The clinician needs to distinguish between toxicity of the inorganic compounds (elemental mercury and the ions: mercuric and mercurial) and the toxicity of organic compounds (alkyls of mercury: methylmercury). Organic methylmercury toxicity causes prominent neuronal loss and gliosis in the cal-carine and parietal cortices and cerebellar folia, as seen in cases of Minamata disease. Inorganic mercury causes cerebral infarctions as well as systemic features, such as pneumonia, renal cortical necrosis, and disseminated intravas-cular coagulopathy. Inorganic mercury impairs adenosine diphosphate (ADP)-dependent protein genesis in animal models, while organic mercury compounds may induce excitotoxicity and dysregulation of the nitric oxide system with subsequent cerebellar damage in rodents (17-19).
Patients presenting with gait ataxia, tremulousness, hearing loss, visual field constriction, dysarthria, and distal limb sensory loss, coupled with cognitive and emotional dysfunction should be evaluated for mercury toxicity, although none of these symptoms is specific (18).
Organic mercury toxicity, seen in Minamata disease and in patients consuming grains contaminated with mercury-based fungicides, often leads to hearing loss and visual field impairments. Distal sensory loss, uncoordinated limb movements, resting tremors, gait ataxia, and a positive Romberg sign are associated with both inorganic and organic types of toxicity. Impairments in the frontal lobe domains (emotional and cognitive) observed with neuropsy-chological testing are somewhat more characteristic of acute inorganic mercury toxicity, although this presentation (the "Mad-Hatter" syndrome) is possible in all cases (19-23).
A 24-hour urine specimen should be obtained for measurement of inorganic mercury levels, while whole blood mercury levels should be measured for alkyls of mercury (organic mercury). Blood and urine levels of mercury should not exceed 10 ng/mL (see Chapter 9). Hair levels are more useful in cases of organic mercury poisoning and should not exceed 2 ng/mL (24).
Electrophysiological studies are necessary and often demonstrate a sensorimotor neuropathy, typically axonal. Visual-evoked potential studies may also present with abnormalities. The utility of MRI appears to be primarily for ruling out other causes of symptomatic presentations, while sural nerve biopsies in patients with Minamata disease caused by organic mercury toxic-ity indicated preferential loss of large myelinated nerve fibers (19,20,25).
Administration of chelating agents that contain thiol groups is the accepted standard of care. For acute, inorganic toxicity, dimercaprol (BAL) has been recommended traditionally, but oral agents are gaining prominence. Chela-tion with DMSA (Succimer) has been shown to result in increased mercury excretion compared to N-acetyl-D,L-penicillamine in adults with acute mercury vapor exposure. DMSA is generally well tolerated in adults and children (16).
Chelation removes only a small portion of the toxin, especially in cases of organic mercury poisoning. The placebo response has been observed in patients concerned with the occupational exposure in dentistry, and there is a general paucity of studies showing neurological improvement following any kind of chelation therapy (25,26).
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