Pathogenesis and Pathophysiology. Organic mercury readily crosses the blood-brain barrier, and its turnover in
the brain is slow. In cases of chronic exposure, approximately 10 percent of the body burden localizes in the brain. Less than 3 percent is degraded into inorganic mercury. In a single case study, histological changes and high mercurial content were noted in the corpus callosum. Excretion occurs primarily through the gastrointestinal tract, mostly through biliary secretion, and the mercury then undergoes almost immediate gastrointestinal reabsorption into the bloodstream. Neuropathological changes noted in 10 cases included damage to peripheral neurons in the myelin sheath accompanied by glial proliferation and mobilization of phagocytes.'^1 Anatomically, the most severe damage was found in the primary visual cortex, followed by the cerebellar cortex, the pre- and postcentral gyri, the transverse gyrus, and the putamen.
Epidemiology and Risk Factors. Sources of organic mercury include contaminated seafood or exposure to alkyl mercury (used in antifungal treatment of seed grains). There have been reports of massive intoxications resulting from ingestion of fish containing methyl mercury or from eating homemade bread prepared from seed treated with methyl mercury fungicide. Ingestion of livestock that have been fed grain treated with mercury-containing fungicides is an additional source.
Routes of absorption of organic mercury are primarily dermal and gastrointestinal. Organic mercury is slowly excreted through the kidneys, and its half-life varies from 40 to 105 days. Organic mercury readily crosses the placenta, resulting in blood concentrations in the fetus that are equal to or greater than those in the maternal blood. There have been several reports of fetal methyl mercury poisoning in asymptomatic mothers. Methyl mercury is also secreted in breast milk.
Clinical Features and Associated Findings. The clinical triad of organic mercury toxicity consists of peripheral neuropathy, ataxia, and cortical blindness. There may be a delay of 2 weeks to several months before symptoms appear after mercury exposure. The earliest symptoms may be paresthesias of the extremities, beginning distally and extending in a glove-stocking distribution. Touch and pain sensations are most impaired. Constriction of the visual fields is generally seen. y
In infants born of intoxicated mothers, severe brain damage may develop including retardation and cerebral palsy. Motor neuron disease resembling amyotrophic lateral sclerosis (ALS) is another notable and prominent clinical pattern. In these patients, gradual weakness develops with features of both upper motor neuron disease (increased reflexes and prominent jaw jerk) and lower motor neuron disease (fasciculations and atrophy).
Differential Diagnosis and Evaluation. It is difficult to diagnose mercury toxicity from laboratory data because the blood and urine measurements vary widely. While measurements in blood and hair are less variable than those in urine, these do not necessarily reflect the degree of mercury toxicity. Hair samples must be collected according to specific protocols. For example, samples must be taken close to the scalp and then washed to remove contaminants such as hair dyes or hair treatments. The advantage of hair samples is that they provide exposure information for the past year. Hair sample levels are usually 300 to 500 times those seen in blood.
Management. Management of mercury toxicity depends first on eliminating the exposure. Other remedies include the use of mercury-binding chelators such as D-penicillamine, BAL, or DMSA, which may accelerate the excretion of mercury. However, because chelation mobilizes mercury from bones, it may cause the clinical symptoms to become worse and allow further deposits of mercury into the brain (especially BAL). Penicillamine may be more effective in improving the CNS effects of mercury. However, the side effects of penicillamine treatment may include hematopoietic suppression, alterations in cognitive and renal function, symptoms of myasthenia gravis, occasional hepatitis, and allergic reactions such as pruritus and swelling. With chelation, blood concentrations usually begin to decline after approximately 3 days. In asymptomatic individuals with increased blood concentrations of mercury, administration of selenium and vitamin E may prevent the development of symptoms. In patients with mild contractures, physical therapy can be helpful.
Prognosis and Future Perspectives. Most patients with severe mercury poisoning die within a few weeks of symptom onset. Some may survive with major neurological disability. In those with mild or moderate neurological symptoms, improvement may occur within the first 6 months, mostly in children and young adults. Isolated cases have been reported in which bedridden individuals regained the ability to walk, and some children who were totally blind regained vision.
Follow-up of the survivors with Minamata disease years after poisioning revealed decreased bilateral attenuation on CT scans in the visual cortex and diffuse atrophy of the cerebellum, especially the vermis.
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