68 Korean J Pain Vol. 23, No. 1, 2010 also been made to treat various types of headaches, lower lumbar pain, myofascial pain syndrome, and CRPS with BoNT-A [6,10-12]. Recent studies have suggested that BoNT-A has an effect on the secretion of neuro- transmitters which are involved in the recognition of pain secondary to the analgesic effect due to muscle relaxation [6-8]. 　　Analgesic mechanisms of BoNT-A can mainly be div- ided into peripheral, spinal, and cerebrocortical mecha- nisms. According to Cui et al. [8], the peripheral mecha- nisms are of interest based on the finding that the sub- cutaneous solar administration of BoNT-A had a sig- nificant analgesic effect in an experimental model of pain induced using formalin in rats. In cases of neurogenic in- flammation, with the initiation of secretions of substances, such as substance P, CGRP, and glutamate, local vaso- dilation, plasma leakage, and the destruction of mast cells occur. Owing to these inflammatory events, bradykinin, ATP, histamine, and serotonin, which are known to provoke hypersensitivity of peripheral nociceptors, accumulate. It has been reported that BoNT-A blocks the early stage of these chain reactions of neurogenic inflammation and thereby reduces pain [8]. Park et al. [13] clarified that BoNT-A effectively reduced mechanical, cold allodynia in an animal experimental model of neuropathy. Subse- quently, according to Ranoux et al. [14], an intradermal in- jection of BoNT-A had a direct analgesic effect in patients with local chronic neuropathy associated with allodynia. These reports provide a theoretical basis for the avail- ability of BoNT-A for the treatment of neuropathies. 　　The activity of central pain receptors immediately af- ter pain stimulation can be measured based on the ex- pression of c-fos, genes associated with the early ex- pression of pain. BoNT-A blocks the secretion of neuro- transmitters which are involved in the pathophysiology of neurogenic inflammation, such as glutamate, secreted from the primary afferent pain receptor fibers. BoNT-A therefore reduces the extensive activity of dorsal horn neurons of the spinal cord, which has been confirmed based on the decreased expression of c-fos [6]. BoNT-A is involved in the blockage of secretion of the above-men- tioned inflammatory mediators and suppresses the ex- pression of c-fos occurring immediately after pain sensa- tion. It can therefore be concluded that BoNT-A sup- presses peripheral sensitization, and this leads to central desensitization [7]. 　　As described herein, in addition to the peripheral and spinal cord effects of BoNT-A, the effects on the central nervous system have also been examined in many studies. With respect to the finding that BoNT-A causes alter- ations in the sensory pattern via the neural axis, including the cerebral cortex, it has been reported that major mech- anisms altering the overall recognition of pain by BoNT-A originate from the neuroplastic reorganization of ex- citatory and inhibitory balances [15]. Through experimental results that BoNT-A has an anti-nociceptive effect via axonal transport to the central nervous system following peripheral injection [16], it has been demonstrated that the central nervous system is involved in the mechanisms by which BoNT-A reduces pain. 　　Alcohol and phenol, which have been commonly used for neurolysis, cannot accurately predict drug spread, and therefore these agents cannot block nerves selectively. Alcohol and phenol cause irreversible destruction. Further- more, alcohol and phenol have been reported to induce novel pain [17]. In cases of pain in which radiofrequency ablation is used, there exist specialized equipment, such as an electrostimulating device and a minute controller. Accordingly, in these cases the selective destruction of nerve fibers is possible. There is a lower possibility that complications might occur in cases in which neurolysis is performed. The size and location of lesions can be controlled. Of the methods for blocking ganglion impar, radiofrequency ablation is excellent [4]. In cases in which ganglion impar is blocked, however, an approach is com- monly made via the anococcygeal ligament. Because a cannula has a linear form, an accurate approach cannot be made to the ganglion impar. The patient presented herein was apprehensive about neurolysis using radio- frequency ablation . Accordingly, as an alternative method to radiofrequency ablation, blockage of the ganglion impar was performed using BoNT-A. Carroll et al. [11] performed blockage of lumbar sympathetic ganglia in patients with CRPS, and compared treatment outcomes between the group in which 0.5% bupivacaine 10 ml was used alone and a group in which concomitant use of 75 U BoNT-A and 0.5% bupivacaine was attempted. As a result, the decrease in VAS was markedly greater and the analgesic period was prolonged in the group in which bupivacaine 10 ml and 75 U BoNT-A was concomitantly used for blockage of the ganglion impar. This is an example demonstrating the sympathetic nerve block effect of BoNT-A based on clin-