Minamata disease (methylmercury poisoning) can affect all ages. In adults all the organs contain increased mercury, but lesions occur mainly in the nervous system, particularly the brain. The neurons, especially nonpyramidal cells in the cerebral and cerebellar cortices, are destroyed. In the cerebrum, there is selective involvement of the calcarine and precentral regions involving neurons in the second and upper third layer and predominantly in the depth of the sulci. In the cerebellum, the granular cells are most susceptible and are lost in the deeper regions of the folia of both hemispheres. In nonfetal infantile Minamata disease there is hypoplasia of various organs, including the brain. There is widespread disintegration of cortical neurons and secondary degeneration of myelin sheaths.


Cerebellar Cortex Cerebral White Matter Fetal Alcohol Syndrome Drug Intoxication Carbon Monoxide Intoxication 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

21 Intoxication

  1. 1.
    Eto K, Oyanagi, Itai Y, Tokunaga H, Takizawa Y, Suda I (1992) A fetal case of Minamata disease: an autopsy case report with special reference to the nervous system. Mol Chem Pathol 16:171–186.Google Scholar
  2. 2.
    Eto K, Yasutake A, Korogi Y, Akima M, Shimozeki T, Tokunaga H, Kuwana T, Kaneko Y (2002) Methylmercury poisoning in common marmosets: MRI findings and peripheral nerve lesions. Toxicol Pathol 30:723–734.PubMedCrossRefGoogle Scholar
  3. 3.
    Takeuchi T, Eto K (1999) The pathology of Minamata disease: a tragic story of water pollution. Kyushuu University Press, Fukuoka.Google Scholar
  4. 4.
    Volpe J. Neurology of the newborn, 4th edn. Saunders, Philadelphia, pp 858–889.Google Scholar
  5. 5.
    Graham D, Montime TJ (2002) Neurotoxicity. In: Graham DI, Lantos PL (eds) Greenfield’s neuropathology, 7th edn. Vo1 1. Arnold, London, pp 799–815.Google Scholar

Copyright information

© Springer 2007

Personalised recommendations