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Abstract Details

Sudden Severe Vision Loss And Persistent Vomiting: From A Suspicion Of Neuromyelitis Optica To A Diagnosis Of Acute Thinner Intoxication
Neuro-ophthalmology/Neuro-otology
P6 - Poster Session 6 (12:00 PM-1:00 PM)
5-006

Case Report

47-YOM was referred to neurology ED with 4-day history of sudden severe bilateral vision loss, preceded of 7-day persistent vomiting and hiccups. He denied past medical complaints. There was remarkable depression and, after some resistance, he revealed thinner inhalation addiction for 2 years. In the past 7 days, he increased the previous unknown intake to massive inhalation of 1-2l/day. Neuro-ophthalmological examination showed VA of light perception RE and 20/200 LE, eye-movement elicited pain and relative afferent pupillary defect in LE.

Retinography with angiofluorescein revealed RE with diffuse disc extravasation, peridisc ischemia, choroidal folds and moderate papilledema, and LE with anellar disc extravasation and temporal disc pallor. Computerized visual field mean deviation -30.47dB RE and -16,51bD LE. Optic coherence tomography showed RE disc edema and LE loss of layers in temporal. 1.5T MRI revealed extensive hypersignal in LE optic nerve. CSF analysis was normal.

Introduction

Thinner sniffing is worldwide concern. The commercialized thinner proportion of toluene, alcohols and hydrocarbons is wide variable.

Immediate effects are hallucinations and delusions, nausea and vomiting are the most common, and, metabolic acidosis and hypoxia are the most threaten. Chronicity affects multisystems and neurologic symptoms vary from cerebellar dysfunction, optic neuropathy, hearing impairment to peripheral neuropathy and more.

Neuroimaging damage are diffuse and multifocal white-matter changes, cerebral, cerebellar, corpus callosum and brainstem atrophies. Time and amount of consumption have positive correlation.

Neuropathologically, there is demyelination and hyalinisation of arterioles, similar to the methanol exposure toxicity.


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Discussion

Development of blindness in addition to possible area postrema syndrome lead to a NMOSD hypothesis. The proper history taking uncovered a toxic-metabolic etiology, corroborating the need to exclude other diagnosis before impute primary demyelination. Current care is directed to supportive measures and psychiatric issues. Evidence on steroids, ascorbic acid, N-acetylcysteine and vitamin B are scarce.

Authors/Disclosures
Emerson de Paula Santos
PRESENTER
No disclosure on file
Belisa Lopes Alvares No disclosure on file
Ana Paula Costa No disclosure on file