The Experts below are selected from a list of 288 Experts worldwide ranked by ideXlab platform
Masazumi Harada - One of the best experts on this subject based on the ideXlab platform.
-
critical appraisal of the 1977 diagnostic criteria for Minamata Disease
Archives of Environmental & Occupational Health, 2013Co-Authors: Takashi Yorifuji, Masazumi Harada, Toshihide Tsuda, Soshi Takao, Sachiko Inoue, Ichiro KawachiAbstract:ABSTRACT Large-scale food poisoning caused by methylmercury was identified in Minamata, Japan, in the 1950s (Minamata Disease). Although the diagnostic criteria for the Disease remain current, few studies have been carried out to assess the diagnostic accuracy of the criteria. From a 1971 population-based investigation, data from 2 villages were selected: Minamata (high-exposure area; n = 779) and Ariake (low-exposure area; n = 755). The authors examined the prevalence of neurologic signs characteristic of methylmercury poisoning and the validity of the criteria. A substantial number of residents in the exposed area exhibited neurologic signs even after excluding officially certified patients. Using paresthesia of the extremities as the gold standard of diagnosis, the criteria had a sensitivity of 66%. The current diagnostic criteria as well as the official certification system substantially underestimate the incidence of Minamata Disease.
-
what has methylmercury in umbilical cords told us Minamata Disease
Science of The Total Environment, 2009Co-Authors: Takashi Yorifuji, Toshihide Tsuda, Saori Kashima, Masazumi HaradaAbstract:Abstract Severe methylmercury poisoning occurred in Minamata and neighboring communities in the 1950s and 1960s. The exposed patients manifested neurological signs, and some patients exposed in utero were born with so-called congenital Minamata Disease. In a previous report, Nishigaki and Harada evaluated the methylmercury concentrations in the umbilical cords of inhabitants and demonstrated that methylmercury actually passed through the placenta (Nishigaki and Harada, 1975). However, the report involved a limited number of cases (only 35) and did not quantitatively evaluate the regional differences in the transition of methylmercury exposure. Therefore, in the present study, we evaluated the temporal and spatial distributions of methylmercury concentrations in umbilical cords, with an increased number of participants and additional descriptive analyses. Then, we examined whether the methylmercury concentrations corresponded with the history of the Minamata Disease incident. A total of 278 umbilical cord specimens collected after birth were obtained from babies born between 1925 and 1980 in four study areas exposed to methylmercury. Then, we conducted descriptive analyses, and drew scatterplots of the methylmercury concentrations of all the participants and separated by the areas. In the Minamata area, where the first patient was identified in 1956, the methylmercury concentration reached a peak around 1955. Subsequently, about 5 years later, the concentrations peaked in other exposed areas with the expected exposure distribution corresponding with acetaldehyde production (the origin of methylmercury). This historical incident several decades ago in Minamata and neighboring communities clearly shows that regional pollution affected the environment in utero. Furthermore, the temporal and spatial distributions of the methylmercury concentrations in the umbilical cords tell us the history of the Minamata Disease incident.
-
What has methylmercury in umbilical cords told us? — Minamata Disease
Science of The Total Environment, 2009Co-Authors: Takashi Yorifuji, Toshihide Tsuda, Saori Kashima, Masazumi HaradaAbstract:Abstract Severe methylmercury poisoning occurred in Minamata and neighboring communities in the 1950s and 1960s. The exposed patients manifested neurological signs, and some patients exposed in utero were born with so-called congenital Minamata Disease. In a previous report, Nishigaki and Harada evaluated the methylmercury concentrations in the umbilical cords of inhabitants and demonstrated that methylmercury actually passed through the placenta (Nishigaki and Harada, 1975). However, the report involved a limited number of cases (only 35) and did not quantitatively evaluate the regional differences in the transition of methylmercury exposure. Therefore, in the present study, we evaluated the temporal and spatial distributions of methylmercury concentrations in umbilical cords, with an increased number of participants and additional descriptive analyses. Then, we examined whether the methylmercury concentrations corresponded with the history of the Minamata Disease incident. A total of 278 umbilical cord specimens collected after birth were obtained from babies born between 1925 and 1980 in four study areas exposed to methylmercury. Then, we conducted descriptive analyses, and drew scatterplots of the methylmercury concentrations of all the participants and separated by the areas. In the Minamata area, where the first patient was identified in 1956, the methylmercury concentration reached a peak around 1955. Subsequently, about 5 years later, the concentrations peaked in other exposed areas with the expected exposure distribution corresponding with acetaldehyde production (the origin of methylmercury). This historical incident several decades ago in Minamata and neighboring communities clearly shows that regional pollution affected the environment in utero. Furthermore, the temporal and spatial distributions of the methylmercury concentrations in the umbilical cords tell us the history of the Minamata Disease incident.
-
global lessons of Minamata Disease a man s worth
Japanese journal of leprosy : official organ of the Japanese Leprosy Association, 2009Co-Authors: Masazumi HaradaAbstract:: Minamata Disease (MD) was first recognized in May 1956. Its first recognized victims were 3 and 5 years old children. Environmental contamination most rapidly and seriously affected the physiologically and socially weak among the residents. Methylmercury (MeHg) had accumulated in fishes and shellfishes and those who ate them had been poisoning with it. MD is an indirect poisoning by MeHg through the food chain as a result of environmental contamination, and is the first known Disease to cause abnormalities in the fetus due to a toxic substances passing through the placenta. In 1962 MeHg poisoning through the placenta was found for the first time in the world. It used to be considered that poisoning was caused by direct exposure to a toxic substance, and that toxic substances did not pass the placenta. MD had implications in various fields. Namely it also stirred up legal, ethical, and eugenic arguments concerning fetal protection. Also man thought about a man's worth.
-
Minamata Disease and the mercury pollution of the globe
Korean Journal of Environmental Health Sciences, 2005Co-Authors: Masazumi HaradaAbstract:Minamata Disease made its first appearance in the world at Minamata City, Kumamoto Prefecture, in May 1956. In 1962 methyl mercury poisoning through the placenta was found for the first time in the world. This was called congenital Minamata Disease. In all cases the clinical symptoms were consistent with those of cerebral palsy. The time and place of outbreak were the same as those for Minamata Disease. Their mothers had eaten fish and shellfish during pregnancy. The principal symptoms of congenital Minamata Disease are mentalretardation (100%); primitive reflexes (100%); disturbance of coordination (100%); dysarthria (100%); limb deformation (100%); growth disorders (100%); nutritional disorders (100%); chorea-athetose (95%); and hypersalivation (95%). However, today, when the world is polluted by mercury in various places and at various levels, the data we need is not represented by those severe cases, but rather by the chronic milder type. Even in Minamata, the issue of Minamata Disease has not been resolved. And likewise, on a global scale the problem of Minamata Disease is not yet over.
Takashi Yorifuji - One of the best experts on this subject based on the ideXlab platform.
-
lessons from an early stage epidemiological study of Minamata Disease
Journal of Epidemiology, 2020Co-Authors: Takashi YorifujiAbstract:The Revisit series in this issue introduced the article by Kitamura and colleagues.1 Dr. Shoji Kitamura, born in 1915, was a medical doctor and a professor of Department of Public Health in the Medical School at Kumamoto University when Minamata Disease happened. The article summarized findings from a very-early-phase epidemiological study conducted by researchers from Kumamoto University immediately after the Minamata Disease incident was officially recognized on May 1, 1956. The epidemiological study was very well-conducted in a timely manner and the article was available as early as January 1957 in an academic journal published by the Medical School at Kumamoto University. This is a very influential report that demonstrated associations between fish intake and the Minamata Disease after careful descriptive and analytical epidemiological studies. Although the Japanese society should have taken some actions to prevent the Disease with the evidence that a research group at Kumamoto University had at that time, the pollution was not stopped until 12 years had passed since the official identification in 1956. Moreover, the struggle with Minamata Disease is still in progress. This unfavorable response by the Japanese society could partly be explained by the important economic role of the causative factory at that time, when Japan had recorded a trade deficit since the end of the Second World War.2 Plastic products of the factory were key Japanese exports helping to reduce this deficit. In this commentary, after introducing the study by Kitamura and colleagues, I discuss the potentials of epidemiology, as well as consequences on public health that occurred when we did not follow the findings from the epidemiological study.
-
accelerated functional losses in ageing congenital Minamata Disease patients
Neurotoxicology and Teratology, 2018Co-Authors: Takashi Yorifuji, Philippe Grandjean, Shigeru TakaokaAbstract:Abstract Severe methylmercury poisoning occurred in Minamata and neighboring communities in Japan during the 1950s and 1960s. A considerable number of children were born with conditions resembling cerebral palsy, later known as congenital Minamata Disease. Although surviving patients are now in their 50s or 60s, few assessments of functional capacities in daily living have been performed. We assessed the changes in Activities of Daily Living (ADL) status of 11 patients over a 10-year period. For assessment of ADL, we applied the Barthel Index (BI) and the Functional Independence Measure (FIM). We obtained the patients' current and previous status information by interview of their caregivers or from medical records and then compared them using the Wilcoxon signed-rank test. Both ADL measures, including the status related with cognition, had significantly declined during the 10 years. The same was true for the overall BI score (p = 0.01). Similarly, all functions of the FIM scores declined (i.e., self-care, sphincter control, mobility, locomotion, communication, and social cognition), and for FIM physical and cognition subscores as well as FIM total score, the declines were statistically significant. The present study indicates that the ADL status of congenital Minamata Disease patients, now in their 50s or 60s, has substantially declined during the last 10 years; a decline that was much steeper in comparison with expectation in subjects of similar ages, but in agreement with accelerated ageing also reported in subjects with cerebral palsy, past polio infection, or epilepsy. While already incapacitated due to the prenatal methylmercury poisoning, their accelerated ageing may suggest that patients with developmental neurotoxicity have less reserve capacity to compensate for normal ageing. These patients will need continuous and increasing medical and welfare support in the community.
-
critical appraisal of the 1977 diagnostic criteria for Minamata Disease
Archives of Environmental & Occupational Health, 2013Co-Authors: Takashi Yorifuji, Masazumi Harada, Toshihide Tsuda, Soshi Takao, Sachiko Inoue, Ichiro KawachiAbstract:ABSTRACT Large-scale food poisoning caused by methylmercury was identified in Minamata, Japan, in the 1950s (Minamata Disease). Although the diagnostic criteria for the Disease remain current, few studies have been carried out to assess the diagnostic accuracy of the criteria. From a 1971 population-based investigation, data from 2 villages were selected: Minamata (high-exposure area; n = 779) and Ariake (low-exposure area; n = 755). The authors examined the prevalence of neurologic signs characteristic of methylmercury poisoning and the validity of the criteria. A substantial number of residents in the exposed area exhibited neurologic signs even after excluding officially certified patients. Using paresthesia of the extremities as the gold standard of diagnosis, the criteria had a sensitivity of 66%. The current diagnostic criteria as well as the official certification system substantially underestimate the incidence of Minamata Disease.
-
what has methylmercury in umbilical cords told us Minamata Disease
Science of The Total Environment, 2009Co-Authors: Takashi Yorifuji, Toshihide Tsuda, Saori Kashima, Masazumi HaradaAbstract:Abstract Severe methylmercury poisoning occurred in Minamata and neighboring communities in the 1950s and 1960s. The exposed patients manifested neurological signs, and some patients exposed in utero were born with so-called congenital Minamata Disease. In a previous report, Nishigaki and Harada evaluated the methylmercury concentrations in the umbilical cords of inhabitants and demonstrated that methylmercury actually passed through the placenta (Nishigaki and Harada, 1975). However, the report involved a limited number of cases (only 35) and did not quantitatively evaluate the regional differences in the transition of methylmercury exposure. Therefore, in the present study, we evaluated the temporal and spatial distributions of methylmercury concentrations in umbilical cords, with an increased number of participants and additional descriptive analyses. Then, we examined whether the methylmercury concentrations corresponded with the history of the Minamata Disease incident. A total of 278 umbilical cord specimens collected after birth were obtained from babies born between 1925 and 1980 in four study areas exposed to methylmercury. Then, we conducted descriptive analyses, and drew scatterplots of the methylmercury concentrations of all the participants and separated by the areas. In the Minamata area, where the first patient was identified in 1956, the methylmercury concentration reached a peak around 1955. Subsequently, about 5 years later, the concentrations peaked in other exposed areas with the expected exposure distribution corresponding with acetaldehyde production (the origin of methylmercury). This historical incident several decades ago in Minamata and neighboring communities clearly shows that regional pollution affected the environment in utero. Furthermore, the temporal and spatial distributions of the methylmercury concentrations in the umbilical cords tell us the history of the Minamata Disease incident.
-
What has methylmercury in umbilical cords told us? — Minamata Disease
Science of The Total Environment, 2009Co-Authors: Takashi Yorifuji, Toshihide Tsuda, Saori Kashima, Masazumi HaradaAbstract:Abstract Severe methylmercury poisoning occurred in Minamata and neighboring communities in the 1950s and 1960s. The exposed patients manifested neurological signs, and some patients exposed in utero were born with so-called congenital Minamata Disease. In a previous report, Nishigaki and Harada evaluated the methylmercury concentrations in the umbilical cords of inhabitants and demonstrated that methylmercury actually passed through the placenta (Nishigaki and Harada, 1975). However, the report involved a limited number of cases (only 35) and did not quantitatively evaluate the regional differences in the transition of methylmercury exposure. Therefore, in the present study, we evaluated the temporal and spatial distributions of methylmercury concentrations in umbilical cords, with an increased number of participants and additional descriptive analyses. Then, we examined whether the methylmercury concentrations corresponded with the history of the Minamata Disease incident. A total of 278 umbilical cord specimens collected after birth were obtained from babies born between 1925 and 1980 in four study areas exposed to methylmercury. Then, we conducted descriptive analyses, and drew scatterplots of the methylmercury concentrations of all the participants and separated by the areas. In the Minamata area, where the first patient was identified in 1956, the methylmercury concentration reached a peak around 1955. Subsequently, about 5 years later, the concentrations peaked in other exposed areas with the expected exposure distribution corresponding with acetaldehyde production (the origin of methylmercury). This historical incident several decades ago in Minamata and neighboring communities clearly shows that regional pollution affected the environment in utero. Furthermore, the temporal and spatial distributions of the methylmercury concentrations in the umbilical cords tell us the history of the Minamata Disease incident.
Toshihide Tsuda - One of the best experts on this subject based on the ideXlab platform.
-
critical appraisal of the 1977 diagnostic criteria for Minamata Disease
Archives of Environmental & Occupational Health, 2013Co-Authors: Takashi Yorifuji, Masazumi Harada, Toshihide Tsuda, Soshi Takao, Sachiko Inoue, Ichiro KawachiAbstract:ABSTRACT Large-scale food poisoning caused by methylmercury was identified in Minamata, Japan, in the 1950s (Minamata Disease). Although the diagnostic criteria for the Disease remain current, few studies have been carried out to assess the diagnostic accuracy of the criteria. From a 1971 population-based investigation, data from 2 villages were selected: Minamata (high-exposure area; n = 779) and Ariake (low-exposure area; n = 755). The authors examined the prevalence of neurologic signs characteristic of methylmercury poisoning and the validity of the criteria. A substantial number of residents in the exposed area exhibited neurologic signs even after excluding officially certified patients. Using paresthesia of the extremities as the gold standard of diagnosis, the criteria had a sensitivity of 66%. The current diagnostic criteria as well as the official certification system substantially underestimate the incidence of Minamata Disease.
-
what has methylmercury in umbilical cords told us Minamata Disease
Science of The Total Environment, 2009Co-Authors: Takashi Yorifuji, Toshihide Tsuda, Saori Kashima, Masazumi HaradaAbstract:Abstract Severe methylmercury poisoning occurred in Minamata and neighboring communities in the 1950s and 1960s. The exposed patients manifested neurological signs, and some patients exposed in utero were born with so-called congenital Minamata Disease. In a previous report, Nishigaki and Harada evaluated the methylmercury concentrations in the umbilical cords of inhabitants and demonstrated that methylmercury actually passed through the placenta (Nishigaki and Harada, 1975). However, the report involved a limited number of cases (only 35) and did not quantitatively evaluate the regional differences in the transition of methylmercury exposure. Therefore, in the present study, we evaluated the temporal and spatial distributions of methylmercury concentrations in umbilical cords, with an increased number of participants and additional descriptive analyses. Then, we examined whether the methylmercury concentrations corresponded with the history of the Minamata Disease incident. A total of 278 umbilical cord specimens collected after birth were obtained from babies born between 1925 and 1980 in four study areas exposed to methylmercury. Then, we conducted descriptive analyses, and drew scatterplots of the methylmercury concentrations of all the participants and separated by the areas. In the Minamata area, where the first patient was identified in 1956, the methylmercury concentration reached a peak around 1955. Subsequently, about 5 years later, the concentrations peaked in other exposed areas with the expected exposure distribution corresponding with acetaldehyde production (the origin of methylmercury). This historical incident several decades ago in Minamata and neighboring communities clearly shows that regional pollution affected the environment in utero. Furthermore, the temporal and spatial distributions of the methylmercury concentrations in the umbilical cords tell us the history of the Minamata Disease incident.
-
What has methylmercury in umbilical cords told us? — Minamata Disease
Science of The Total Environment, 2009Co-Authors: Takashi Yorifuji, Toshihide Tsuda, Saori Kashima, Masazumi HaradaAbstract:Abstract Severe methylmercury poisoning occurred in Minamata and neighboring communities in the 1950s and 1960s. The exposed patients manifested neurological signs, and some patients exposed in utero were born with so-called congenital Minamata Disease. In a previous report, Nishigaki and Harada evaluated the methylmercury concentrations in the umbilical cords of inhabitants and demonstrated that methylmercury actually passed through the placenta (Nishigaki and Harada, 1975). However, the report involved a limited number of cases (only 35) and did not quantitatively evaluate the regional differences in the transition of methylmercury exposure. Therefore, in the present study, we evaluated the temporal and spatial distributions of methylmercury concentrations in umbilical cords, with an increased number of participants and additional descriptive analyses. Then, we examined whether the methylmercury concentrations corresponded with the history of the Minamata Disease incident. A total of 278 umbilical cord specimens collected after birth were obtained from babies born between 1925 and 1980 in four study areas exposed to methylmercury. Then, we conducted descriptive analyses, and drew scatterplots of the methylmercury concentrations of all the participants and separated by the areas. In the Minamata area, where the first patient was identified in 1956, the methylmercury concentration reached a peak around 1955. Subsequently, about 5 years later, the concentrations peaked in other exposed areas with the expected exposure distribution corresponding with acetaldehyde production (the origin of methylmercury). This historical incident several decades ago in Minamata and neighboring communities clearly shows that regional pollution affected the environment in utero. Furthermore, the temporal and spatial distributions of the methylmercury concentrations in the umbilical cords tell us the history of the Minamata Disease incident.
-
Minamata Disease catastrophic poisoning due to a failed public health response
Journal of Public Health Policy, 2009Co-Authors: Toshihide Tsuda, Masaya Miyai, Takashi Yorifuji, Soshi Takao, Akira BabazonoAbstract:We present the history of Minamata Disease in a chronological order from the public health point of view. Because the appropriate public health response – to investigate and control the outbreak – as set out in the Food Sanitation Act was not conducted, no one knew how many became ill following the outbreak. Exposure could not be stopped. In our discussion, we offer two reasons as to why the Japanese public health agencies did not apply the Act: social circumstances in the 1950s and 1960s that placed emphasis on industrial development, and the Japanese medical community’s lack of knowledge about the Act. The history of Minamata Disease shows us the consequences when public health responses are not implemented. Minamata Disease should be an invaluable lesson for future public health responses.
-
methylmercury level in umbilical cords from patients with congenital Minamata Disease
Science of The Total Environment, 1999Co-Authors: Masazumi Harada, Hirokatsu Akagi, Toshihide Tsuda, T Kizaki, H OhnoAbstract:Abstract A total of 151 umbilical cords during the period from 1950 to 1969 were collected from the residents of the Minamata area (including 25 patients with congenital Minamata Disease) for methylmercury (MeHg) analysis. When the MeHg discharge from the Chisso Company’s Minamata factory into the Minamata Bay is compared with the incidence of congenital Minamata Disease, the abrupt increase of the former in 1952 [Nishimura H. Chem. Today 1998;323:60–66] was found to precede that of the latter by approximately 2 years, thereby indicating that MeHg is the cause of the disaster. This was confirmed by the elevated levels of MeHg in the umbilical cords from residents of the Minamata area [from 0.35±0.30 (S.D.) ppm in 1952 to 0.96±0.75 ppm in 1955], the MeHg levels (1.60±1.00 ppm) in the cords from patients with congenital Minamata Disease showing the highest values [ P
Philippe Grandjean - One of the best experts on this subject based on the ideXlab platform.
-
accelerated functional losses in ageing congenital Minamata Disease patients
Neurotoxicology and Teratology, 2018Co-Authors: Takashi Yorifuji, Philippe Grandjean, Shigeru TakaokaAbstract:Abstract Severe methylmercury poisoning occurred in Minamata and neighboring communities in Japan during the 1950s and 1960s. A considerable number of children were born with conditions resembling cerebral palsy, later known as congenital Minamata Disease. Although surviving patients are now in their 50s or 60s, few assessments of functional capacities in daily living have been performed. We assessed the changes in Activities of Daily Living (ADL) status of 11 patients over a 10-year period. For assessment of ADL, we applied the Barthel Index (BI) and the Functional Independence Measure (FIM). We obtained the patients' current and previous status information by interview of their caregivers or from medical records and then compared them using the Wilcoxon signed-rank test. Both ADL measures, including the status related with cognition, had significantly declined during the 10 years. The same was true for the overall BI score (p = 0.01). Similarly, all functions of the FIM scores declined (i.e., self-care, sphincter control, mobility, locomotion, communication, and social cognition), and for FIM physical and cognition subscores as well as FIM total score, the declines were statistically significant. The present study indicates that the ADL status of congenital Minamata Disease patients, now in their 50s or 60s, has substantially declined during the last 10 years; a decline that was much steeper in comparison with expectation in subjects of similar ages, but in agreement with accelerated ageing also reported in subjects with cerebral palsy, past polio infection, or epilepsy. While already incapacitated due to the prenatal methylmercury poisoning, their accelerated ageing may suggest that patients with developmental neurotoxicity have less reserve capacity to compensate for normal ageing. These patients will need continuous and increasing medical and welfare support in the community.
-
methylmercury dose estimation from umbilical cord concentrations in patients with Minamata Disease
Environmental Research, 1998Co-Authors: Hirokatsu Akagi, Philippe Grandjean, Yukio Takizawa, Pal WeiheAbstract:Abstract The methylmercury exposure of patients with congenital or infantile Minamata Disease is known only from a small number of analyses of umbilical cords. Four laboratories in Japan have analyzed a total of 176 samples of umbilical cord tissue obtained from Minamata. The highest concentrations were seen in cord tissue from children born during 1950–1965, i.e., the peak period of acetaldehyde production in Minamata before installation of waste water treatment. Twenty-four samples from patients diagnosed with Minamata Disease showed a median mercury concentration of 1.63 μg/g and differed significantly from levels seen in cord tissue from control children. However, children diagnosed with mental retardation had mercury concentrations in cord that were intermediate between the two other groups. Using regression coefficients obtained at a study conducted at the Faroe Islands, the median cord mercury concentration from the children with Minamata Disease is estimated to correspond to about 216 μg/L cord blood and 41 μg/g in maternal hair. Based on correlations reported in the literature, the median daily mercury intake of the women whose children developed Minamata Disease can then be estimated at about 225 μg. Although these children had fully developed Minamata Disease, the estimates of median mercury levels are only four to five times higher than current mercury exposure limits.
Mineshi Sakamoto - One of the best experts on this subject based on the ideXlab platform.
-
characteristics of hand tremor and postural sway in patients with fetal type Minamata Disease
Journal of Toxicological Sciences, 2016Co-Authors: Toyoto Iwata, Shigeru Takaoka, Mineshi Sakamoto, Eri Maeda, Masaaki Nakamura, Katsuyuki MurataAbstract:: About forty certified patients aged around 50 years old existed as living witnesses to fetal-type Minamata Disease (methylmercury poisoning due to in utero exposure) in Minamata, Japan in 2006. Computerized hand tremor and postural sway tests with spectral analysis were conducted for 24 of them and in matched control subjects to examine the pathophysiological feature of neuromotor function. The tremor intensities of the patients with fetal-type Minamata Disease were significantly larger than those of the 67 controls at every frequency band for both hands. In the patients, proportions for intensity at 1-6 Hz of both hands were larger, but those of the intensity at 6-10 Hz were smaller compared with the controls. The center frequency of a tremor was significantly lower in the patients than in the controls. Only eight males of the 24 patients were examined to evaluate postural sway because of extremely low scores in activities of daily living in the remaining. Most of the postural sway parameters obtained with eyes open and closed were significantly larger in the patients than in the male controls. Likewise, Romberg quotients of postural sway in anterior-posterior direction were significantly higher in the patients. In conclusion, the patients with fetal-type Minamata Disease of our study showed a larger tremor of low frequency at less than 6 Hz and postural instability. Spectral analyses of computerized hand tremor and postural sway are suggested to be useful for assessing the pathophysiological change, related to a lesion of the cerebellum, resulting from prenatal methylmercury exposure.
-
comparison of current activities of daily living adl scores of fetal type Minamata Disease patients with their adl scores 15 years ago and communication disorders of these patients
Japanese journal of hygiene, 2007Co-Authors: Mineshi Sakamoto, Takeko Kato, Miwako Okamoto, Kimiyoshi ArimuraAbstract:OBJECTIVES: The main purposes of this study are to compare the current statuses and activities of daily living (ADL) scores with the same parameters 15 years ago in fetal-type Minamata Disease patients and to identify the communication disorders in these patients. METHODS: An interview survey was conducted on 31 fetal-type Minamata Disease patients mainly in 2002 concerning family structure, present status of care, their demand for care, communication status, and ADLs. Changes in ADLs during the past 15 years were also studied in 22 of the patients. RESULTS: Their mean ages were 45.5+/-3.5 (n=20) for males, and 46.1+/-1.9 (n=ll) for females. The average numbers of family of the patients was 2, and 15 patients lived alone. An analysis of ADLs showed that about 50% of the patients could not walk or take a bath, and 30 to 40% of the patients could not eat, excrete, change their clothes, or wash their face alone. Approximately 80% of the patients could understand daily conversation to some degree. However, their ability to express their demands and thoughts, put an idea into action, remember events, and live like ordinary people were significantly worse than their ability to understand daily conversation. The changes in the ADLs of the 22 patients were not significant for the past 15 years. However, two patients showed a rapid decrease for ADL of movement and 2 other patients died after an interview before 50 years of age. CONCLUSIONS: Appropriate care in daily living is an important issue for fetal-type Minamata Disease patients. Further, the individual health care of such patients is an urgent issue and can prevent their health from rapidly deteriorating.
-
widespread neuronal degeneration in rats following oral administration of methylmercury during the postnatal developing phase a model of fetal type Minamata Disease
Brain Research, 1998Co-Authors: Mineshi Sakamoto, Hitoshi Takahashi, Akiyoshi Kakita, Koichi Wakabayashi, Tatsumi Adachi, Atsuhiro NakanoAbstract:The neurotoxicity of methylmercury (MeHg) treatment during the postnatal developing phase in rats was studied. Rats on postnatal day 1 were orally administered 5 mg/kg/day methylmercury chloride (MMC) for more than 30 consecutive days. Body weight loss began 26 days after MMC was administered, and severe paralysis of the hind-limbs and unsteadiness appeared subsequently. Histopathologically, the widespread neuronal degeneration was observed in the cerebral neocortex, neostriatum, red nucleus, brainstem, cerebellum and spinal dorsal root ganglia on day 32. The widespread distribution of the lesions was quite similar to that in fetal cases of MeHg intoxication in Minamata, Japan. These findings suggest that MMC treatment during the postnatal development phase in rats produce a good model of fetal-type Minamata Disease.
-
Profile of Subjective Complaints and Activities of Daily Living among Current Patients with Minamata Disease after 3 Decades1
Neurobehavioral Methods and Effects in Occupational and Environmental Health, 1994Co-Authors: Yoshihide Kinjo, Mineshi Sakamoto, Atsuhiro Nakano, Hirofumi Higashi, Ryoji SakaiAbstract:We surveyed 1144 current patients with Minamata Disease (MD) aged 40 or over in the Minamata area and the same number of neighbor controls matched with age and sex by questionnaire interview with regard to subjective complaints and activities of daily living (ADL). From analysis of subjective complaints, it was found that MD patients had significantly higher rates of all complaints than controls (P < 0.05). Multivariate analysis showed that subjective complaints in controls were clearly separated into the following two categories: sensory disturbances and movement nerve disturbances, but all complaints in MD patients formed one cluster. Such variation seemed to be due to methylmercury exposure to the central nervous system. ADL analysis revealed that the difference in the ADL disability between MD patients and controls significantly increased with age (P < 0.05) and that ADL disability in MD patients was aggravated by aging. © 1993 Academic Press, Inc.
-
profile of subjective complaints and activities of daily living among current patients with Minamata Disease after 3 decades
Environmental Research, 1993Co-Authors: Yoshihide Kinjo, Mineshi Sakamoto, Atsuhiro Nakano, Hirofumi Higashi, Ryoji SakaiAbstract:We surveyed 1144 current patients with Minamata Disease (MD) aged 40 or over in the Minamata area and the same number of neighbor controls matched with age and sex by questionnarie interview with regard to subjective complaints and activities of daily living (ADL). From analysis of subjective complaints, it was found that MD patients had significantly higher rates of all complaints than controls (P < 0.05). Multivariate analysis showed that subjective complaints in controls were clearly separated into the following two categories: sensor disturbances and movement nerve disturbances, but all complaints in MD patients formed one cluster. Such variation seemed to be due to methylmercury exposure to the central nervous system. ADL analysis revealed that the difference in the ADL disability between MD patients and controls significantly increased with age (P < 0.05) and that ADL disability in MD patients was aggravated by aging. 25 refs., 4 figs., 5 tabs.