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Chronic arsenic intoxication is known to cause multisystem impairment and is still a major threat to public health in many countries. In Toroku, a small village in Japan, arsenic mines operated from 1920 to 1962, and residents suffered serious sequelae of arsenic intoxication. We have performed annual medical examinations of these residents since 1974, allowing us to characterize participants’ long-term health following their last exposure to arsenic. The participants could not be described as having “chronic arsenic intoxication,” because their blood arsenic levels were not measured. In this study, we defined them as having “probable arsenic intoxication.” Symptoms frequently involved the sensory nervous system, skin, and upper respiratory system (89.1–97.8%). In an analysis of neurological findings, sensory neuropathy was common, and more than half of the participants complained of hearing impairment. Longitudinal assessment with neurological examinations and nerve conduction studies revealed that sensory dysfunction gradually worsened, even after exposure cessation. However, we could not conclude that arsenic caused the long-term decline of sensory function due to a lack of comparisons with age-matched healthy controls. This is the first study to characterize the longitudinal sequelae after probable arsenic exposure. Our study will be helpful to assess the prognosis of patients worldwide who still suffer from chronic arsenic intoxication.

Background: Cardiac ¹²³I-metaiodobenzylguanidine scintigraphy (MIBG) previously demonstrated an uptake reduction in patients with Parkinson's disease (PD). However, epidemiologic research showed that electrocardiography (ECG) abnormalities occurred prior to motor signs in PD. Here we investigated whether the electrical conduction system of the heart was impaired in PD. Methods: Clinical features, ECG and MIBG parameters were analyzed in 191 patients with PD, 42 with multiple system atrophy (MSA) and 124 normal controls (NL). Results: The PR interval was significantly longer in patients with PD than in NL. The PR interval was significantly negatively correlated with early and delayed heart-to-mediastinum ratios in MIBG scintigraphy in PD and MSA patients. In 19 PD patients with PR prolongation, 17 patients also had abnormal MIBG findings, and the other 2 showed normal MIBG. Conclusions: The PR prolongation must show some sympathetic system abnormality because it is mainly controlled by the sympathetic nervous system. PR prolongation supports the objective biomarker value of MIBG for PD diagnosis.

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Case 1: A 66-year-old man was admitted because of progressive gait disturbance and dysphagia after developing red rash. He was diagnosed as Guillain-Barré syndrome (GBS) and treated by intravenous immunoglobulin therapy (IVIg). Two weeks later, he could swallow and walk without any abnormalities. Case 2: A 58-year-old woman was admitted because of gait disturbance, bilateral peripheral facial nerve palsies, and respiratory failure one week after developing fever and rash. She was diagnosed as GBS and treated with IVIg. She underwent mechanical ventilation, while she could wean off it one month later and her limb strengths improved. We confirmed both patients had scrub typhus by serological studies. Peripheral neuropathy is one of the complications of scrub typhus. In addition, this disease sometimes leads to severe GBS. GBS should be included in differential diagnosis when peripheral neuropathies develop in the course of treating scrub typhus, and we should keep in mind that scrub typhus is one of the causes of GBS.

In previous studies of human T-lymphotropic virus type 1-associated myelopathy/tropical spastic paraparesis (HAM/TSP), areas of slow blood flow in the spinal cord were related to pathological changes. While the pathological changes in the brain are milder than those in the spinal cord, they are also more significant in sites with slow blood flow. In this study, we investigated brain glucose metabolism in slow blood flow areas using fluorine-18 fluorodeoxyglucose positron emission tomography ((18)F-FDG-PET). Clinical features and brain (18)F-FDG-PET parameters were analyzed in six patients with HAM/TSP. For comparison of PET data, eight healthy volunteers were enrolled as normal controls (NLs). Glucose metabolism in the watershed areas of the middle and posterior cerebral arteries, as compared with that in the occipital lobes as a control, was significantly lower in HAM/TSP patients than in NLs. This result confirmed the relationship between slow blood flow areas and hypometabolism in HAM/TSP, and is consistent with previous findings that pathological changes are accentuated in sites with slow blood flow.

As a result of population growth and the development of tube wells, humans’ exposure to arsenic has increased over the past few decades. The natural course of organ damage secondary to arsenic exposure is not yet well understood. In Toroku, Japan, an arsenic mine was intermittently operated from 1920 to 1962, and residents were exposed to high concentrations of arsenic. In this paper, we analyzed 190 consecutive residents for whom detailed records of neurological symptoms and findings were obtained from 1974 to 2005. All participants were interviewed regarding the presence of general, skin, hearing, respiratory, and neurological symptoms. Neurological symptoms were classified into extremity numbness or pain, constipation, dyshidrosis, sensory loss, and muscle atrophy. Superficial and vibratory sensation was also evaluated. More than 80% of participants experienced extremity numbness, and numbness was the most common neurological symptom. Numbness was associated with superficial sensory disturbance, and was correlated with the subsequent development of other neurological symptoms, including autonomic and motor symptoms. No previous studies have investigated the natural course of chronic arsenic intoxication; thus, these data serve as a guide for detecting early symptoms due to arsenic exposure.

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