Vulvodynia consists of unprovoked stinging, burning, irritation, rawness, or pain anywhere on the vulva and can be constant or episodic.
Though antibiotics may yield transient improvement,9 management most often consists of 25-mg hydrocortisone suppositories (or compounded as 100 mg for severe cases) at bedtime for 14 days, then every other day for 14 days. After this course of therapy has been completed, clinicians must reevaluate the patient to determine whether she needs extended therapy (in severe cases) or can begin maintenance with a weekly suppository (for cases that are mild but chronic).
If dyspareunia does not resolve after the inflammation abates, superimposed neuroinflammatory pain (vestibulitis) will need treatment.
CAUSE 5Vulvodynia or vulvar vestibulitis
Vulvodynia (generalized vulvar dysesthesia). This condition—which consists of unprovoked stinging, burning, irritation, rawness, or pain anywhere on the vulva—may be constant or episodic. Dyspareunia in these cases may involve postcoital exacerbation of symptoms.
The cause is unknown, but some suspect a lesion of the pudendal nerve in its long course from the spine to the vulva.
There may be virtually no physical findings, or there may be areas of tenderness, hyperesthesia, or hypoesthesia. A biopsy will be nonspecific. Vulvodynia is therefore diagnosed by ruling out infectious, dermatologic, or other causes of genital pain.
The following treatments are usually successful:
- tricyclic antidepressants such as nortriptyline, starting with a bedtime dose of 10 mg and working up to 50 mg to 150 mg
- the antiepileptic agent gabapentin, starting with a bedtime dose of 100 mg and working up to as much as 1,000 mg (this is usually substituted for the tricyclic antidepressant if that therapy alone is ineffective)
This condition may be either primary or secondary. With primary vestibulitis, a woman experiences pain with her first use of a tampon, her first exposure to a speculum, and the initiation of sexual relations. For those with secondary vestibulitis, pain on contact results after a period of comfortable sexual relations.
This pain is thought to stem from inflammation or trauma that initially sensitizes nociceptors in the vestibular mucosa, leading to prolonged neuronal firing. This in turn sensitizes the wide-dynamic-range neurons in the dorsal horn to respond abnormally, converting the sensation of touch into pain (allodynia).11 There often is a history of an unresolved irritative event such as Candidal infection, repeated genital infection,12 topical treatments,13 and early and sustained use of oral contraceptives.14 All are suspected causes.
Diagnosis is made once other pathology has been ruled out and a Q-tip test has demonstrated that contact elicits pain in the vestibule.
Numerous treatment protocols have been described, but current interest focuses on addressing neuroinflammatory pain. This can be done at the peripheral afferents by reducing inflammation and hyperexcitability with topical xylocaine 5% in a compounded sterol-lanolin base 5 times daily; centrally, this is accomplished using tricyclics in doses of 50 mg to 150 mg.
Note that primary vestibulitis is extremely difficult to treat; vestibulectomy and perineoplasty improve the condition by 60% to 90% when medical management fails.15
- Vaginismus, an involuntary spasm of the perineal and levator muscles, may occur in patients with vestibulitis. While primary vaginismus is psychologic in origin, secondary vaginismus represents a conditioned response to pain,16 usually vestibulitis. In patients with secondary disease, pelvic-floor motor instability has been well-demonstrated; these women have a reduced ability to contract or relax the pelvic floor and increased muscular instability at rest.17
Dyspareunia: Is it organic or psychological
Recent studies of the vestibule and vagina provide new insights into an organic explanation of dyspareunia in women who are otherwise healthy.
Clinicians have long known that the vulva and vestibule are innervated by the pudendal nerve, composed of both somatic motor efferents and sensory afferents. But autonomic nerve fibers from the inferior hypogastric plexus and caudal sympathetic chain ganglia also provide genital sensation and may contribute to the perpetuation of neuroinflammatory pain.1 Although the vulvar vestibule is by definition visceral tissue, it is considered to havenonvisceral innervation.2 Thus, sensations to touch, temperature, and pain are similar to sensations evoked in the skin and can be exquisitely painful.
The traditional view that the vagina has a paucity of nerve endings was contradicted with demonstration of profound innervation, with greater numbers of nerve fibers in the distal areas than in more proximal parts.3 The vagina itself can hurt.
In addition, the presence of luteinizing hormone and human chorionic gonadotropin receptors on the bladder trigone supports the complaint of cyclic worsening of pelvic dyspareunia.4 Circumvaginal motor spasm from hypertonicity of the levator plate5 is an evolving area of study.
Shifting views. Nineteenth-century gynecologists approached dyspareunia primarily from a surgical perspective, using a wide variety of operative interventions. In time, the surgical approach was replaced by an emphasis on psychosocial issues: Women who complained of dyspareunia were frequently classified as “frigid,” while physiological correlates were largely ignored.6 Still later, “deep-thrust” dyspareunia was considered suggestive of an organic source, whereas superficial or entrance dyspareunia was thought to derive from emotional or psychological issues.7
Gradually, an integrated and pain-model approach has evolved. It is now theorized that an instigating pain event is perpetuated by other factors.8
REFERENCES
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4. Tao YX, Heit M, Lei ZM, et al. The urinary bladder of a woman is a novel site of luteinizing hormone-human chorionic gonadotropin receptor gene expression. Am J Obstet Gynecol. 1998;179:1026-1031.
5. Glazer HI, Jantos M, Hartmann EH, Swencionis C. Electromyographic comparisons of the pelvic floor in women with dysesthetic vulvodynia and asymptomatic women. J Reprod Med. 1998;43:959-962.
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