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Subjective symptoms such as lightheadedness and dizziness appear to persist, however, suggesting CNS damage. We evaluated CNS damage due to DPAA by detecting abnormal eye movements.\n\nMethods\nSubjects comprised 29 victims of exposure to DPAA in whom this substance had been detected in the nails. Investigations were performed more than 3 years following cessation of DPAA exposure. Abnormal eye movements were monitored using electronystagmography. We analysed unpaired t-test between exposure subjects who exhibited upbeat nystagmus and those who did not. Upbeat nystagmus parameters were measured, and mean values were calculated. Associations between the properties of upbeat nystagmus and maximum concentrations of DPAA among DPAA exposure were also investigated.\n\nResults\nUpbeat nystagmus was common among exposure victims, occurring in 23 of 29 subjects (79.0%). The subjects with upbeat nystagmus had significantly higher ratio than those without upbeat nystagmus in the points of subjective symptoms and DPAA concentration of drinking water (p \u003c 0.01). The slow-phase amplitude of upbeat nystagmus enlarged with increasing DPAA concentrations, showing a significant positive correlation (p \u003c 0.05). These findings suggest that the level of exposure to DPAA affects the properties of nystagmus. 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Residual central nervous system damage due to organoarsenic poisoning
http://hdl.handle.net/2241/00157158
http://hdl.handle.net/2241/0015715833cb00e2-ad72-41f0-8545-75359b9d06a5
名前 / ファイル | ライセンス | アクション |
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NT_37 (711.6 kB)
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Item type | Journal Article(1) | |||||||||||||||||
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公開日 | 2019-07-19 | |||||||||||||||||
タイトル | ||||||||||||||||||
タイトル | Residual central nervous system damage due to organoarsenic poisoning | |||||||||||||||||
言語 | ||||||||||||||||||
言語 | eng | |||||||||||||||||
資源タイプ | ||||||||||||||||||
資源 | http://purl.org/coar/resource_type/c_6501 | |||||||||||||||||
タイプ | journal article | |||||||||||||||||
著者 |
中馬越, 清隆
× 中馬越, 清隆
WEKO
151469
× 小金澤, 禎史
WEKO
204273
× 石井, 一弘× 玉岡, 晃× Fujizuka, Natsu× Shimizu, Kotone× Takiguchi, Shino× Horaguchi, Takahiro |
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抄録 | ||||||||||||||||||
内容記述タイプ | Abstract | |||||||||||||||||
内容記述 | Background Drinking well water contaminated with the organoarsenic compound diphenylarsinic acid (DPAA) causes central nervous system (CNS) disorders that improve within several years after last drinking such water. Subjective symptoms such as lightheadedness and dizziness appear to persist, however, suggesting CNS damage. We evaluated CNS damage due to DPAA by detecting abnormal eye movements. Methods Subjects comprised 29 victims of exposure to DPAA in whom this substance had been detected in the nails. Investigations were performed more than 3 years following cessation of DPAA exposure. Abnormal eye movements were monitored using electronystagmography. We analysed unpaired t-test between exposure subjects who exhibited upbeat nystagmus and those who did not. Upbeat nystagmus parameters were measured, and mean values were calculated. Associations between the properties of upbeat nystagmus and maximum concentrations of DPAA among DPAA exposure were also investigated. Results Upbeat nystagmus was common among exposure victims, occurring in 23 of 29 subjects (79.0%). The subjects with upbeat nystagmus had significantly higher ratio than those without upbeat nystagmus in the points of subjective symptoms and DPAA concentration of drinking water (p < 0.01). The slow-phase amplitude of upbeat nystagmus enlarged with increasing DPAA concentrations, showing a significant positive correlation (p < 0.05). These findings suggest that the level of exposure to DPAA affects the properties of nystagmus. High-frequency pathological square-wave jerks (SWJ) were seen in 14 of 29 patients (48.0%), and mean SWJ frequency was 112.4 ± 16.7/min. Conclusions Detection of abnormal ocular movements may be useful in evaluating residual/persistent/chronic CNS damage due to organoarsenic poisoning. |
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書誌情報 |
Neurotoxicology and teratology 巻 37, p. 33-38, 発行日 2013-05 |
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ISSN | ||||||||||||||||||
収録物識別子タイプ | ISSN | |||||||||||||||||
収録物識別子 | 08920362 | |||||||||||||||||
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収録物識別子タイプ | NCID | |||||||||||||||||
収録物識別子 | AA1066890X | |||||||||||||||||
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識別子タイプ | PMID | |||||||||||||||||
関連識別子 | 23454008 | |||||||||||||||||
DOI | ||||||||||||||||||
識別子タイプ | DOI | |||||||||||||||||
関連識別子 | 10.1016/j.ntt.2013.02.007 | |||||||||||||||||
権利 | ||||||||||||||||||
権利情報 | © 2013 Elsevier Inc. | |||||||||||||||||
権利 | ||||||||||||||||||
権利情報 | NOTICE: This is the author's version of a work that was accepted for publication in Neurotoxicology and Teratology. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms, may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Neurotoxicology and Teratology, 37, 2013, 10.1016/j.ntt.2013.02.007. | |||||||||||||||||
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値 | author | |||||||||||||||||
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出版者 | Elsevier |