Toxic optic neuropathies: an updated review

Grzybowski, Andrzej; Zülsdorff, Magdalena; Wilhelm, Helmut; Tonagel, Felix

doi:10.1111/aos.12515

Cited by 160 publications

(151 citation statements)

References 84 publications

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“…The optic neuropathy of familial dysautonomia closely resembles that seen in mitochondrial optic neuropathies such as Leber hereditary optic neuropathy (15,19), autosomal dominant optic atrophy (20), and tobacco/alcoholic (21), Cuban epidemic (22), B 12 deficiency, and drug-related optic neuropathies (23). Pathological studies in Leber hereditary optic neuropathy and dominant optic atrophy have shown relatively preservation of melanopsin-containing ganglion cells in spite of extensive loss of the predominantly small midget/ parvocellular P-ganglion cells (17,24).…”

Section: Discussionmentioning

confidence: 92%

Pathological Confirmation of Optic Neuropathy in Familial Dysautonomia

Mendoza‐Santiesteban

Palma

Hedges

et al. 2017

Journal of Neuropathology &Amp; Experimental Neurology

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Clinical data suggest that optic neuropathy and retinal ganglion cell loss are the main cause of visual decline in patients with familial dysautonomia, but this has not previously been confirmed by pathological analyses. We studied retinas and optic nerves in 6 eyes from 3 affected patients obtained at autopsy. Analyses included routine neurohistology and immunohistochemistry for neurofilaments, cytochrome c oxidase (COX), and melanopsin-containing ganglion cells. We observed profound axon loss in the temporal portions of optic nerves with relative preservation in the nasal portions; this correlated with clinical and optical coherence tomography findings in 1 patient. Retinal ganglion cell layers were markedly reduced in the central retina, whereas melanopsin-containing ganglion cells were relatively spared. COX staining was reduced in the temporal portions of the optic nerve indicating reduced mitochondrial density. Axonal swelling with degenerating lysosomes and mitochondria were observed by electron microscopy. These findings support the concept that there is a specific optic neuropathy and retinopathy in patients with familial dysautonomia similar to that seen in other optic neuropathies with mitochondrial dysfunction. This raises the possibility that defective expression of the IkB kinase complex-associated protein (IKAP) resulting from mutations in IKBKAP affects mitochondrial function in the metabolism-dependent retinal parvocellular ganglion cells in this condition.

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Section: Discussionmentioning

confidence: 92%

Pathological Confirmation of Optic Neuropathy in Familial Dysautonomia

Mendoza‐Santiesteban

Palma

Hedges

et al. 2017

Journal of Neuropathology &Amp; Experimental Neurology

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“…The principle of the detoxification is depicted in figure 4. Currently, folic acid is recommended as an antidote in cases of methanol poisoning in human medicine 118,119 . Additionally, it was proved that formic acid is suitable for mitigating neurotoxicity pursuant to chronic ethanol intake 120 .…”

Section: Treatment Of Poisoning With the Alcoholsmentioning

confidence: 99%

Toxicology and the biological role of methanol and ethanol: Current view

Pohanka¹

2016

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

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Background. Alcohol variants such as ethanol and methanol are simple organic compounds widely used in foods, pharmaceuticals, chemical synthesis, etc. Both are becoming an emerging health problem; abuse of ethanol containing beverages can lead to disparate health problems and methanol is highly toxic and unfit for consumption. Methods and Results. This review summarizes the basic knowledge about ethanol and methanol toxicity, the effect mechanism on the body, the current care of poisoned individuals and the implication of alcohols in the development of diseases. Alcohol related dementia, stroke, metabolic syndrome and hepatitis are discussed as well. Besides ethanol, methanol toxicity and its biodegradation pathways are addressed. Conclusions. The impact of ethanol and methanol on the body is shown as case reports, along with a discussion on the possible implication of alcohol in Alzheimer's disease and antidotal therapy for methanol poisoning. The role of ethanol in cancer and degenerative disorders seems to be underestimated given the current knowledge. Treatment in case of poisoning is another issue that remains unresolved even though effective protocols and drugs exist.

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“…Formate causes direct retinal damage and mitochondrial damage in the optic nerve, leading to edema and atrophy . About half of methanol‐poisoned patients develop ocular symptoms, and if the patient survives, most ocular symptoms improve or resolve …”

Section: Introductionmentioning

confidence: 99%

Folate as an Adjuvant Therapy in Methanol Poisoning

Theobald

Lim

2019

Nut in Clin Prac

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Folate and its derivatives have long been used as an adjunctive treatment in methanol poisoning. Methanol is ultimately metabolized to formate, the toxic compound. The accumulation of formate can lead to acidemia, retinal damage, visual impairment, and death. Formate is converted to carbon dioxide and water in a folate-dependent manner, and folate is often given in cases of methanol poisoning. In this paper, the evidence for folate as an adjunctive therapy in methanol poisoning is reviewed. (Nutr Clin Pract.

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Toxic optic neuropathies: an updated review

Cited by 160 publications

References 84 publications

Pathological Confirmation of Optic Neuropathy in Familial Dysautonomia

Pathological Confirmation of Optic Neuropathy in Familial Dysautonomia

Toxicology and the biological role of methanol and ethanol: Current view

Folate as an Adjuvant Therapy in Methanol Poisoning

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