SMON

SMON, which stands for subacute myelo-optico-neuropathy, was a severe neurological disorder that gained significant attention in Japan during the 1950s and 1960s. The condition was characterized by a rapid onset of symptoms affecting the spinal cord and optic nerves. Key clinical manifestations included abdominal pain, diarrhea, and vomiting, followed by sensory disturbances in the lower limbs, muscle weakness, and paralysis. Ocular symptoms were also prominent, with blurred vision, visual field defects, and in some cases, blindness.

The cause of SMON was eventually identified as the widespread use of clioquinol, an oral medication used to treat intestinal infections and amoebiasis. Clioquinol was widely prescribed and readily available over the counter in Japan during the period when SMON cases surged. Research and epidemiological studies strongly linked the consumption of clioquinol to the development of SMON, establishing it as a iatrogenic illness, meaning it was caused by medical treatment.

While the exact mechanism by which clioquinol induced SMON was not fully elucidated, it was believed to involve neurotoxicity. The drug appeared to accumulate in the nervous system, leading to damage of nerve fibers and cells. Following the identification of clioquinol as the causative agent, its use was drastically restricted, and eventually banned in many countries, including Japan. This intervention led to a dramatic decline in new SMON cases, effectively ending the epidemic. Individuals who developed SMON often experienced long-term neurological deficits, and rehabilitation was a significant challenge for many survivors.