J Korean Med Sci.  2017 Feb;32(2):371-376. 10.3346/jkms.2017.32.2.371.

Neurological Complications Resulting from Non-Oral Occupational Methanol Poisoning

• Choi JH
• Lee SK
• Gil YE
• Ryu J
• Jung-Choi
• Kim H
• Choi JY
• Park SA
• Lee HW
• Yun JY

• KMID: 2364185
• DOI: http://doi.org/10.3346/jkms.2017.32.2.371

Abstract

Methanol poisoning results in neurological complications including visual disturbances, bilateral putaminal hemorrhagic necrosis, parkinsonism, cerebral edema, coma, or seizures. Almost all reported cases of methanol poisoning are caused by oral ingestion of methanol. However, recently there was an outbreak of methanol poisoning via non-oral exposure that resulted in severe neurological complications to a few workers at industrial sites in Korea. We present 3 patients who had severe neurological complications resulting from non-oral occupational methanol poisoning. Even though initial metabolic acidosis and mental changes were improved with hemodialysis, all of the 3 patients presented optic atrophy and ataxia or parkinsonism as neurological complications resulting from methanol poisoning. In order to manage it adequately, as well as to prevent it, physicians should recognize that methanol poisoning by non-oral exposure can cause neurologic complications.

Keyword

Methanol; Poisoning; Neurological Manifestations; Metabolic Encephalopathies

MeSH Terms

Acidosis
Ataxia
Brain Diseases, Metabolic
Brain Edema
Coma
Eating
Humans
Korea
Methanol*
Necrosis
Neurologic Manifestations
Optic Atrophy
Parkinsonian Disorders
Poisoning*
Renal Dialysis
Seizures
Methanol

Figure

• 

  Fig. 1 Brain MRI images. (A, B, C) For patient 1, brain MRI performed on the day of admission showed diffusion restrictions in the bilateral putamen and anterior insular cortices in diffusion weighted imaging (A), high signal intensities in T2 weighted imaging over the same regions (B), and focal hemorrhage was not detected in susceptibility weighted imaging (C), which may have been due to toxic metabolic encephalopathy. (D, E, F) For patient 2, brain MRI performed on the fifth day after admission showed diffusion restriction in the bilateral putamen and frontal cortices in diffusion weighted imaging (D), high signal intensities in T2 weighted imaging over the same regions (E), and focal hemorrhage in the left putamen in susceptibility weighted imaging (F). (G, H, I) For patient 3, brain MRI performed 2 months after symptom onset showed low signal intensity in the bilateral putamen, frontal cortices, and subcortices in diffusion weighted imaging (G), high signal intensities in the bilateral putamen, frontal cortices and subcortices, and insular cortices in T2 weighted imaging (H), and focal hemorrhage in the bilateral putamen and frontal subcortices in susceptibility weighted imaging (I). MRI = magnetic resonance image.

• 

  Fig. 2 Images of fundus examination. (A, B) Patient 1 with both edematous optic nerves (arrowheads). (C, D) Patient 2 with bilateral pale optic disks (arrows). (E, F) Patient 3 showing bilateral pale optic disks (arrows).

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