UNSW Embryo- Abnormal Development-Mercury Poisoning.Selected References |
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Note: A Selected List of References for Mercury Poisoning or Minamata disease from PubMed April 1999 back. |
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Internet access computers will be able to get abstract directly from PubMed (when available) by clicking Author's name below. If the Journal is available online then this is also listed at the end of the Reference citation. |
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Articles
Reviews
- Pathology of Minamata disease.
Eto K Toxicol Pathol 1997 Nov-Dec;25(6):614-23- Abstract Minamata disease, or methylmercury
poisoning, was first discovered in 1956 around
Minamata Bay, Kumamoto Prefecture, Japan. A similar
epidemic occurred in 1965 along the Agano River,
Niigata Prefecture, Japan. The neuropathology of
Minamata disease has been well studied; this review
focuses on human cases of Minamata disease in Kumamoto
Prefecture. Nervous system lesions associated with
Minamata disease have a characteristic distribution.
In the cerebral cortex, the calcarine cortex was found
to be involved in all cases of Minamata disease,
particularly along the calcarine fissure. The
destruction of nerve tissue was prominent in the
anterior portions of the calcarine cortex.
Occasionally, the centrifugal route from the visual
and visual association areas (internal sagittal
stratum) showed secondary degeneration in prolonged
cases after acute onset. Postcentral, precentral, and
temporal transverse cortices showed similar changes,
though they were less severe. Intense lesions in the
precentral cortex caused the development of secondary
bilateral degeneration of the pyramidal tracts. In the
cerebellum, the lesions occurred deeper in the
hemisphere. The granule cell population was most
affected. In the peripheral nerves, sensory nerves
were more affected than motor nerves. Secondary
degeneration of Goll's tracts was occasionally seen in
prolonged or chronic cases.
- Abstract Minamata disease, or methylmercury
poisoning, was first discovered in 1956 around
Minamata Bay, Kumamoto Prefecture, Japan. A similar
epidemic occurred in 1965 along the Agano River,
Niigata Prefecture, Japan. The neuropathology of
Minamata disease has been well studied; this review
focuses on human cases of Minamata disease in Kumamoto
Prefecture. Nervous system lesions associated with
Minamata disease have a characteristic distribution.
In the cerebral cortex, the calcarine cortex was found
to be involved in all cases of Minamata disease,
particularly along the calcarine fissure. The
destruction of nerve tissue was prominent in the
anterior portions of the calcarine cortex.
Occasionally, the centrifugal route from the visual
and visual association areas (internal sagittal
stratum) showed secondary degeneration in prolonged
cases after acute onset. Postcentral, precentral, and
temporal transverse cortices showed similar changes,
though they were less severe. Intense lesions in the
precentral cortex caused the development of secondary
bilateral degeneration of the pyramidal tracts. In the
cerebellum, the lesions occurred deeper in the
hemisphere. The granule cell population was most
affected. In the peripheral nerves, sensory nerves
were more affected than motor nerves. Secondary
degeneration of Goll's tracts was occasionally seen in
prolonged or chronic cases.
- Epidemiological and clinical features of Minamata
disease.
Igata A Environ Res 1993 Oct;63(1):157-69- Abstract Minamata disease is methyl mercury intoxication from fish contaminated by a chemical factory in Minamata city. Based on the results of our regional survey, cardinal clinical features of the disease were clarified by a multivariant analysis of all symptoms in inhabitants in the polluted area. The clinical features were found to be essentially the same as those of Hunter Russell syndrome; however, some additional symptoms were also found. Those symptoms are influenced by many factors, such as degree of exposure and duration of pollution. The disposition of each inhabitant also plays a role in clinical manifestation. This analysis contributes to a correct individual diagnosis and to the correct estimation of patients in polluted areas. Long-term studies also uncovered a few inhabitants who claimed to have begun to experience some neurological symptoms after pollution ceased. These symptoms were attributed mainly to aging. As many inhabitants with mild neurological complaints were not easily diagnosed, a questionable borderline group should be postulated for social settlement of Minamata disease. The characteristics of Minamata disease are discussed and compared to cases of methyl mercury poisoning in other parts of the world.