And whats the reason that mercury based filling might not tip the balance in
an already mercury toxic person...
http://www.emedicine.com/neuro/topic617.htm
Mercury
Last Updated: April 10, 2002 Rate this Article
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Synonyms and related keywords: mad hatter's syndrome, metal fume fever,
erethism, Minamata disease, methylmercury
AUTHOR INFORMATION Section 1 of 10
Author Information Introduction Clinical Differentials Workup Treatment
Medication Follow-up Miscellaneous Bibliography
Author: David A Olson, MD, Consulting Staff, Department of Neurology, Dekalb
Medical Center
David A Olson, MD, is a member of the following medical societies: American
Academy of Neurology
Editor(s): Joseph Quinn, MD, Assistant Professor, Department of Neurology,
Portland VA Medical Center, Oregon Health Sciences University; Francisco
Talavera, PharmD, PhD, Senior Pharmacy Editor, Pharmacy, eMedicine; Richard J
Caselli, MD, Chairperson, Department of Neurology, Professor, Department of
Neurology, Mayo Clinic of Scottsdale; Matthew J Baker, MD, Consulting Staff,
Collier Neurologic Specialists, Naples Community Hospital; and Nicholas
Lorenzo, MD, eMedicine Chief Publishing Officer, Chief Editor, eMedicine
Neurology; Consulting Staff, Neurology Specialists and Consultants
INTRODUCTION Section 2 of 10
Author Information Introduction Clinical Differentials Workup Treatment
Medication Follow-up Miscellaneous Bibliography
Background: At least some of the toxic effects of mercury have been well known
since the 18th century. In 1889, Charcot's Clinical Lectures on Diseases of
the Nervous System attributed some rapid oscillatory tremors to mercury
exposure. In Wilson's classic textbook of neurology, published in 1940, Wilson
concurred with Charcot's attribution of tremors to mercury poisoning. Wilson
also identified mercury-induced cognitive impairments, such as inattention,
excitement, and hallucinosis. In 1961, researchers in Japan correlated
elevated urine mercury levels with the features of the previously mysterious
Minamata disease. Before the etiology of Minamata disease was discovered, it
plagued the residents around Minamata Bay in Japan with tremors, sensory loss,
ataxia, and visual field constriction.
Toxicity from mercury exposure occurs with both organic and inorganic forms.
Minamata disease is an example of organic toxicity. In Minamata Bay, a factory
discharged inorganic mercury into the water. The mercury was methylated by
bacteria and subsequently ingested by fishes and then by humans.
Inorganic mercury toxicity occurs in several forms: metallic mercury (Hg),
mercurous mercury (Hg1+), or mercuric mercury (Hg2+). Toxicity from inorganic
mercury can result from direct contact through the skin or gastrointestinal
tract or from inhalation of mercury vapors. Vaporous mercury diffuses through
the alveoli, becomes ionized in the blood, and ultimately deposits in the CNS.
Pathophysiology: Organic methylmercury toxicity and inorganic mercury toxicity
show different pathologic effects. Organic methylmercury toxicity causes
prominent neuronal loss and gliosis in the calcarine and parietal cortices and
cerebellar folia, as seen in cases of classic Minamata disease. Inorganic
mercury causes cerebral infarctions as well as systemic features, such as
pneumonia, renal cortical necrosis, and disseminated intravascular
coagulopathy. A more diffuse direct neuronal toxicity may exist with organic
mercury, as the brain weights of patients with Minamata disease are
substantially lower than those of controls.
The mechanism by which mercury ultimately causes disruption of the CNS and
peripheral nervous system is not clear. Multiple processes seem to be
affected. Inorganic mercury impairs adenosine 5' diphosphate (ADP)-dependent
protein genesis in rat neurons. Recently, researchers have identified
excessive excitotoxins and dysregulation of the nitric oxide system with
cerebellar damage in rodents exposed to methylmercury. Others have discovered
alterations of nerve growth factor in the basal forebrain of the offspring of
rats that were exposed to methylmercury during pregnancy and nursing.
Frequency:
In the US: Despite the serious, even fatal, consequences of toxicity,
prevalence and incidence rates are not readily available, partly because some
sequelae of low-level exposure are controversial.
Mortality/Morbidity:
Mercury toxicity is a function of the frequency and intensity of exposure as
well as the chemical form of mercury involved. Acute fulminant intoxication
with methylmercury resulted in coma and death in the Minamata catastrophe. In
a recent case, death resulted several months following absorption of
dimethylmercury through the skin. Mercury vapors also can result in both acute
neurological and generalized symptoms.
Morbidity manifesting as peripheral neuropathy and tremulousness can persist
for several decades after toxic exposure to mercury vapors.
Race: No racial predisposition has been identified clearly.
Sex: No gender predisposition has been identified clearly.
Age: Toxicity probably affects developing fetuses and children preferentially
compared to other age groups, but even on this point the data are incomplete.
Prenatal exposure through maternal consumption of predominantly whale meat has
been shown to impair development among children in the Faeroe Islands, while
maternal mercury exposure from fish consumption in the Seychelles did not
result in significant developmental problems among children exposed
prenatally. In one family exposed to methylmercury through the ingestion of
contaminated pork, the more severe clinical manifestations were found in the
younger children. CLINICAL Section 3 of 10
Author Information Introduction Clinical Differentials Workup Treatment
Medication Follow-up Miscellaneous Bibliography
History: The symptoms of mercury intoxication are manifold. Patients can
present with complaints of numbness, tingling, hearing loss, visual
difficulties, gait unsteadiness, and tremulousness, as well as emotional and
cognitive difficulties. Obviously, assessing the risk of exposure, which can
be acute or long term, is paramount to making a diagnosis.
Some unique features of mercury poisoning have generated their own
nomenclature.
Metal fume fever occurs in the acute phase of mercury vapor toxicity and is
manifested by fatigue, weakness, fever, chills, dizziness, headache, abdominal
cramping, dyspnea, dysuria, and ejaculatory pain.
Acrodynia also occurs acutely and predominates in children. A pink peeling
rash, along with generalized pain, sweating, and tachycardia are
characteristic.
Erethism is the constellation of irritability, excitability, anxiety,
insomnia, and social withdrawal. Erethism traditionally is seen in the chronic
phase of the toxicity.
Physical: Although no physical findings are pathognomonic for mercury
toxicity, the constellation of gait ataxia, tremulousness, hearing loss,
visual field constriction, dysarthria, and distal limb sensory loss, coupled
with cognitive and emotional dysfunction, is suggestive.
Hearing loss and visual field impairments more often occur with organic
poisoning, as in Minamata disease.
Distal sensory loss, uncoordinated limb movements, resting tremors, gait
ataxia, and a positive Romberg sign have been described after exposure to both
organic and inorganic mercury.
Emotional instability and cognitive impairments can be present in both types
of exposure; however, these deficits are more characteristic of acute
inorganic mercury toxicity. Neuropsychological testing in these cases has
revealed pronounced impairments in traditional frontal lobe domains.
Causes:
One major risk factor is industrial contamination.
Workers, particularly those employed in the manufacturing of mirrors,
thermometers, incandescent lights, and x-ray machines, are at risk for
inorganic mercury toxicity.
Organic mercury poisoning can occur among exposed workers in the paper and
pulp industries.
In the United States, exposure to organic mercury is primarily through
ingestion of contaminated fish. Those who consume large amounts of seafood
from contaminated waters have an increased risk of toxicity. Surveys indicate
that public awareness of the risks of mercury-contaminated fish is limited.
Exposure to contaminated grains, on which mercury was used as a fungicide, has
resulted in mercury toxicity in the third world.
More unusual sources of exposure have included numerous pools of standing and
vaporizing liquid mercury in a renovated building in New Jersey. Several
residents of this building exhibited urinary mercury levels in the neurotoxic
range.
Also, the Centers for Disease Control and Prevention (CDC) identified at least
3 residents of the southwestern United States who developed toxic effects from
a Mexican beauty cream that contained 6-8% mercurous chloride.
Traditional religious and healing practices are risk factors for mercury
exposure. Mercury has been identified as a contaminant of Chinese herbal
balls, and it has been used deliberately for its putative supernatural
attributes in amulets in the Santeria religion.
Even the mercury vapors from dental amalgam have been implicated as a
possible, though controversial, source of exposure among dental workers and
the general population.
Finally, recent concerns about the mercury content of childhood vaccines that
utilized mercury derivatives for their antimicrobial and preservative
qualities have led to the increased availability of mercury-free vaccines.
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