Methylmercury has a half-life in human blood of about 50 days.Several studies indicate that methylmercury is linked to subtle developmental deficits in children exposed in utero such as loss of IQ points, and decreased performance in tests of language skills, memory function and attention deficits. Methylmercury exposure in adults has also been linked to increased risk of cardiovascular disease including heart attack. Some evidence also suggests that methylmercury can cause autoimmune effects in sensitive individuals. Despite some concerns about the relationship between methylmercury exposure and autism, there are few data that support such a link. Although there is no doubt that methylmercury is toxic in several respects, including through exposure of the developing fetus, there is still some controversy as to the levels of methylmercury in the diet that can result in adverse effects. Recent evidence suggests that the developmental and cardiovascular toxicity of methylmercury may be mitigated by co-exposures to omega-3 fatty acids and perhaps selenium, both found in fish and elsewhere.There have been several episodes in which large numbers of people were severely poisoned by food contaminated with high levels of methylmercury, notably the dumping of industrial waste that resulted in the pollution and subsequent mass poisoning in Minamata and Niigata, Japan and the situation in Iraq in the 1960s and 1970s in which wheat treated with methylmercury as a preservative and intended as seed grain was fed to animals and directly consumed by people (see Basra poison grain disaster).
The cause is thought to be predominantly related to abnormal ammonia metabolism. Asterixis is seen most often in drowsy or stuporous patients with metabolic encephalopathies, especially in decompensated cirrhosis or acute liver failure. It is also seen in some patients with kidney failure and azotemia. It can also be a feature of Wilsons disease. Asterixis is also seen in respiratory failure due to carbon dioxide toxicity (hypercapnia). Some drugs are known to cause asterixis, particularly phenytoin (when it is known as phenytoin flap). Other drugs implicated include benzodiazepines, salicylates, barbiturates, valproate, gabapentin, lithium, ceftazidime, and metoclopramide. History
R.D. Adams and J.M. Foley first described asterixis in 1949 in patients with severe liver failure and encephalopathy. Initially Foley and Adams referred to asterixis simply as "tremor" but realized that they needed a more appropriate term. On a literature search they found a poorly described phenomenon in similar patients mentioned by German physicians called “jactitations” but the reference was vague. Foley consulted Father Cadigan, a Jesuit classics scholar, who suggested “anisosterixis” (an "negative"–iso "equal"–sterixis "firmness") but Foley shortened this to asterixis due to the former being too difficult to pronounce. They introduced the term in 1953 by way of a medical abstract and later Adams solidified its medical use as he was an author and editor of the widely influential Harrisons Principles of Internal Medicine. References
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