Vulvodynia has been defined by the International Society for the Study of Vulvovaginal Diseases (ISSVD) as vulvar discomfort, which is most often described as a burning pain, occurring in the absence of relevant visible findings or a specific, clinically identifiable, neurological disorder (1). Much remains to be understood regarding the patho genesis, natural history, and management of this distressing condition. As postulated for many chronic pain syndromes, the involvement of both peripheral and central sensitization mechanisms in the pathogenesis of vulvodynia has been suggested (2, 3). The characteristics of the pain experienced by patients with vulvodynia suggests the involvement of a neuropathic component in vulvodynia; this includes: hyperalgesia, paraesthesia, dysesthesia and allodynia. In addition, the ineffectiveness of common pain-killers, the effectiveness of certain anticonvulsants (4), anti-depressants and transcutaneous electrical nerve stimulation (TENS) (5) are occasionally reported in association with vulvodynia. The primary objective of the present study was to generate further evidence in support of the existence of a neuropathic component underlying the pathogenesis of vulvodynia. An additional aim was to determine the presence of anxiety, depression and other chronic pain conditions in patients with vulvodynia.