Brain fluorodeoxyglucose positron emission tomography (¹⁸FDG PET) in patients with acute thallium intoxication

Objective. Thallium toxicity induces cellular injury through impaired Na-K-ATPase activity. The aim of this study was to investigate functional imaging and the long-term clinical-imaging correlations of thallium toxicity. Materials and methods. We measured thallium concentrations in blood, urine, stools, and hair of a 48-year-old woman and a 52-year-old man (patients 1 and 2) in the first 3 months after exposure to thallium containing water, and studied their neuropsychological functions. Using fluorodeoxyglucose positron emission tomography (¹⁸FDG PET) scans, we examined the brain involvement and correlated the image findings with the clinical presentations. Results. On the 1st, 30th, and 61st days after exposure, the thallium concentrations in patient 1 were 2056,311, and 7.5 μg/L in the blood, and 11400,4570, and 36.4 μg/L in the urine. The concentrations in patient 2 were 956,235, and 15.6 |lg/L in the blood, and 11900,2670, and 101 μg/L in the urine. On the 40th, 50th and 89th days after exposure, the thallium concentration in the stools were 21.6, 3.6, and 0.35 μg/g in patient 1, and 22.2, 3.2, and 0.37 μg/g in patient 2. Executive function, perceptual motor speed, and learning memory were initially abnormal but recovered particularly within the first year. The first ¹⁸FDG PET studies of both patients disclosed a decreased uptake of glucose metabolism in the cingulate gyrus, bilateral frontal, and parietal lobes 2-5 months after exposure. The follow-up ¹⁸FDG PET scan of patient 2 revealed a partial recovery. Conclusion. This study indicates that damage to the central nervous system after acute thallium poisoning may be reversible after a long-term follow-up. Brain ¹⁸FDG PET demonstrated the brain involvement and was correlated with cognitive impairment.