1990 Archives of Ophthalmology
doi: 10.1001/archopht.1990.01070100012001
This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables.
1990 Archives of Ophthalmology
doi: 10.1001/archopht.1990.01070100012001
This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables.
1990 Archives of Ophthalmology
doi: 10.1001/archopht.1990.01070100013002
This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables.
1990 Archives of Ophthalmology
doi: 10.1001/archopht.1990.01070100014003
This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables.
1990 Archives of Ophthalmology
doi: 10.1001/archopht.1990.01070100019004pmid: 2248664
Abstract To the Editor. —I was very interested to read the expedited publication in the December 1989 issue of the Archives by Sergott et al1 claiming that surgical optic nerve sheath decompression improved visual function in patients with "progressive" nonarteritic anterior ischemic optic neuropathy (NA-AION). They hypothesized that in NA-AION, "progressive visual loss after the initial ischemic event could be due to interference with rapid axoplasmic transport produced by [cerebrospinal fluid] CSF pressure within the anatomically restricted confines of the perineural optic nerve space. Drainage of the CSF might allow recovery of fast axoplasmic transport with subsequent improvement in vision." This theory raises some very important issues that need comment before they are accepted as scientifically valid concepts.My comments are based on the following: (1) my prospective studies on NA-AION in more than 600 patients; (2) my studies of the blood supply of the optic nerve head for the References 1. Sergott RC, Cohen MS, Bosley TM, Savino PJ. Optic nerve decompression may improve the progressive form of nonarteritic ischemic optic neuropathy . Arch Ophthalmol . 1989;107:1743-1754.Crossref 2. Hayreh SS. Pathogenesis of oedema of the optic disc (papilloedema) . Br J Ophthalmol . 1964;48:522-543.Crossref 3. Hayreh SS. Optic disc edema in raised intracranial pressure, V: pathogenesis . Arch Ophthalmol . 1977;95:1553-1565.Crossref 4. Hayreh SS. Optic disc edema in raised intracranial pressure, VI: assocated visual disturbances and their pathogenesis . Arch Ophthalmol . 1977;95:1566-1579.Crossref 5. Hayreh SS. The sheath of the optic nerve . Ophthalmologica . 1984;189:54-63.Crossref 6. Hayreh SS. Anterior ischaemic optic neuropathy, III: treatment, prophylaxis, and differential diagnosis . Br J Ophthalmol . 1974;58:981-989.Crossref
Sergott, Robert C.;Cohen, Marc S.;Bosley, Thomas M.;Savino, Peter J.
1990 Archives of Ophthalmology
doi: 10.1001/archopht.1990.01070100019005
Abstract In Reply. —We would like to address each of Dr Hayreh's concerns. In NAION, is the visual loss due to blockage of the axoplasmic flow? Dr Hayreh states, and we agree, that in papilledema visual dysfunction is secondary to ischemia. Because optic nerve sheath decompression (ONSD) has been demonstrated to reverse severe visual loss in pseudotumor cerebri,1 we considered ONSD for other optic neuropathies in which ischemia may be involved. Dr Hayreh continues that "axoplasmic flow plays no role in the conduction of nerve impulses." While this statement is true in the strict neurophysiologic sense, alteration of axoplasmic flow has produced blockage of impulse conduction in several carefully studied experimental and human conditions. First, giant axonal swellings have been produced in rats by the administration of β-β1-iminodipropionitrile, a toxin that disrupts the cytoskeletal elements of axons.2 In this model, iminodipropionitrile blocks slow axonal transport more than References 1. Keltner JL. Optic nerve sheath decompression: how does it work? Has its time come? Arch Ophthalmol . 1988;106:1365-1369.Crossref 2. Stanley EF, Griffen JW, Fahnestock KE. Effects of IDPN-induced axonal swellings on conduction in motor nerve fibers . J Neurol Sci . 1985;69:183-200.Crossref 3. Sladky JT, Tschoepe RL, Brown MJ. Nodal dysfunction in peripheral nerves subjected to chronic ischemia . Neurology . 1988;38( (suppl 1) ):351. 4. Beck RW, Servais GE, Hayreh SS. Anterior ischemic optic neuropathy, IX: cup-to-disc ratio and its role in pathogenesis . Ophthalmology . 1987;94:1503-1508.Crossref 5. Miller NR: Anterior ischemic optic neuropathy . In: Walsh and Hoyt's Clinical Neuro-Ophthalmology . 4th ed. Baltimore, Md:Williams & Wilkins; 1982:212-226. 6. Boghen DR, Glaser JS. Ischemic optic neuropathy: the clinical profile and natural history . Brain . 1975;98:689-708.Crossref
1990 Archives of Ophthalmology
doi: 10.1001/archopht.1990.01070100021006
Abstract To the Editor. —In their article in the December 1989 issue of the Archives, Sergott et al1 state that "... and lysis of presumed arachnoidal adhesions within the subdural space resulted in additional CSF [cerebrospinal fluid] drainage...." Surely they mean they opened the subarachnoid space. The subdural space is only a potential space between the dura and arachnoid and ordinarily does not contain cerebrospinal fluid.2,3 References 1. Sergott RC, Cohen MS, Bosley TM, Savino PJ. Optic nerve decompression may improve the progressive form of nonarteritic ischemic optic neuropathy . Arch Ophthalmol . 1989;107:1743-1754.Crossref 2. Miller N. Walsh and Hoyt's Clinical Neuro-ophthalmology . 4th ed. Baltimore, Md: Williams & Wilkins; 1982;1:56. 3. Warwick R. Eugene Wolff's Anatomy of the Eye and Orbit . 7th ed. London, England: H. K. Lewis; 1976:336-341.
1990 Archives of Ophthalmology
doi: 10.1001/archopht.1990.01070100021008pmid: 2383185
Abstract To the Editor. —While I think the article by Sergott et al1 in the December 1989 issue of the Archives is very interesting, and while I realize the authors have used the word "may" in the title, I still feel that there are some difficult questions that need further clarification.First of all, the number of patients in one sense is relatively small, at 14. In another sense, 14 patients with progressive nonarteritic ischemic optic neuropathy is actually a rather large number. In other words, I find it unusual that the authors were able to find 14 patients of a progressive nature in such a short period of time.The second issue has to do with what we are calling ischemic optic neuropathy. In the first place, we do not even know for sure whether this entity is ischemic. We know that the optic nerves tend to be small, References 1. Sergott RC, Cohen MS, Bosley TM, Savino PJ. Optic nerve decompression may improve the progressive form of nonarteritic ischemic optic neuropathy . Arch Ophthalmol . 1989;107:1743-1754.Crossref
Sergott, Robert C.;Cohen, Marc S.;Bosley, Thomas M.;Savino, Peter J.
1990 Archives of Ophthalmology
doi: 10.1001/archopht.1990.01070100021007
This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables. Abstract In Reply. —We appreciate Dr Kellen's comments regarding our recent publication. He is indeed correct in that we meant to say "the subarachnoid space," since he correctly indicates that this is where the cerebrospinal fluid is contained. We thank him for drawing this to our attention.
Mutlukan, Erkan;Cullen, James F.
1990 Archives of Ophthalmology
doi: 10.1001/archopht.1990.01070100022010pmid: 2383186
Abstract To the Editor. —We read with great interest the article by Sergott et al1 in the December 1989 issue of the Archives.We find it difficult to determine the exact nature of their decompressive procedure. The authors persistently mention multiple linear incisions of the meningeal sheath and lysis dissection of arachnoidal adhesions within the subdural space, and they refer to the presence of cerebrospinal fluid and blood elsewhere within the subdural space. The subdural space is only a potential space and is normally empty, and frequent adhesions between dura and arachnoid are found in normal individuals.2,3 Cerebrospinal fluid is present and circulates in the subarachnoid space and it has been well established that an increase of pressure in this area is associated with papilledema, which can be relieved by decompression of the optic nerve sheath, but the arachnoid must be opened to achieve this goal. In the specimens References 1. Sergott RC, Cohen MS, Bosley TM, Savino PJ. Optic nerve decompression may improve the progressive form of nonarteritic ischemic optic neuropathy . Arch Ophthalmol . 1989;107:1743-1754.Crossref 2. Duke-Elder S, Wybar KC. The Anatomy of the Visual System: System of Ophthalmology . London, England: Henry Kimpton; 1961;2:283. 3. Anderson DR. Ultrastructure of meningeal sheaths, normal human and monkey optic nerves . Arch Ophthalmol . 1969;82:659.Crossref 4. Smith JL, Hoyt WF, Newton TH. Optic nerve sheath decompression for relief of chronic monocular choked disc . Am J Ophthalmol 1969;68:633-639. 5. Kirkali P, Kansu T, Erzen C, Cila A. A radiological insight into primary empty sella syndrome with visual dysfunction . Neuro-ophthalmology . 1989;9:259-265.Crossref
Sergott, Robert C.;Cohen, Marc S.;Bosley, Thomas M.;Savino, Peter J.
1990 Archives of Ophthalmology
doi: 10.1001/archopht.1990.01070100021009
Abstract In Reply. —We appreciate Dr Wilson's comments regarding our article on optic nerve sheath decompression for progressive nonarteritic ischemic optic neuropathy (NAION). Our relatively large number of patients with progressive NAION reflects the clinical activity of the Wills Eye Hospital Neuro-Ophthalmology Service, Philadelphia, Pa, where we see over 4000 patients a year. The incidence of progressive visual loss in our population correlates well with the incidence reported by Boghen and Glaser.1 We agree with Dr Wilson that conclusive evidence is lacking to support a completely ischemic pathogenesis for NAION and believe that the alternative hypothesis proposed by Borchert and Lessell2 may have merit.However, we doubt that an inflammatory etiology for NAION has been overlooked, because the most complete histopathologic study of this entity did not demonstrate any vascular or neural inflammation.3 We believe that the focal ischemic neuropathies of diabetes mellitus satisfy the criteria for another References 1. Boghen DR, Glaser JS. Ischemic optic neuropathy: the clinical profile and natural history . Brain . 1975;98:689-708.Crossref 2. Borchert M, Lessell S. Progressive and recurrent non-arteritic ischemic optic neuropathy . Am J Ophthalmol . 1988;106:443-449. 3. Quigley HA, Miller NR, Green WR. The pattern of optic nerve fiber loss in anterior ischemic optic neuropathy . Am J Ophthalmol . 1985;100:769-776. 4. Asbury AK. Proximal diabetic neuropathy . Ann Neurol . 1977;2:179-180.Crossref 5. Repka MX, Savino PJ, Schatz NJ, Sergott RC. Clinical profile and long-term implications of anterior ischemic optic neuropathy . Am J Ophthalmol . 1983;96:478-483.
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