Optical coherence tomography findings in methanol toxicity

Abstract

Background Methanol toxicity poses a significant public health problem in developing countries, and in Southeast Asia, where the most common source of poisoning is via adulterated liquor in local drinks. Methanol toxicity can have devastating visual consequences and retinal specialists should be aware of the features of this toxic optic neuropathy. The authors report a case of severe systemic methanol toxicity and relatively mild optic neuropathy demonstrating unique retinal changes on optical coherence tomography (OCT).Case presentation A previously healthy student developed ataxia, difficulty breathing and loss of consciousness hours after drinking homemade alcohol while traveling in Indonesia. She was found to have a serum pH of 6.79 and elevated methanol levels. She was treated with intravenous ethanol, methylprednisolone and sodium bicarbonate. When she awoke she had bilateral central scotomas. At presentation, she had central depression on visual field testing. OCT of the retinal nerve fiber layer (RNFL) was normal but ganglion cell layer analysis (GCL) showed highly selective loss of the nasal fibers in both eyes. Further, OCT of the macula demonstrated inner nuclear layer (INL) microcysts in the corresponding area of selective GCL loss in both eyes.ConclusionsThe selective involvement of the papillomacular bundle fibers is common in toxic optic neuropathies and represents damage to the small caliber axons rich in mitochondria. Despite severe systemic toxicity, the relative sparing of the optic nerve in this case enabled characterization of the evolution of methanol toxicity with segmental GCL involvement and preservation of the RNFL, corresponding to the papillomacular bundle. This is the first reported case of INL microcysts in methanol optic neuropathy and supports that they are a non-specific finding, and may represent preferential damage to the papillomacular bundle.

Accumulation of formaldehyde causes motor deficits in an in vivo model of hindlimb unloading

“…The above data indicated that HU caused motor deficits associated with formaldehyde accumulation in the muscle and cerebellum. Unexpectedly, exogenous formaldehyde or methanol (a precursor of formaldehyde) has been shown to induce cerebellar ataxias in rats 15 and humans 16 . These data suggest that excessive formaldehyde in the cerebellum may be a direct trigger of acute cerebellar ataxia in the HU mouse model.…”

“…Unsurprisingly, excessive formaldehyde had been found to markedly inactivate ATM protein and induce cell death 58 . Exogenous formaldehyde and methanol directly causes cerebellar ataxia in mice 15 and humans 16 . Formaldehyde can cause a reduction in the numbers and sizes of Purkinje cells and granular cells, and in the thickness of the granular layer in mice 59 .…”

“…Under microgravity conditions, the expression of semicarbazide-sensitive amine oxidase (SSAO, a formaldehyde-generating enzyme) was elevated about 2-fold in a system of SSAO-transformed Escherichia coli BL21 13 . Notably, exogenous formaldehyde or methanol (MeOH, a precursor of formaldehyde 14 ) poisoning also induced severe cerebellar ataxias in mice 15 and humans 16 . Recent studies revealed that the accumulated formaldehyde induces muscle atrophy and osteoporosis in the mice with double-knockout of alcohol dehydrogenase-5 (ADH5) and aldehyde dehydrogenase-2 (ALDH2) (two enzyme of clearance formaldehyde) 17 , 18 .…”

Neuropatía óptica bilateral e irreversible por ingestión de disolvente de pintura

“…También es característica en esta fase de atrofia un aumento de la excavación papilar 10 , así como un progresivo adelgazamiento de la capa de fibras peripapilares, sobre todo temporales, valorado mediante OCT; ambos hallazgos estaban presentes en nuestro paciente. Se han descrito otras alteraciones retinianas, como la aparición de microquistes en la capa nuclear interna 11 , ausentes en nuestro caso.…”

Severe visual loss by inhalation of methanol

“…The resulting outcome then gets metabolized by aldehyde dehydrogenase into formic acid. Formic acid is toxic and it inhibits the mitochondrial cytochrome oxidase causing tissue hypoxia, and lactic acid [ 3 ].…”