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Pathological changes of human sural nerves in Minamato disease (methylmercury poisoning). Light and electron
Abstract:
Biopsy of the sural nerve was performed on six patients with relatively mild Minamata disease of 10-year or longer duration. All of the six patients presented characteristic pathologic changes. Light microscopy disclosed the formation of irregularly shaped myelin sheaths and fine axons, an increase in them, which is suggestive of incomplete regeneration, cicatrization following the loss of nerve fibers, increase in Schwann's nuclei, and formation of Büngner's bands. Electron microscopy revealed incomplete myelinated fibers and ultrafine unmyelinated fibers associated with incomplete regeneration, formation of regeneration units, and collagen increase. The laminar encapsulation with the processes of Schwann's cells were often observed in ultrafine fibers. In view of the fact that small quantities of mercury-contaminated fishes are still being caught in the Minamata district, myelin degeneration, glycogen deposits and appearance of dense bodies in axons, and vesiculation and fragmentation of endoplasmic reticulum were observed as degenerative changes due to the effects of mercury accumulation.
Insights
Sural nerve biopsies in mild Minamata disease patients reveal nerve fiber damage and regeneration signs. Mercury accumulation likely causes these pathological changes, even with long-term exposure.
Area of Science:
- Neurology
- Toxicology
- Pathology
Background:
- Minamata disease is a severe neurological disorder caused by methylmercury poisoning.
- Long-term exposure to low levels of methylmercury can still cause neurological damage.
Observation:
- Sural nerve biopsies were performed on six patients with mild Minamata disease (duration >10 years).
- Light microscopy showed irregular myelin sheaths, increased fine axons, and signs of nerve fiber loss and regeneration.
- Electron microscopy revealed incomplete myelination, ultrafine unmyelinated fibers, and collagen increase, indicative of regeneration attempts.
Findings:
- Pathological changes consistent with nerve damage and attempted regeneration were observed in all patients.
- Specific findings included irregular myelin, increased Schwann's nuclei, and Büngner's bands.
- Mercury accumulation was linked to myelin degeneration, axonal changes (glycogen deposits, dense bodies), and endoplasmic reticulum damage.
Implications:
- These findings highlight the persistent neuropathological effects of chronic mercury exposure.
- Understanding these nerve changes is crucial for diagnosing and managing Minamata disease.
- The study underscores the ongoing risk posed by mercury-contaminated fish in affected regions.