VESTIBULITIS / VESTIBULODYNIA - Dr. (part 1)

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Here is a good one from Dee. It was written by Dr. , but it was so long I broke it up into two posts. I'm not sure how old it is, but it does contain a lot a good info. I hope it helps! ~ChelleDeeTroll wrote: Forgive my own highlights, I do that for myself to find things quickly or what I think is important to highlight for me with my own notes... but I always add my initials if I do.... This is exceptionally long so be forewarned, but I hope it helps. HUGSDee` ========================================== _________________________________________________________ VERY LONG AND TECHNICAL AND IS A 'FEE' CHARGED ARTICLE I PAID FOR, OR I'D SEND THE URL. Dee Vulvar pain syndromes: Vestibulodynia (formerly Vestibulitis) By Gunther ,MD Note**(She has a good book out called 'The V-Book', an excellent book for all women, Dee T DEFINITION — Vulvodynia refers to a syndrome of unexplained vulvar itching, burning, and/or pain that causes physical, sexual, and psychological distress. This combination of symptoms has been given many confusing descriptors and subtypes in the past. The International Society for the Study of Vulvovaginal Disease (ISSVD) has proposed specific pain terminology: Generalized vulvar dysesthesia (VDY), formerly known as dysesthetic or essential vulvodynia (DV) refers to diffuse and constant pain anywhere on the vulva that is 'not' evoked. Localized vulvar dysesthesia refers to pain that 'is' evoked and can be consistently localized by point pressure mapping within

specific areas of the vulva. There are three subtypes within this category: vestibulodynia (formerly vulvar vestibulitis syndrome), clitorodynia, and other localized forms of vulvodynia. Most localized vulvar dysesthesia is attributable to vestibulodynia (VBY), which represents the largest subset of VDY. Mixed dysesthesia refers to pain upon touching the vulvar vestibule or other areas of the vulva. The definitions will change continuously until vulvodynia is fully understood. Conditions previously considered subsets of vulvodynia, such as vulvar dermatoses, cyclic vulvovaginitis,

and papillomatosis, have other etiologies and are 'not' part of vulvar dysesthesia. The etiology, diagnosis, and treatment of vestibulodynia will be reviewed here. Vulvodynia (unexplained vulvar pain of various types) is discussed separately. CRITERIA FOR VESTIBULODYNIA — (was called vestibulitis) Criteria for vestibulodynia (VBY) include: severe pain upon vestibular touch or attempted vaginal entry, tenderness to pressure localized within the vulvar vestibule, and physical findings limited to vestibular erythema.

These features are chronic, typically of at least three to six months duration and lasting years. The diagnosis should not be made in women complaining of vestibular pain of only a few weeks' duration. VBY (vestibulitis) can be primary or secondary. Primary VBY refers to introital dyspareunia dating from initiation of sexual activity or among women who have never been sexually active intolerable pain consistently present upon insertion of a tampon or vaginal speculum. Secondary VBY describes women who have introital dyspareunia that develops after a period of comfortable sexual relations, tampon use, or speculum examinations. There are no unique

histological findings in primary versus secondary disease. However, the difference in clinical history suggests the possibility of separate etiologies. INCIDENCE AND EPIDEMIOLOGY — The incidence of VBY is unknown, but the disease is not uncommon. One British study, for example, found the prevalence of VBY was 1 to 3 percent among 150 consecutive new female patients attending a walk-in genitourinary medicine clinic. In an American series, 18.5 percent of women reported evoked or unevoked pain in the genitals persisting longer than three months. Most women with VBY are white, young (mean age 32 years), and nulliparous. (meaning have not beared a live birth) Disease prevalence is not related to socioeconomic level. HISTOLOGY AND PATHOGENESIS — Inflammation of the minor vestibular glands was originally considered a pathologic finding; however, the same nonspecific inflammatory infiltrate has now been demonstrated in healthy vestibular tissue. The

ducts of the vestibular glands contain intraepithelial axons that are closely applied to serotonin-containing neuroendocrine cells. Substance P immunoreactive axons have also been found in submucosal nerves of the vestibule and in the duct epithelium . Both serotonin and substance P are inflammatory mediators that may be the source of neurogenic inflammation operant in vestibular pain. (see "Pain theory" further below that I added). For

example, a study comparing biopsies from 32 women with vestibulitis to 30 normal controls demonstrated complement along the dermoepithelial junction, perivascular IgM, and fibrinogen. The authors proposed that vascular injury leading to fibrinogen leakage, antigenic stimulation of IgM, and leakage of other tissue injury products that activate the complement cascade was mediated by altered central neuronal processing initiated by release of vasodilatory substance P from C fibers of the vestibule. In another study, moderate to severe inflammation in tissue sections from women with VBY was associated with an increase in the number of neuroendocrine cells expressing serotonin and CXCR2, the shared interleukin-8 receptor. The inflammatory cytokines, interleukin–1b and tumor necrosis factor-a, have also been found to be elevated in women with VBY. ETIOLOGY — No single agent or factor can be held responsible for the majority of cases of VBY, (vestibulitis) which is best categorized as a chronic pain syndrome of unknown etiology . However, several risk factors and associations have been observed. Infection — A history of vulvovaginal candidiasis (yeast infection, dt) is the single most consistently reported feature reported by women with VBY.(vestibulitis) Candida has been proposed as a causative organism , but the presence of yeast has not been found to be more prevalent in patients with VBY than in asymptomatic women and antifungal treatment usually failed to relieve VBY (and may aggravate symptoms). An autoimmune association between Candida and VBY has also been proposed, although not documented. Human papillomavirus (HPV) and other sexually

transmitted diseases do 'not' appear related to VBY. Hyperoxaluria — Excessive urinary oxalate excretion has been proposed as an etiology of vulvar pain, based upon a case report of only one patient in whom complete remission of symptoms occurred with a low oxalate diet and use of calcium citrate. The low-oxalate diet and treatment with calcium citrate (to bind the oxalate) has been strongly endorsed by many women with VBY and VDY; however, a controlled study of urinary oxalate excretion did 'not' show any differences in women with and without pain.

By comparison, in another series 14 percent of women with pain improved with a low oxalate diet and calcium citrate. It is a slight possibility that oxalate acts as an irritant to aggravate ongoing pain of VBY, but is 'not' a primary cause of VBY. Allergy — (Mast cells/ cromolyn) Levels of IgE consistent with vaginal allergy have been detected in vaginal fluid of women with VBY, but treatment with antihistamines has not been that

effective . Mast cells have also been noted in biopsy specimens from women with VBY. A double-blind, randomized study showed no reduction in pain in women with VBY taking cromolyn compared to those administered placebo. (I myself would doubt that statement as I've seen relief happen with Benedryl gel applied, and/or taking other oral antihistamines for relief, Dee T) Gene polymorphism — Homozygosity of allele 2 of the gene encoding the interleukin 1 receptor antagonist occurs in just over fifty percent of women with VBY. This suggests polymorphism in this gene may be a factor influencing susceptibility to VBY, severity of symptoms, or both [30]. Hormones — Many women complain their pain is worse around the time of menses [31,32], while others only obtain pain relief during their menstrual periods. One study linked oral contraceptive pill (OCP) use, especially in women under age 17, to an increased risk of vestibular pain [33]. (More articles have stated the same since that one, check out this link.) dee http://www.kaisernetwork.org/daily_reports/rep_index.cfm?DR_ID=12809 However, this may represent a marker for early age of first sexual intercourse, which is also a risk factor for VBY. Both normal and low serum estrogen levels have been found in women with VBY. There are many 'numerous' anecdotal reports of efficacy of topical estrogen for relief of vestibular pain. (*note * Using Estrace cream topically to 'me' can

definitely improve the quality of the V skin and it helps those nerve endings, Dee) A strong association of VBY with the postpartum (after giving birth, dt) period has been reported. Thirty-nine percent of women delivering first or second babies developed nonfocal introital dyspareunia (median duration 5.5 months)and cesarean delivery was not protective. Somatization — A psychiatric basis for vulvar pain should be a diagnosis of exclusion . There is no definitive evidence for a causal relationship between VBY and psychological problems, childhood sexual or physical abuse, or partners with psychosexual abnormalities . Pain that

interferes with sexual functioning is a cause of secondary depression in women . A study of women suffering from VBY found these women had more bodily complaints than unaffected controls, and considered this an indication of a psychosomatic component to their illness . However, another controlled study did not report differences in nongenital aches and pains between women affected and unaffected with VBY. Disorders of the pelvic floor — Muscles of the pelvic floor may be destabilized, either from cutaneous vulvar disturbances or from joint abnormalities of the spine or pelvis. This destabilization perpetuates vulvar tissue inflammation by its effects on local autonomic (sympathetic)

mediated activity, leading to vascular changes and histamine release. Patients with VBY demonstrate muscular instability at rest, poor muscle recovery, elevated resting baseline tension, reduced muscle activity, and reduced contraction strength. A protocol of internal and external soft tissue mobilization, internal and external therapeutic exercise, and pelvic floor retraining with biofeedback results in improvement in women who have evidence of such muscle dysfunction. Interstitial cystitis — Interstitial cystitis (IC) refers to a syndrome of

urinary frequency, nocturia, hypogastric pain, bladder tenderness on palpation, and negative urine cultures. It is as poorly understood as VBY. Diagnostic criteria include a history of frequency, nocturia and dyspareunia, with bladder and urethral tenderness on bimanual examination. A small number of cases of IC associated with VBY (vestibulitis) have been reported. The epidermis of the vestibule, bladder mucosa, and urethra share a common embryological derivation from the urogenital sinus. Neural hyperplasia noted in VBY is also found in biopsies from women with IC. However, defects in the

urogenital epithelium of the bladder of patients with IC detected by special staining could not be found in patients with VBY. I (dee) added this pain theory just FYI. Pain theory — A chronic inflammatory condition from one of a variety of insults in the mucous membrane of the vestibule may ultimately result in inflammatory or nociceptive pain. (nociceptive are the nerve endings that feel pain, the pathways.) The sensory innervation of the posterior vulva is from branches of the pudendal nerve; the anterior vulva is supplied by branches of the ilioinguinal nerve and the genital branch of the genitofemoral

nerve. These nerve fibers consist of two types: Type A-beta fibers, which are responsible for touch Type C fibers, which mediate perception of noxious stimuli (nociception). In addition, the vulva has an autonomic nerve supply via the hypogastric plexus located in the pararectal tissue. Sympathetic innervation comes via the hypogastric nerve and parasympathetic input comes from the pelvic nerve. Interactive neuronal pathways from higher origins in the brain have been identified, but need further elucidation. Inflammatory mediators are released in tissue

with chronic inflammation and are elevated in women with VBY (vestibulitis) compared to asymptomatic controls. These chemical intermediates (eg, interleukin-1b, tumor necrosis factor, serotonin, bradykinin, histamine,) sensitize C fibers, which are normally subresponsive to mechanical stimulation. In addition, the synthesis of sensory neuropeptides (eg, calcitonin gene-related peptide (CGRP) and substance P) from

the activated C fibers is increased during inflammation. These substances have pro-inflammatory effects and reinforce the inflammatory response in affected tissue. The cytokines may not be the final common pathway to hyperalgesia, instead they may act on the unique neural organization of the vestibule secondarily through the release of neurokinins such as substance P. Prolonged firing of C fibers in the vestibule results in hyperalgesia. In addition to these events in the vestibule, transport of CGRP and substance P to the dorsal horn of the spinal cord sensitizes central neurons in the cord. These sensitized wide-dynamic range (WDR)

neurons then respond to light touch on the vulva by passing through the large myelinated A-fiber mechanoreceptors to the cord; they change the signal sent to the brain from one of light touch to one of pain (allodynia). Eventually, spontaneous signals arising in the dorsal horn can pass by the sympathetic efferent nerves to the A-fiber mechanoreceptors. Continuous stimulation of the A-fiber mechanoreceptors and misreading by the WDR neurons results in continuous burning or pain in the vulva. In summary, sensitization of vestibular type C nerve fibers occurs by insults that vary from woman to woman. Ongoing release of cytokines and neurokines leads to prolonged neuronal firing that sensitizes the

WDR neurons in the dorsal horn to respond abnormally so that the sensation of touch is transformed into that of pain (allodynia). This theory is supported by two studies that have shown a significant increase in the number of intraepithelial nerve endings in women with VBY(vestibulitis) compared to controls. NOTE* see http://www.bmj.com/cgi/eletters/328/7450/1214#63008 to read more. dt Neurochemical characterization of these nerve fibers revealed only calcitonin gene-related peptide, known to exist in nociceptive afferent nerves,

suggesting that the free nerve endings within the epithelium were nociceptors . A statistically significant linear correlation was found between inflammation and nerve bundle density. In addition, women with VBY have increased superficial blood flow and erythema in the posterior vestibule, most probably caused by neurogenic inflammation. Quantitative sensory testing in these women showed allodynia to mechanical testing with von Frey filaments, a lower pain threshold to heat, and a higher threshold to cold compared to controls. These findings support the hypothesis that women with VBY have increased innervation and/or sensitization of thermoreceptors and nociceptors in the vestibular

mucosa. CLINICAL MANIFESTATIONS — VBY (vestibulitis) is asymptomatic unless the vestibule is touched. All women with VBY have introital pain with attempted intercourse; both thermal and incisive pressure type pain have been described and constitute the major feature of this syndrome. In one study over one-third of the patients had constant burning in the vestibule, three-quarters had excessive vaginal discharge,

and ten percent had chronic urinary tract symptoms. Other complaints include discomfort with insertion of a tampon or speculum, tight clothing (eg, pants with a prominent inseam), washing or wiping the vestibule, sitting, biking, or horseback riding. Pelvic pain and deep dyspareunia are not features of VBY, but may occur if interstitial cystitis or endometriosis is also present. Some women experience constant irritative symptoms often misinterpreted as Candidal infection. Longstanding VBY may result in chronic burning in the vestibule misinterpreted as vaginal burning by women who are unfamiliar with the

vestibule. DIAGNOSIS History — Diagnosis of primary VBY can often be made by history alone: dyspareunia with first attempt at sexual activity or inability to use a tampon or tolerate a vaginal speculum. Secondary vestibulitis, developing after a period of comfortable sexual relations or vaginal procedures, may appear after childbirth, repeated infection, long-term dermatosis, or treatment of the vestibule with laser or chemicals. A sexual history is essential to confirm that the relationship is loving and not abusive and that sexual technique

is adequate. Nonreceptive and unlubricated intercourse could cause VBY. Symptoms suggestive of VBY are listed in Table 1. Associated symptoms — Associated symptoms include urinary frequency, urethral or bladder burning, and a history of frequent urinary tract infections with negative cultures. Common diagnoses are trigonitis, chronic cystitis, interstitial cystitis, and urethral syndrome. Irritable bowel syndrome, fibromyalgia, migraines, depression, chronic fatigue syndrome, temporomandibular joint syndrome, and endometriosis are pain conditions that may be associated with VBY. Physical examination — The vulva should be evaluated to confirm normal architecture and exclude dermatoses or other medical conditions. The mouth and skin

should also be checked for lesions suggesting lichen sclerosus or lichen planus. Palpation over the labia and perineum and in the interlabial folds is performed to determine if tender areas exist outside the vestibule. With the labia minora gently parted, the examiner uses a moist cotton-tipped applicator to discern whether there is pain with pressure at one or more points around the vestibule. Such tenderness is easily overlooked in general gynecology evaluations without careful exposure and Q-tip evaluation of the vestibule. Erythema is often present and can be diffuse, in

patches, or focal red spots near the minor vestibular gland openings. Fissuring, especially posteriorly at the 6 o'clock location, may occur. However, the mucosa may also appear normal. A bimanual exam will confirm that the examining hand does not elicit vaginal, cervical, or pelvic tenderness after it passes beyond the vestibule. If there is tenderness over the bladder or upon palpation through the anterior vaginal wall, interstitial cystitis is a consideration. Laboratory — A vaginal pH, wet mount, and yeast culture should be performed to exclude vaginitis or infections. Excessive discharge that is normal by microscopy may represent altered neural control of

vestibular gland secretions. Paradoxically, women with VBY complain of and have excessive vaginal discharge, but may feel extremely dry. Herpes, gonorrhea, and chlamydia cultures should be obtained, if suspected. Colposcopy is helpful in evaluation of the vulva for possible abnormality of the epidermis, but is not routinely used. Acetic acid (vinegar wash) significantly worsens vulvar pain. DIFFERENTIAL DIAGNOSIS —

Differentiating Candida from VBY (vestibulitis) is problematic since both can produce irritative symptoms and tenderness in the vestibule. Yeast must be excluded by examining the woman when she has maximum symptoms, which have not been treated by oral or topical antifungals in the preceding two weeks, and by obtaining a yeast culture on Sabaraud's medium. If a woman has had repeated yeast infections, her inflammatory symptoms will require at least six to eight weeks of antifungal suppression (eg, fluconazole 150 mg PO weekly) before regressing. Persistent dyspareunia with a negative Sabaraud's culture after appropriate antifungal suppression suggests VBY. PCR testing could be a helpful adjunct to yeast cultures. (See "Overview of vaginitis" section on

Candida vulvovaginitis). Dermatoses involving the vestibule can account for significant dyspareunia. (See "Dermatitis of the vulva"). Lichen sclerosus and lichen planus cause well described lesions, synechiae, and introital narrowing contributing to dyspareunia. Biopsy may be necessary. If the dermatoses are controlled by ultrapotent topical steroids, ongoing vestibular tenderness may represent VBY. (See "Lichen sclerosus" and see "Vulvar lichen planus"). TREATMENT — The huge sense of relief from having a concrete diagnosis cannot be underestimated. Confirmation that the pain is real and the condition is not malignant or communicable is also reassuring. Provision of accurate informational handouts is important. Both vulvar pain societies, the National Vulvodynia Association and the Vulvar Pain Foundation, have newsletters, outreach for women, and Web sites . Couples and sexual counseling are valuable, but are limited until the pain is controlled. Open communication between partners and pursuing alternatives to vaginal sex can be encouraged. Zawislak AA, McCarron PA, McCluggage WG, Donnelly RF, Price

JH, McClelland HR, Woolfson AD. Department of Gynaecology, Belfast City Hospital; School of Pharmacy, Queen's University Belfast, UK. OBJECTIVE: To assess the applicability of photodynamic therapy (PDT) in the management of vulvodynia whereby a novel, patch-type system, loaded with 5-aminolevulinic acid (ALA), was used to administer PDT to vulvar regions

displaying the characteristics of vulvodynia. STUDY DESIGN: Eleven patients underwent PDT using a bioadhesive patch to deliver ALA over 4 hours. A nonlaser light source delivered 100 J cm(-2) to the target area using red light of 630 nm. Fluorescence of protoporphyrin IX was observed under ultraviolet light illumination, with no significant difference found between that produced after the first and second applications of the patch. RESULTS: There was a significant reduction (p= 0.0077) in overall symptoms after completion of treatment. No significant alleviation (p = 0.1088) in pain during intercourse was observed following treatment. Eight patients experienced a symptomatic response, while 3 exhibited no improvements in symptoms. No adverse reactions or worsening of reported symptoms was reported. CONCLUSION: The results suggest that PDT is of value in the management of vulvodynia, most probably as a viable option to conventional approaches. Further studies involving

larger numbers of patients are required to confirm the efficacy of PDT in the management of vulvodynia. PMID: 17847765 [PubMed - in process