Minamata-Table-02

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Table 4

Chronographical onset of Minamata disease

Year	Congenital	Infant	Adult	Total
1953		1		1
1954		5	7	12
1955	5	2	8	15
1956	7	21	23	51
1957	6		2	8
1958	2		3	5
1959	3	1	16	20
1960			4	4
Total	23	30	63	116

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Table 5

Mercury contents (ppm) in the hair of the patient of congenital Minamata disease and of their mothers

No.	Birth	date	Patient			Mother
			1959-61	1963	1966	1960-61	1961-63
1	1956	7	59.0	12.0	3.56	72.9	6.0
2	1957	2	34.3	6.0	9.0	65.4	8.0
3	1957	5	61.9	39.0	14.0	101.0
4	1957	5	4.0	5.0
5	1956	4	51.8	18.0			5.0
6	1956	5	57.8			191.0	32.0
7	1957	10	37.7	54.0	3.5
8	1956	7	26.2	7.0	9.35		4.4
9	1958	9	35.0
10	1958	11	5.25	1.0		6.5	2.0
11	1955	8	11.3	12.0		12.7
12	1956	4	8.14	7.0	2.5	1.8
13	1956	6	10.6
14	1955	11	100.0			90.0
15	1955	8	73.5	19.0	5.79	16.0
16	1956	12	14.9	13.0	10.1	7.03	10.0
17	1955	1	6.0	4.0	5.1
19	1957	8		29.0			32.0*
22	1959	9		28.0	0.0

Note:
1. Cases 6 and 7 were sisters.
2. * measured in 1963.

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Table 6

Comparison in pathology of Minamata disease among the congenital, non-fetal, and adult cases (Takeuchi, 1968)

	Pathological features	Congenital	Infantile	Adult
1	Cortical disturbance of cerebrum	+++	+++	+++
2	Cerebellar disturbance of granular cell type	+++	+++	+++
3	Central type of granular atropy	+	++	++
4	Intense reduction of brain	+++	+++~++	+
5	Wide distribution of lesions	+++	+++	+
6	Preferential localization of lesions	±	++	+++
7	Degree of the granular cell disturbance	+	+++	+++
8	Hypoplastic change of cytoarchitecture*	+++	-	-
9	Malformation of neurons	+++	-	-

*: remaining matrix cells, evidence of nerve cells in cerebral medulla, abnormal cytoarchitecture (columnar block, etc.), hypoplastic narrowing of granular layer in cerebellum, and hypoplastic corpus callosum

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