To investigate the therapeutic efficacy of cyclosporin A (CyA) in the treatmen t of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), a microem ulsion form of this drug (Neoral) was orally given to seven patients with the disease who were unresponsive or resistant to conventional therapies.The daily d ose of CyA was carefully controlled in order to keep the plasma trough concentra tion between 100 and 150 ng/ml. Within 1 month of initiation of CyA, all patient s subjectively showed improvement of clinical symptoms, while both modified Rank in and INCAT disability scores were significantly decreased (p < 0.05) and grip strength was significantly increased (p < 0.05) 3 months after initiation compar ed with before. Total protein in the cerebrospinal fluid was significantly decre ased 3 and 6 months after starting CyA (p < 0.05). Although the maximal motor ne rve conduction velocity showed a significant improvement in the median nerve 1 t o 1.5 years after commencement of CyA (p < 0.05), there were no significant chan ges in any other neurophysiological parameters. One patient with anti sulphoglu curonyl paragloboside IgM antibodies gradually became resistant to CyA, but the rest have since been in good neurological con dition without complications ascribable to this drug. These results suggest that oral CyA may be effective even for refractory cases with CIDP. CyA should be ac tively considered as a therapeutic option when patients with CIDP are resistant to conventional treatment. To investigate the therapeutic efficacy of cyclosporin A (CyA) in the treatmen t of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), a microem ulsion form of this drug (Neoral ) was orally given to seven patients with the disease who were unresponsive or resistant to conventional therapies. The daily d ose of CyA was carefully controlled in order to keep the plasma trough concentra tion between 100 and 150 ng / ml. Within 1 month of initiation of CyA, all patient s subjectively showed improvement of clinical symptoms, while both modified Rank in and INCAT disability scores were significantly decreased (p <0.05) and grip strength was significantly increased (p <0.05) 3 months after initiation compar ed with before. Total protein in the cerebrospinal fluid was significantly decresed ased 3 and 6 months after starting CyA (p <0.05). Although the maximal motor ne rve conduction velocity showed a significant improvement in the median nerve 1 to 1.5 years after commencement of CyA (p <0.05), there were no significant chan ges in any other neurophysiological parameters. One patient with anti sulphoglu curonyl paragloboside IgM is often resistant to CyA, but the rest have since been in good neurological condition without complications ascribable to the results suggest that oral CyA may be effective even for refractory cases with CIDP. CyA should be acively considered as a therapeutic option when patients with CIDP are resistant to conventional treatment.