Background: The relationship between varicella-zoster virus (VZV)-associated myelitis and aquaporin-4 immunoglobulin-G (AQP4-IgG) remains unknown.Case Report: We report a case of acute radiculomyelitis with longitudinal extensive hyperintensity signals traversing the brainstem until the upper thoracic cord in a 55-year-old healthy woman following herpes zoster infection in the left C4-T3 dermatome. VZV-specific IgG in the cerebrospinal fluid (CSF) and AQP4-IgG positivity on enzyme-linked immunosorbent assay (ELISA) were undetectable. Thus, she was diagnosed with immune-competent VZV radiculomyelitis. Forty-two months later, she experienced a relapse, and AQP4-IgG positivity was detected on ELISA. A cell-based assay (CBA) showed AQP4-IgG positivity not only at the time of recurrence but also retrospectively at 1 month after the initial symptoms. We concluded that AQP4-IgG-positive neuromyelitis optica spectrum disorder (NMOSD) was concurrent with VZV myelitis. After the second attack, she was treated with azathioprine and has had no relapse since then.Conclusion: We reported a case of VZV radiculomyelitis with confirmed concurrent AQP4-IgG positivity. NMOSD induced by herpes zoster has been recently identified, but distinguishing it from VZV myelitis can be difficult and whether these two diseases aggravate each other is unknown. Awareness of the potentially varied presentation of VZV myelitis can enable earlier recognition and proper treatment.

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We herein report two patients harboring the mutation N279K in microtubule-associated protein tau (MAPT), who showed parkinsonism with a disease duration within three years from the onset, evaluated by dopamine transporter (DAT) [123I]N-ω-fluoroprophyl-2β-carbomethoxy-3β-(4-iodophenyl) tropane single-photon emission computed tomography. We performed a quantification analysis, comparing five age- and severity-matched PD patients and six normal controls. The patients with the N279K mutation showed a more marked reduction in their DAT densities, especially in the caudate nucleus and anterior putamen, than the others. An early marked reduction in the DAT densities in the caudate nucleus and anterior putamen may be an early biomarker of patients with MAPT mutations.

A 42-year-old man presented with coma from methanol intoxication (178 mg/dL; its metabolite, formic acid, 860 mg/mL). Continuous hemodiafiltration improved his disturbance of consciousness, but he subsequently developed cognitive dysfunction and parkinsonism, which were finally alleviated by rehabilitation and amantadine therapy. Brain MRI revealed acute basal ganglionic and hippocampal lesions and chronic developmental white matter lesions (figures 1 and 2).Formic acid disrupts mitochondria, resulting in cytotoxic hypoxia and oxygen free radical production, which might cause acute putaminal and hippocampal injuries.1 Oxygen free radicals contribute to the development of white matter lesions.2 In our case, toxic encephalopathy likely resulted from diverse mechanisms.Haruka Takeshige, MD, Yuji Ueno, MD, PhD, Fuyuko Sasaki, MD, Akira Namera, PhD, Takehisa Matsukawa, PhD, Kazuhito Yokoyama, MD, DMSc, Nobutaka Hattori, MD, PhD Author contributions: Dr. Takeshige: drafting the manuscript, acquisition of data. Dr. Ueno: drafting the manuscript, study conception, interpretation of data, acquisition of data. Dr. Sasaki: interpretation of data, acquisition of data. Dr. Namera: interpretation of data, acquisition of data. Dr. Matsukawa: interpretation of data, acquisition of data. Dr. Yokoyama: interpretation of data, acquisition of data. Dr. Hattori: critical revision of the manuscript for important intellectual content, study supervision. Study funding: No targeted funding reported.Disclosure: The authors report no disclosures relevant to the manuscript. Go to Neurology.org for full disclosures.Correspondence to Dr. Ueno: yuji-u@juntendo.ac.jp