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Delayed Functional Loss in Glaucoma LII Edward Jackson Memorial Lecture
This study is a systematic exploration of why some patients with glaucoma continue to lose visual field long after therapeutic normalization of their increased intraocular pressures. Three cases of glaucoma are described that had increased intraocular pressures and good initial visual fields. The fo...
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Published in: | American journal of ophthalmology 1996-05, Vol.121 (5), p.473-483 |
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container_end_page | 483 |
container_issue | 5 |
container_start_page | 473 |
container_title | American journal of ophthalmology |
container_volume | 121 |
creator | BRUBAKER, RICHARD F. |
description | This study is a systematic exploration of why some patients with glaucoma continue to lose visual field long after therapeutic normalization of their increased intraocular pressures.
Three cases of glaucoma are described that had increased intraocular pressures and good initial visual fields.
The following four hypotheses are offered to explain delayed functional loss in these patients: (1) A process independent of intraocular pressure is killing ganglion cells. (2) Unmeasured increases of pressure are killing ganglion cells. (3) The ganglion cells have a genetically determined hypersensitivity to intraocular pressure. (4) The ganglion cells have been rendered hypersensitive to intraocular pressure by irreversible damaging effects of previously increased intraocular pressures.
The current state of knowledge does not permit the elimination of any of the four hypotheses. An additional hypothesis is that the final stage of ganglion cell death is mediated by apoptosis. If so, a potential new treatment for glaucoma would be to inhibit the apoptotic pathway. |
doi_str_mv | 10.1016/S0002-9394(14)75421-2 |
format | article |
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Three cases of glaucoma are described that had increased intraocular pressures and good initial visual fields.
The following four hypotheses are offered to explain delayed functional loss in these patients: (1) A process independent of intraocular pressure is killing ganglion cells. (2) Unmeasured increases of pressure are killing ganglion cells. (3) The ganglion cells have a genetically determined hypersensitivity to intraocular pressure. (4) The ganglion cells have been rendered hypersensitive to intraocular pressure by irreversible damaging effects of previously increased intraocular pressures.
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Three cases of glaucoma are described that had increased intraocular pressures and good initial visual fields.
The following four hypotheses are offered to explain delayed functional loss in these patients: (1) A process independent of intraocular pressure is killing ganglion cells. (2) Unmeasured increases of pressure are killing ganglion cells. (3) The ganglion cells have a genetically determined hypersensitivity to intraocular pressure. (4) The ganglion cells have been rendered hypersensitive to intraocular pressure by irreversible damaging effects of previously increased intraocular pressures.
The current state of knowledge does not permit the elimination of any of the four hypotheses. An additional hypothesis is that the final stage of ganglion cell death is mediated by apoptosis. If so, a potential new treatment for glaucoma would be to inhibit the apoptotic pathway.</description><subject>Adult</subject><subject>Apoptosis</subject><subject>Awards and Prizes</subject><subject>Biological and medical sciences</subject><subject>Cell Death</subject><subject>Female</subject><subject>Glaucoma - pathology</subject><subject>Glaucoma - physiopathology</subject><subject>Glaucoma and intraocular pressure</subject><subject>Humans</subject><subject>Intraocular Pressure</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Ophthalmology</subject><subject>Retinal Ganglion Cells - pathology</subject><subject>Societies, Medical</subject><subject>Vision Disorders - physiopathology</subject><subject>Visual Fields - physiology</subject><issn>0002-9394</issn><issn>1879-1891</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><recordid>eNqFkE9LwzAYh4Moc04_wqAHET1UkyZN2pPI3Oak4kE9hzR5C9H-mUmr7NvbbmNXTy_h9_zyJg9CU4JvCSb87g1jHIUpTdk1YTciZhEJoyM0JolIQ5Kk5BiND8gpOvP-sz9ywcQIjRJOsEjxGC0foVQbMMGiq3Vrm1qVQdZ4H9g6WJaq002lgmy1CubmVzkTPCv95Zs6eIGqcXaAQbedg3N0UqjSw8V-TtDHYv4-ewqz1-Vq9pCFmsVxGxYmzzU3pogNp6nKITWEgobY5AoDUZRQBn0gNOUsz7kwRRIDVzQpuNGG0Qm62t27ds13B76VlfUaylLV0HReigTjNCIDGO9A7frvOCjk2tlKuY0kWA4C5VagHOxIwuRWoIz63nS_oMsrMIfW3lifX-5z5bUqC6dqbf0Bo1jQKIp77H6HQS_jx4KTXluoNRjremPSNPafh_wBXBSM4w</recordid><startdate>19960501</startdate><enddate>19960501</enddate><creator>BRUBAKER, RICHARD F.</creator><general>Elsevier Inc</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>19960501</creationdate><title>Delayed Functional Loss in Glaucoma LII Edward Jackson Memorial Lecture</title><author>BRUBAKER, RICHARD F.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c455t-fdbbc6ddf5d639abe9d13ece5dba0e1a3134e39a7c364bb67df85e6a38f6dcd43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1996</creationdate><topic>Adult</topic><topic>Apoptosis</topic><topic>Awards and Prizes</topic><topic>Biological and medical sciences</topic><topic>Cell Death</topic><topic>Female</topic><topic>Glaucoma - pathology</topic><topic>Glaucoma - physiopathology</topic><topic>Glaucoma and intraocular pressure</topic><topic>Humans</topic><topic>Intraocular Pressure</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Ophthalmology</topic><topic>Retinal Ganglion Cells - pathology</topic><topic>Societies, Medical</topic><topic>Vision Disorders - physiopathology</topic><topic>Visual Fields - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>BRUBAKER, RICHARD F.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>American journal of ophthalmology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>BRUBAKER, RICHARD F.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Delayed Functional Loss in Glaucoma LII Edward Jackson Memorial Lecture</atitle><jtitle>American journal of ophthalmology</jtitle><addtitle>Am J Ophthalmol</addtitle><date>1996-05-01</date><risdate>1996</risdate><volume>121</volume><issue>5</issue><spage>473</spage><epage>483</epage><pages>473-483</pages><issn>0002-9394</issn><eissn>1879-1891</eissn><coden>AJOPAA</coden><abstract>This study is a systematic exploration of why some patients with glaucoma continue to lose visual field long after therapeutic normalization of their increased intraocular pressures.
Three cases of glaucoma are described that had increased intraocular pressures and good initial visual fields.
The following four hypotheses are offered to explain delayed functional loss in these patients: (1) A process independent of intraocular pressure is killing ganglion cells. (2) Unmeasured increases of pressure are killing ganglion cells. (3) The ganglion cells have a genetically determined hypersensitivity to intraocular pressure. (4) The ganglion cells have been rendered hypersensitive to intraocular pressure by irreversible damaging effects of previously increased intraocular pressures.
The current state of knowledge does not permit the elimination of any of the four hypotheses. An additional hypothesis is that the final stage of ganglion cell death is mediated by apoptosis. If so, a potential new treatment for glaucoma would be to inhibit the apoptotic pathway.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>8610790</pmid><doi>10.1016/S0002-9394(14)75421-2</doi><tpages>11</tpages></addata></record> |
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ispartof | American journal of ophthalmology, 1996-05, Vol.121 (5), p.473-483 |
issn | 0002-9394 1879-1891 |
language | eng |
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source | ScienceDirect Freedom Collection |
subjects | Adult Apoptosis Awards and Prizes Biological and medical sciences Cell Death Female Glaucoma - pathology Glaucoma - physiopathology Glaucoma and intraocular pressure Humans Intraocular Pressure Male Medical sciences Middle Aged Ophthalmology Retinal Ganglion Cells - pathology Societies, Medical Vision Disorders - physiopathology Visual Fields - physiology |
title | Delayed Functional Loss in Glaucoma LII Edward Jackson Memorial Lecture |
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