The disease is an autosomal dominant genetic disease. In the process of bilirubin synthesis by porphyrin metabolism, due to the lack of urobilinogen synthase, urobilinogen can't metabolize and accumulate in the body, which reduces bilirubin synthesis. The activity of δ-aminolevulinic acid synthase can be increased through feedback, leading to the increase of δ-aminolevulinic acid and urobilinogen in vivo. Their increase may have toxic effects on nerve transmission function through direct or indirect mechanisms, and then cause the onset of this disease. The disease is an autosomal dominant genetic disease. In the process of bilirubin synthesis by porphyrin metabolism, due to the lack of urobilinogen synthase, urobilinogen can't metabolize and accumulate in the body, which reduces bilirubin synthesis. The activity of δ-aminolevulinic acid synthase can be increased through feedback, leading to the increase of δ-aminolevulinic acid and urobilinogen in vivo. Their increase may have toxic effects on nerve transmission function through direct or indirect mechanisms, and then cause the onset of this disease.