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Decreased regional cerebral blood flow in patients with diphenylarsinic acid intoxication
Author(s) -
Ishii K.,
Nemoto K.,
Iwasaki N.,
Takeda T.,
Masuda T.,
Shibata Y.,
Tamaoka A.
Publication year - 2019
Publication title -
european journal of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.881
H-Index - 124
eISSN - 1468-1331
pISSN - 1351-5101
DOI - 10.1111/ene.13783
Subject(s) - medicine , cerebral blood flow , asymptomatic , blood flow , nuclear medicine
Background and purpose Diphenylarsinic acid ( DPAA ) intoxication caused by drinking contaminated well water was found in Kamisu, Japan. The symptoms indicated cerebellar–brainstem and temporo‐occipital involvement. However, it remains unclear how it affects the human brain. To elucidate the effect of DPAA on the human brain, we analyzed cerebral blood flow ( CBF ) data after the drinking of DPAA ‐contaminated water was stopped and investigated the correlation between DPAA exposure level and CBF by single‐photon emission computed tomography ( CBF ‐ SPECT ). Methods The DPAA ‐exposed inhabitants ( n = 78) were divided into 35 symptomatic and 43 asymptomatic subjects and compared with 38 healthy controls. The DPAA concentration in nails or hair and well water was measured using a high‐performance liquid chromatography system and coupled plasma mass spectrometry after adequate extraction treatment. CBF ‐ SPECT data, obtained within 1 year after the drinking of contaminated well water was stopped, were analyzed by statistical parametric mapping. We also examined the relationship between variations in CBF ‐ SPECT signals and variations in DPAA concentrations in the hair or nails of the subjects. Results Compared with control subjects, CBF in symptomatic DPAA ‐exposed subjects was significantly lower in the occipital lobe, including the cuneus and inferior occipital gyri. The DPAA concentration in the nails or hair of subjects was inversely and significantly related to their CBF . Conclusion These data suggest that CBF ‐ SPECT may be useful as a clinical marker to infer the effect of accumulated DPAA on the brain.