Chronic severe methanol intoxication after repeated mask cleansing due to fear of COVID-19: A new risk of coronaphobia.

BACKGROUND: Disproportionate fear of contracting COVID-19 (coronaphobia) may result in inappropriate use of preventive measures that could, in turn, result in severe harm to the patient. OBJECTIVE: To describe a patient with subacute parkinsonism and cognitive dysfunction and magnetic resonance imaging (MRI) evidence of bilateral deep white matter and basal ganglia damage. CASE PRESENTATION: A 56-year-old female presented with a 4-week history of insomnia, cognitive decline, and parkinsonism. Brain MRI revealed a bilateral lesion of both globus pallidus, deep white matter, and cerebellar hemispheres. Her son reported that, for the previous month, she had been cleaning her facial mask three times a day with a pure methanol solution as a disinfectant due to an intense fear of acquiring COVID-19. Previously, she had used 97% isopropyl alcohol and had inadvertently switched to methanol. After the exposure ended, she slowly improved but 4 months later she remains severely disabled. CONCLUSIONS: The repeated exposure to methanol vapor, the MRI findings, and the absence of other etiologies for her cognitive and parkinsonian features led to the diagnosis of chronic methanol intoxication with severe central nervous system damage. Misinformation is a likely contributory factor to such scenario. Efforts should be made by the scientific community to educate the general public on avoiding self-damaging behaviors as a result of coronaphobia.

Migraña episódica frecuente y péptido relacionado con el gen de la calcitonina. Influencia del tratamiento con topiramato y zonisamida en los niveles del péptido / Frequent episodic migraine and calcitonin gene-related peptide. Influence of treatment with topiramate and zonisamide on levels of the peptide

Introducción. La fisiopatología del dolor en la migraña se relaciona con la activación del sistema trigeminovascular por medio de la liberación de neuropéptidos vasoactivos, y el más importante es el péptido relacionado con el gen de la calcitonina (CGRP), que causa una inflamación neurógena en los vasos leptomeníngeos. Objetivo. Investigar si el CGRP está incrementado en la migraña episódica frecuente y si el tratamiento preventivo con topiramato o zonisamida modifica sus niveles. Sujetos y métodos. Se estudiaron 28 pacientes con migraña episódica con o sin aura, cumpliendo los criterios de la Sociedad Internacional de Cefaleas, con una frecuencia de 4-14 días/mes. En todos los pacientes se determinaron los niveles plasmáticos del CGRP durante un período intercrítico (> 72 h sin dolor). Los pacientes se aleatorizaron en dos grupos de tratamiento, uno con 50 mg/día de topiramato y otro con 50 mg/día de zonisamida, durante tres meses. Al finalizar el período activo se analizó nuevamente el nivel del CGRP. El grupo control lo constituyeron nueve sujetos sanos. Resultados. El CGRP fue significativamente superior en el grupo de migraña episódica comparado con el grupo control (50,61 ± 22,5 pg/mL frente a 34,96 ± 17,03 pg/mL; p = 0,037). Después del tratamiento con neuromoduladores no se hallaron diferencias significativas en el nivel de CGRP (46,11 ± 24,2 pg/mL basal frente a 47,5 ± 24,88 pg/mL postratamiento). Tampoco se hallaron diferencias al analizar los grupos de topiramato y zonisamida de forma individualizada. Conclusiones. El nivel plasmático del CGRP está incrementado en la migraña episódica y sus niveles no son modificados por el tratamiento con dosis bajas de topiramato o zonisamida (AU)

Introduction. The pathophysiology of pain in migraine is related to the activation of the trigeminovascular system by releasing vasoactive neuropeptides, the most important of which is calcitonin gene-related peptide (CGRP), which causes a neurogenic inflammation in the leptomeningeal vessels. Aim. To study whether CGRP is increased in frequent episodic migraine and whether preventive treatment with topiramate or zonisamide modifies its levels. Subjects and methods. We studied 28 patients with episodic migraine with or without aura, in accordance with the International Headache Society criteria, with a frequency of 4-14 days/month. Plasma levels of CGRP were determined in all the patients during an interictal period (> 72 hours without pain). Patients were divided at random into two treatment groups, one with 50 mg/day of topiramate and the other with 50 mg/day of zonisamide, for three months. At the end of the active period the CGRP level was analysed again. The control group consisted of nine healthy subjects. Results. CGRP was significantly higher in the episodic migraine group than in the control group (50.61 ± 22.5 pg/mL versus 34.96 ± 17.03 pg/mL; p = 0.037). After treatment with neuromodulators no significant differences were found in the level of CGRP (46.11 ± 24.2 pg/mL basal versus 47.5 ± 24.88 pg/mL post-treatment). Neither were any differences found on analysing the topiramate and zonisamide groups individually. Conclusions. The plasma level of CGRP is increased in episodic migraine, and its levels are not modified by treatment with low doses of topiramate or zonisamide (AU)