In 1880, T.G. Thomas was the first to describe vulvar pain in the medical literature, characterizing it as “an abnormal sensitiveness; ’a plus state of excitability’ in the diseased nerve” [4]. Until recently, however, little was known about the prevalence of chronic vulvar pain. In 2003, the authors of a landmark population-based study estimated the prevalence of vulvodynia in an ethnically diverse sample of 4915 women and concluded that as many as 14 million women in the United States will experience chronic vulvar pain during their lifetime [5]. Contrary to earlier assessments, Caucasian and African-American women reported a similar lifetime prevalence; however, Hispanic women were 80% more likely to experience chronic vulvar pain than their Caucasian and African-American counterparts. Even if only a small percentage of these women have true vulvodynia, the number of women suffering from this pain is staggering. Unfortunately, at least 30% will suffer without seeking medical care [5].

The etiology of GVD remains elusive, but it most likely occurs from a variety of sources and represents many different disease processes. In 2003, leaders at a National Institute of Health sponsored conference on vulvodynia concluded that GVD is described most accurately when conceptualized as a combined neuropathic pain process (e.g., pudendal neuralgia) and complex regional pain syndrome (CRPS), similar to other CRPSs (e.g., fibromyalgia, interstitial cystitis) [6]. As with patients with neuropathic pain, women with GVD exhibit dysesthesia (an abnormal, unpleasant pain sensation) characterized by allodynia (pain in response to a normally nonpainful stimulus), hyperpathia (pain in response to light touch), and hyperalgesia (increased response to a painful stimulus) [7] .

In addition, like patients with CRPS, women with GVD exhibit enhanced systemic pain perception, a process likely due to central nervous system (CNS) sensitization [8], which develops when neuronal synapses within the CNS change in response to a persistent barrage of nociceptive impulses, thereby prolonging andamplifyingpain perception [9]. In addition, women with GVD are more likely to have other CRPSs (e.g., interstitial cystitis) [10]; this co-occurrence may be due to “wind-up,” in which there is progressively increasing activity in the dorsal horn cells of the spinal cord following repetitive activation of primary afferent C-fibers [11],

It has also been suggested that the nerves innervating the pelvis and vulva are especially prone to injury due to the complex anatomical structure of the pelvis and lower spine [ 12]. The vulva is innervated by the pudendal nerve originating from S2 to S4 and from the genitofemoral nerve arising from LI to L2. The location and winding course of the pudendal nerve subjects it to potential injury through entrapment (in Alcock’s canal), crush (e.g., falls on the buttocks, pressure from bicycle seats, hypertonus of the levator ani muscles), scarring (e.g., endometriosis), stretching (e.g., during childbirth), and infection (e.g., herpes) [12],

Perhaps consistent with pudendal nerve injury is the suggestion that women with GVD have pelvic floor muscle dysfunction. Although few studies have systematically investigated this issue, evidence indicates that affected women display abnormalities in resting amplitude; contractile amplitudes during tonic, phasic, and endurance contractions; and postcontractile pelvic floor muscle stability as compared with control women [13]. Supporting the involvement of the pelvic floor musculature is the improvement in pain and sexual function measures after electromyography-assisted pelvic floor muscle rehabilitation [14].

Although researchers have failed to find a consistent association between childhood victimization and GVD, one study demonstrated that women with chronic vulvar pain (including GVD and provoked vestibulodynia, or PVD) were more likely to have reported poor family social support and child physical abuse [15]. Theoretically, a stressor such as sexual abuse can lead to alternations in the pain pathways of the CNS [16]; however, this finding is in need of replication as several other controlled studies have failed to show this association [17].

Also, despite hints in the earlier literature of associations between psychosocial function and GVD such that psychological distress preceded the development of the pain, it is currently acknowledged that the presence of the pain of GVD and its associated disability leads to profound psychosocial ramifications including anxiety, depression, and disruption of interpersonal relationships [18–20].

All women with vulvar pain should have a thorough physical examination with the goal of finding evidence of an identifiable disease that can cause vulvovaginal pain but would not be classified as vulvodynia (i.e. infections, trauma, dermatitis, interstitial cystitis, etc.). A thorough description of this exam can be found in Chapter 4.

Unfortunately, most treatment recommendations for vulvodynia are not based on controlled trials. In addition, many studies do not distinguish between PVD and GVD. As such, this chapter will focus on treatments that are more applicable to GVD (PVD treatment is discussed in Chapter 8). For certain women displaying both types of symptoms, the treatments discussed in both chapters may be applicable.

Strategies to Minimize Vulvar Irritation

Most practitioners recommend numerous strategies to minimize vulvar irritation [21]. A common recommendation is to use 100% cotton underwear washed only in hot water to avoid irritation that may be caused by residual fabric detergents or softeners. Also, patients should be counseled to use mild soap for bathing without applying soap directly to the vulva because the interlabial sulci and vestibule can be easily cleaned with water and a gentle touch. Daily use of panty-liners can be irritating; unscented and dye-free cotton menstrual pads during menstruation are good alternatives. Adequate lubrication during intercourse is also suggested; for example, Slippery Stuff™ does not contain propylene glycol which can act as an allergen or irritant [22]. Rinsing the vulva after urination and gently patting the area dry after urination and bathing may also be helpful in some cases.

Topical Treatments

While topical treatments are more applicable to PVD, some women with GVD may benefit from them. Topical anesthetics may cause initial burning and stinging upon application; the discomfort lasts for a few minutes until the area is numb. The longer the ointment is on the area, the deeper the anesthesia. The most commonly prescribed anesthetic is lidocaine (Xylocaine™ jelly 2% or ointment 5%) [23]. The long-term use of overnight topical lidocaine has been proposed as a specific therapy for PVD, but may be useful for women with GVD, as it is theorized that the regular application of lidocaine interrupts repetitive activation of peripheral C-afferent nociceptors, thereby inhibiting the process of “wind-up” at the dorsal horn of the spinal cord [24]. However, several topical anesthetics may in fact sensitize the tissue and lead to unwanted outcomes (e.g., Benzocaine™); these should be avoided.

Topical therapies that patients describe as not