J Korean Ophthalmol Soc.  2016 Dec;57(12):1987-1993. 10.3341/jkos.2016.57.12.1987.

A Case of Optic Neuropathy Associated with Methyl Bromide Intoxication

Affiliations
  • 1Department of Ophthalmology, Dong-A University College of Medicine, Busan, Korea. wyryu@dau.ac.kr
  • 2Department of Neurology, Dong-A University College of Medicine, Busan, Korea.

Abstract

PURPOSE
In this study, a case of toxic encephalopathy and optic neuropathy due to methyl bromide poisoning is reported.
CASE SUMMARY
A 31-year-old male presented with dysarthria, gait disturbance and bilateral visual impairment. He was treated with intravenous methylprednisolone for bilateral optic neuritis 1 year prior. He previously worked in a fumigation warehouse and was exposed to methyl bromide in the past 3 years. His corrected visual acuity was 20/30 in both eyes. The patient had reduced color vision and enlarged central scotoma in both eyes. His mentality was alert but exhibited slow response, ataxia and dysarthria. Brain magnetic resonance imaging (MRI) revealed high signals in the brainstem, cerebellum and midbrain. His serum and urine methyl bromide concentrations were significantly elevated. The patient was treated with intravenous methylprednisolone 1.0 g/day for 5 days. MRI showed resolution of the multiple brain lesions observed previously. Ten days after steroid therapy, his visual acuity was 20/20 in both eyes and his neurologic manifestations were completely recovered at 2 months after treatment.
CONCLUSIONS
Taking a detailed occupational history is necessary in patients with optic neuropathy. The probability of toxic optic neuropathy should be considered when patients are exposed to toxic materials.

Keyword

Methyl bromide intoxication; Methyl bromide poisoning; Secondary optic neuropathy; Toxic encephalopathy; Toxic optic neuropathy

MeSH Terms

Adult
Ataxia
Brain
Brain Stem
Cerebellum
Color Vision
Dysarthria
Fumigation
Gait
Humans
Magnetic Resonance Imaging
Male
Mesencephalon
Methylprednisolone
Neurologic Manifestations
Neurotoxicity Syndromes
Optic Nerve Diseases*
Optic Neuritis
Poisoning
Scotoma
Vision Disorders
Visual Acuity
Methylprednisolone

Figure

  • Figure 1. Visual field and fundus photography at initial attack. The patient presented with the central scotoma and mild optic disc swelling in both eyes at the initial attack.

  • Figure 2. Visual field and fundus photography at second attack. The patient presented with mild central scotoma and the optic disc was temporally pallor at the second attack.

  • Figure 3. Magnetic resonance images. Fluid-attenuated inversion recovery images for a patient showing high signal changes in peri-aqueductal gray matter of midbrain (arrow) (A), the pons, the medulla, and cerebellum (arrow) (B). Ten days after treatment, the brain lesions previously observed was rapidly disappeared (arrows) (C, D).

  • Figure 4. Visual field and disc optical coherence tomography at one and one-half years after treatment. One and one-half years after treatment, the patient was presented with mild central scotoma and decreased retinal nerve fiber thickness of temporal area in optic coherence tomography. RNFL = retinal nerve fiber layer; OD = oculus dexter; OS = oculus sinister; C/D = cup/disc; TEMP = temporal; SUP = superior; NAS = nasal; INF = inferior; S = superior; N = nasal; I = inferior; T = temporal.


Reference

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