Methanol-Induced Optic Nerve Cupping

Sharma, Mithlesh C; Volpe, Nicholas J.; Dreyer, Evan B.

doi:10.1001/archopht.117.2.286

Cited by 44 publications

(40 citation statements)

References 7 publications

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“…5 The mechanism of subsequent optic atrophy in patients with methanol poisoning is still unknown, it was suggested to be due to progressive demyelination. 8 The distinct glaucomatous-like cupping of the optic disc suggests extensive loss of retina ganglion cells, which has been thought to result from retrograde degeneration of optic nerve axons. 8 The bilateral haemorrhagic necrosis of the putamen and oedema in the deep white matter of our patient are the characteristic MRI findings of severe methanol intoxication.…”

Section: Commentmentioning

confidence: 99%

“…8 The distinct glaucomatous-like cupping of the optic disc suggests extensive loss of retina ganglion cells, which has been thought to result from retrograde degeneration of optic nerve axons. 8 The bilateral haemorrhagic necrosis of the putamen and oedema in the deep white matter of our patient are the characteristic MRI findings of severe methanol intoxication. 9 Besides the optic disc oedema, the oedematous changes involving optic tracts and optic radiations shown on MRI might contribute to the profound vision loss in our case.…”

Section: Commentmentioning

confidence: 99%

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Ocular manifestations and MRI findings in a case of methanol poisoning

Yang

Tsai²,

Lirng

2004

Eye

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Section: Commentmentioning

confidence: 99%

Section: Commentmentioning

confidence: 99%

Ocular manifestations and MRI findings in a case of methanol poisoning

Yang

Tsai²,

Lirng

2004

Eye

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“…However, "cupping" is also used as a synonym for the pathophysiology of glaucomatous damage to the ONH 44,[73][74][75] . Because the clinical and pathophysiologic contexts for "cupping" are seldom clarified there is a confusing literature regarding the presence, importance and meaning of "cupping" in a variety of optic neuropathies 21,[76][77][78][79][80][81][82][83][84][85][86][87][88][89] .…”

Section: Onh Biomechanics and Onh Cuppingmentioning

confidence: 99%

Premise and Prediction???How Optic Nerve Head Biomechanics Underlies the Susceptibility and Clinical Behavior of the Aged Optic Nerve Head

Burgoyne¹,

Downs²

2008

Journal of Glaucoma

194

169

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We propose that age-related alterations in optic nerve head (ONH) biomechanics underlie the clinical behavior and increased susceptibility of the aged ONH to glaucomatous damage. The literature which suggests that the aged ONH is more susceptible to glaucomatous damage at all levels of intraocular pressure is reviewed. The relevant biomechanics of the aged ONH are discussed and a biomechanical explanation for why, on average, the stiffened peripapillary scleral and lamina cribrosa connective tissues of the aged eye should lead to a shallow (senile sclerotic) form of cupping is proposed. A logic for why age-related axon loss and the optic neuropathy of glaucoma in the aged eye may overlap is discussed. Finally, we argue for a need to characterize all forms of clinical cupping into prelaminar and laminar components so as to add precision to the discussion of clinical cupping which does not currently exist. Such characterization may lead to the early detection of ONH axonal and connective tissue pathology in ocular hypertension and eventually aid in the assessment of etiology in all forms of optic neuropathy including those that may be purely age-related. The Susceptibility of the Aged Optic Nerve Head (ONH)A variety of data suggest that the ONH becomes more susceptible to progressive glaucomatous damage as it ages, though this concept remains unproven through direct experimentation, and may not be true for every aged eye. These data can be summarized as follows. First, in most [1][2][3][4][5] , but not all 6,7 , population based studies, intraocular pressure (IOP) either does not increase with age or if it does, the magnitude of increase is not likely to be clinically important. Thus, the fact that the prevalence of the neuropathy increases with age 8 is likely explained by a greater susceptibility to IOP and other non-IOP-related risk factors, rather than a higher prevalence of IOP elevation, with increasing age. Second, in an extensive review of the literature, we can find only a few reports of the onset and progression of normal tension glaucoma (NTG) in infants, children and young adults 9 . While we acknowledge that accurate NTG prevalence estimates require long-term telemetric characterization of untreated IOP and rigorous population based ONH and visual field examinations, all existing studies suggest that NTG is most commonly a disease of the elderly [10][11][12][13][14][15] in the young 9 . Third, age is an independent risk factor for both the prevalence 16 and progression of the neuropathy at all stages of damage [17][18][19] . The Clinical Behavior of the Aged ONHApart from the issue of ONH susceptibility, we predict that if all aspects of insult are equal (alterations in IOP, the volume flow of blood and nutrient transfer from the laminar capillary to the ONH astrocyte are all of the same magnitude, duration and fluctuation), the aged eye will demonstrate clinical cupping that is on average shallow and pale (at all stages of field loss) compared to the eye of a child or young adult. This clini...

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“…Acute methanol intoxication causes severe visual dysfunction, optic nerve head disease, and sometimes death in humans [1][2][3][4][5][6][7][8]. At the acute stage of methanol poisoning, optic disk edema occurs.…”

Section: Introductionmentioning

confidence: 99%

Serum Methanol Levels in Subjects with or without Optic Nerve Head Disease

Hayasaka

Hayasaka²,

Hiraki³

et al. 2000

Ophthalmic Res

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We evaluated serum methanol levels in subjects with or without optic nerve head disease. Serum methanol levels were determined using gas chromatography in 71 patients with optic nerve head disease and in 127 subjects without optic nerve head disease. Their ages ranged from 17 to 89 years. Serum methanol levels in 127 subjects without optic nerve head disease ranged from 0.12 to 3.86 µg/ml (mean ± standard deviation, 1.72 ± 0.86 µg/ml). In the subjects without optic nerve head disease, the differences in the levels between those with cataract versus retinal detachment, men versus women, and between each age-group (50–80 years) were not significant. The methanol levels in patients with optic neuritis (n = 2), Wolfram syndrome (n = 1), Leber hereditary optic neuropathy at the late stage (n = 2), retinitis pigmentosa (n = 23), and primary open-angle glaucoma (n = 16) were less than 3.86 µg/ml. Methanol levels in 1 patient with Leber hereditary optic neuropathy at the acute stage was 5.28 µg/ml. Of 10 patients with primary angle-closure glaucoma, 1 had a slightly elevated level and 9 had levels less than 3.86 µg/ml. Of 17 patients with normal tension glaucoma, 5 had methanol levels higher than 3.86 µg/ml, and 12 patients had levels less than 3.86 µg/ml. The present study shows that serum methanol levels in subjects without optic nerve head disease ranged from 0.12 to 3.86 µg/ml and were much lower than the levels that produce acute ocular symptoms of methanol intoxication. It is possible that high serum methanol levels may play a part in the acute stage of Leber hereditary optic neuropathy and normal tension glaucoma in certain patients. It is unlikely that increased serum methanol levels participate in primary angle-closure glaucoma.

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Methanol-Induced Optic Nerve Cupping

Cited by 44 publications

References 7 publications

Ocular manifestations and MRI findings in a case of methanol poisoning

Ocular manifestations and MRI findings in a case of methanol poisoning

Premise and Prediction???How Optic Nerve Head Biomechanics Underlies the Susceptibility and Clinical Behavior of the Aged Optic Nerve Head

Serum Methanol Levels in Subjects with or without Optic Nerve Head Disease

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