A follow-up study ten years later discovered that many had died from "unknown causes". Congenital Minamata disease
Local doctors and medical officials had noticed for a long time an abnormally high frequency of cerebral palsy and other infantile disorders in the Minamata area. In 1961, a number of medical professionals, including Masazumi Harada (later to be honored by the United Nations for his body of work on Minamata disease), set about re-examining children diagnosed with cerebral palsy. The symptoms of the children closely mirrored those of adult Minamata disease patients, but many of their mothers did not exhibit symptoms. The fact that these children had been born after the initial outbreak and had never been fed contaminated fish also led their mothers to believe they were not victims. At the time the medical establishment believed the placenta would protect the foetus from toxins in the bloodstream, which is indeed the case with most chemicals. What was not known at the time was that exactly the opposite is the case with methylmercury: the placenta removes it from the mothers bloodstream and concentrates the chemical in the foetus. After several years of study and the autopsies of two children, the doctors announced that these children had an as-yet unrecognised congenital form of Minamata disease. The certification committee convened on 29 November 1962 and agreed that the two dead children and the sixteen children still alive should be certified as patients, and therefore liable for "sympathy" payments from Chisso, in line with the 1959 agreement.
Conditions such as reduced corneal thickness, are observed in people with cases of polycoria, as well as keratoconus (keratoconus is a corneal disease has the possibility of leading to blindness and/or astigmatism). However, there are some proposals that it is caused by a dissociation of the pupil margins, a partial coloboma which is a hole in the eye, or abnormal eye tissue composition. Causes
There is not any known direct mechanisms involved in the development of true polycoria or pseudopolycoria. There are some proposed ideas, one being that after the sphincter muscle is fully formed and developed in the eye there is a severing of the pupillary margins leading to the distinction of the extra pupil and the principal pupil. Polycoria can also be caused any hole in ones iris to develop a sphincter muscle development. Another proposed theory about the cause of polycoria is intrauterine trauma, or postpartum iris trauma.If the development of the iris is hindered, the ectoderm of the eye (which forms the lens and corneal epithelium) may split, which could lead to pseudopolycoria. Genetics
The gene that is the cause of this disorder is the PRDM5 gene. The PRDM5 gene has also been linked to Brittle Cornea syndrome, which is a tissue disorder of the eye, as well as Axenfeld syndome. PRDM5 plays crucial roles in the molecular composition of the eye, as well as the tissue thickness. Axenfeld syndrome occurs in the patient in a case of the mutation of the FOXC1 gene, which is a heterozygous mutation.