It is said that PHN occurs in approximately 13% of patients with herpes zoster.5 Pain during the acute period of herpes zoster is principally due to inflammation. However, the mechanism by which the pain occurs in patients with PHN has not been elucidated. Currently, it is believed that PHN belongs to the category of neuropathic pain, and some theories, such as the virus breaking down the gate control system,1have been presented. Another important theory is that the sympathetic nerve participates in generating pain. In reality, there is no direct relationship between the sympathetic nerve and the somatic nerve; however, when the peripheral nociceptor is injured, a strong excitation is transmitted to the wide dynamic range neuron (WDRN) at the dorsal horn of the spinal cord. The WDRN is excited most strongly by pain stimulus and, at the same time, is in a long-term hypersensitive state. The hypersensitive WDRN can be excited by a non-noxious stimulus transmitted through non-noxious mechanoreceptor fibers, thus generating pain. An impulse by efferent sympathetic fibers is easily transmitted to non-noxious mechanoreceptor fibers and excites the WDRN, thus generating pain.2 When hyperesthesia of the sympathetic nerve is the cause of pain, a blocking transmission of sympathetic excitation and increasing blood flow to the region controlled by the nerve seems to be effective for pain suppression, as was observed in our patient.