perilimbal lacerations. Rupture pressures by each technique averaged 3065, 4972, and 5648 mmHg.nnnCONCLUSIONnPeribulbar injection can produce inadvertent ocular explosion.


Ophthalmology | 1999

Ocular explosions from periocular anesthetic injections: A clinical, histopathologic, experimental, and biophysical study☆

John D. Bullock; Ronald E. Warwar; W. Richard Green

OBJECTIVESnAn increasing number of cases are being recognized in which a periocular anesthetic for cataract surgery has been inadvertently injected directly into the globe under high pressure until the globe ruptures or explodes. The objectives of the current study were to (1) analyze this injury clinically and histopathologically through a series of seven case reports; (2) reproduce the injury experimentally in human eyebank eyes, live anesthetized rabbit eyes, and human cadaveric eyes; (3) investigate the biophysical basis of the injury; and (4) outline recommendations to help decrease the risk of ocular rupture with periocular injections. DESIGNS/PARTICIPANTS: Clinical, histopathologic, experimental animal, autopsy eye, and theoretical biophysical study.nnnMETHODSnThe clinical and histopathologic findings of the patients eyes were documented. Human eyebank eyes, live anesthetized rabbit eyes, and human cadaveric eyes were exploded via direct intraocular saline injection. The laws of Bernoulli, LaPlace, Friedenwald, and Pascal were used to investigate theoretically the biophysics of the injury.nnnRESULTSnThe findings of anterior and posterior scleral rupture, retinal detachment, vitreous hemorrhage, and lens extrusion were observed clinically and experimentally. In some clinical and experimental cases, the anterior segment appeared entirely normal despite a posterior rupture. The surgeon proceeded with and completed the cataract surgery in two of the seven clinical cases without knowledge of the rupture. The pressure required to produce such an injury is in the range of 2800 to 6400 mmHg, and this pressure is more easily attained with a 3-ml syringe than with a 12-ml syringe.nnnCONCLUSIONSnExplosion of an eyeball during the injection of anesthesia for ocular surgery is a devastating injury that may go unrecognized. The probability of an ocular explosion can be minimized by (1) the use of a blunt needle and a 12-ml syringe, (2) aspirating the plunger and wiggling the syringe before injection, (3) discontinuing the injection if corneal edema or resistance to injection is noted, and (4) inspecting the globe for evidence of intraocular injection before ocular massage or placement of a Honan balloon. On recognition of an ocular explosion, immediate referral to and intervention by a vitreoretinal surgeon is optimal.

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Douglas A. Jabs

Icahn School of Medicine at Mount Sinai

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Eduardo S. Soriano

Johns Hopkins University School of Medicine

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Gregory R. Dunkelberger

Johns Hopkins University School of Medicine

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Irina S. Barequet

Johns Hopkins University School of Medicine

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Stanley A. Vinores

Johns Hopkins University School of Medicine

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Abha Amin

Johns Hopkins University School of Medicine

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