Optic nerve involvement in a case of methanol poisoning.

Naeser, Peter

doi:10.1136/bjo.72.10.778

Cited by 31 publications

(22 citation statements)

References 8 publications

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“…A variety of paint thinners and adhesives consist of methyl alcohol or toluene, and a number of reports have presented cases of poisoning by those components. [3][4][5][6][7] In the present case, the patient was exposed to dichloromethane that had a purity greater than 99%, thus the possibility of contamination with another organic solvent, such as methyl alcohol, could be excluded. This is the first-known, reported case of optic neuropathy caused by dichloromethane poisoning, though a case of facial nerve palsy related to dichloromethane poisoning has been presented.…”

Section: Discussionmentioning

confidence: 90%

“…5 The conditions generally progress rapidly after a short latency period, even after isolation from the organic solvent, and a number of patients have shown limited recovery. [3][4][5][6][7] Organic solvent poisoning occurs in various situations, such as with occupational use, thinner sniffing, accidental ingestion, and suicide attempts. A variety of paint thinners and adhesives consist of methyl alcohol or toluene, and a number of reports have presented cases of poisoning by those components.…”

Section: Discussionmentioning

confidence: 99%

“…Paint thinners and adhesives contain organic solvents, such as methyl alcohol and toluene, as well as others, and a number of reports regarding organic solvent toxic optic neuropathy from various agents have been published. [3][4][5][6][7] In addition, studies of organic poisoning caused by dichloromethane, which is primarily used in commercial applications, have been reported. [8][9][10][11][12][13][14][15][16][17][18] Dichloromethane is a clear, lipophilic liquid that is widely used as a chlorinated organic solvent in paint removers, paint and varnish thinners, and aerosol propellants, as well in other industrial processes.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Severe Optic Neuropathy Caused by Dichloromethane Inhalation

Kobayashi

Andõ

Tagami

et al. 2008

Journal of Ocular Pharmacology and Therapeutics

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Based on our findings, we considered that the central nervous system, including the optic nerve, was more severely damaged than the retina due to the normal findings in the ocular fundus and ERG examinations. Since dichloromethane produces carbon monoxide when catabolized in the liver, carbon monoxide toxicity together with the direct toxic effect of dichloromethane were considered to contribute to optic neuropathy in this case. The outcome for the present patient was poor.

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Section: Discussionmentioning

confidence: 90%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Severe Optic Neuropathy Caused by Dichloromethane Inhalation

Kobayashi

Andõ

Tagami

et al. 2008

Journal of Ocular Pharmacology and Therapeutics

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“…A dense central or paracentral scotoma is also observed [1]. Postmortem histologic sudies have shown degeneration of retinal ganglion cells and optic nerve [1,4,6]. A small amount of methanol is Hayasaka/Hayasaka/Hiraki/Kadoi/Nagaki/ Matsumoto found in normal human breath, in blood samples of normal subjects, and in patients with chronic alcoholism [9][10][11].…”

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 poisoning causes acute visual impairment, optic atrophy, coma, and sometimes death in man (Benton & Calhaun 1952;Duke-Elder & Scott 1971;McMartin et al 1980;Roe 1982;Sharpe et al 1982;Sejersted et al 1983;Chen et al 1985;Naeser 1988;Matsui et al 1991;Hantson et al 1999;Onder et al 1999;Sharma et al 1999). Ocular toxicity is thought to be due to the formation of toxic metabolites, formaldehyde or formate.…”

mentioning

confidence: 99%

Ocular Changes after Intravitreal Injection of Methanol, Formaldehyde, or Formate in Rabbits

Hayasaka

Nagaki

2001

Pharmacology & Toxicology

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Abstract:We evaluated the effects of intravitreal injection of methanol, formaldehyde, or formate on rabbit eyes. One hundred ml of 1% methanol, 1% or 0.1% formaldehyde, or 1% formate was injected in the vitreous cavity of the right eyes of rabbits. The eyes were examined by biomicroscopy and ophthalmoscopy weekly. One month after injection, the eyes were enucleated and examined histologically. One week after treatment the animals that received 0.1% formaldehyde showed retinal vessel dilation, and the rabbits that received 1% formaldehyde showed mild posterior subcapsular cataract and retinal vessel dilation and haemorrhages. One month after treatment, the animals that received 0.1% or 1% formaldehyde developed mild posterior subcapsular cataract and retinal lesions. Animals that received 1% methanol or 1% formate showed nearly normal optical media and fundi. Histologically disorganized retina and optic nerve were seen in eyes that received 0.1% or 1% formaldehyde. Eyes that received 1% methanol or 1% formate appeared histologically normal. Our findings indicate that intravitreal injection of formaldehyde causes retinal and optic nerve damage, while methanol and formate are not or less toxic to ocular tissues.

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Optic nerve involvement in a case of methanol poisoning.

Cited by 31 publications

References 8 publications

Severe Optic Neuropathy Caused by Dichloromethane Inhalation

Severe Optic Neuropathy Caused by Dichloromethane Inhalation

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

Ocular Changes after Intravitreal Injection of Methanol, Formaldehyde, or Formate in Rabbits

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