Case Report Bilateral Optic Neuropathy with Bilateral Putaminal Lesions: A Case Report Jumpei Togawa, MD, Takekazu Ohi, MD, PhD From the Department of Neurology, Otsu Red Cross Hospital, Otsu, Japan (JT); and Department of Neurology, Kyoto Hakuaikai Hospital, Kyoto, Japan (TO).

ABSTRACT Bilateral optic neuropathy with bilateral putaminal lesions may be caused by methanol or cyanide poisoning or mitochondrial disorders including Leber hereditary optic neuropathy and Leigh syndrome. We report the case of a 34-year-old Japanese man who developed bilateral visual loss 5 days after the development of gastrointestinal symptoms. Magnetic resonance imaging of the brain on admission revealed high-intensity signal areas in the bilateral putamina on diffusion-weighted and T2-weighted images as well as a high-intensity signal area in the left middle cerebellar peduncle that had been identified 3 years previously. We diagnosed bilateral optic neuropathy with bilateral putaminal lesions caused by preceding infection-triggered demyelination. We administered methylprednisolone, but his vision did not recover.

Keywords: Bilateral putaminal lesions, optic neuropathy, Leber hereditary optic neuropathy, Leigh syndrome, neuromyelitis optica. Acceptance: Received August 16, 2013, and in revised form May 28, 2014. Accepted for publication June 1, 2014. Correspondence: Address correspondence to Jumpei Togawa, MD, Department of Neurology, Otsu Red Cross Hospital 1-1-35 Nagara, Otsu, Shiga 520-8511, Japan, Phone: +81-77-5224131, Fax: +81-77-525-8018, E-mail: [email protected]. Conflicts of Interest: None. J Neuroimaging 2015;25:514-516. DOI: 10.1111/jon.12153

Introduction Bilateral visual loss and bilateral putaminal lesions may be caused by methanol or cyanide poisoning, Leber hereditary optic neuropathy, or Leigh syndrome.1–4 We report the case of a 34-year-old Japanese man who developed bilateral visual loss 5 days after the development of gastrointestinal symptoms. Neuroimaging revealed bilateral putaminal lesions.

Case Report A 34-year-old Japanese man was admitted to our hospital with a chief complaint of bilateral visual loss that had developed 3 days before admission. The patient was well until 5 days before the onset of blindness, when he developed nausea, vomiting, and diarrhea. Neurological examination revealed bilateral pupillary diameters of 7 mm and a slow direct light reflex; he could not count the number of fingers, but could see brightness and darkness. His venous serum lactate level was 10.8 mg/dL (reference range, 5-20 mg/dL). Immunoglobulin M antibody to the ganglioside N-acetylgalactosaminyl GD1a (IgM anti-GalNAcGD1a antibody) was positive in his acute-phase serum. No pathological mutation was detected in his whole mitochon-

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drial deoxyribonucleic acid (mtDNA) assay, and no deletions were detected on either Southern blotting analysis or long polymerase chain reaction amplification. Methanol was not detected in urine taken on the second day after admission. The patient’s cerebrospinal fluid (CSF) cell count, protein level, and glucose level were normal. The concentration of myelin basic protein in his CSF was 276 pg/mL (reference,

Bilateral optic neuropathy with bilateral putaminal lesions: a case report.

Bilateral optic neuropathy with bilateral putaminal lesions may be caused by methanol or cyanide poisoning or mitochondrial disorders including Leber ...
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