Goldstein, MD and article

[Guest guest]

Has anyone seen him or been treated by

him? I just talked with him on the phone, and told me that dyesthetic

vulvodynia is nerve damage. He says you have to hit it hard

with nerve numbing medications (neurontin, cymbalta, etc,) and introvaginal

physical therapy at the same time. He says biofeedback stinks by

itself.

If I went to see him, his first visit

would be 600-1000 dollars. He has offices in Ny and Washington DC. He does not take

any insurance.

He says he has about a 80% success rate,

with success being defined as 8-90% reduction in pain and functioning.

Wondering if anyone has any experiences with

him?

Thanks,

Anne

http://www.ourgyn.com/article_retrieve_printer.php?articleid=63

Vaginal Pain and Itching with No Known Cause?

By:

Goldstein, MD

It Could be Vulvodynia. Here’s a Book-Mark Guide

READER CAUTION NOTE: This article

contains medically graphic images of female genitalia to illustrate the

symptoms of vulvodynia.

Your

visit to the gynecologist has ended with you thinking that you’re

crazy. You’ve got vaginal burning, pain, and rawness that won’t

go away. Your genital area may be red and irritated looking. Your doctor has

said that there is no infection, nor any other disease that is causing the

problem. You’ve tried creams, over-the-counter yeast infection

treatments, and every other itching treatment available. It’s not in

your head; you are not losing your mind. It could be vulvodynia.

The

International Society for the Study of Vulvovaginal Disease (ISSVD) defines

Vulvodynia as chronic vulvar discomfort or pain, characterized by burning,

stinging, irritation or rawness of the female genitalia in cases in which

there is no infection or skin disease of the vulva or vagina causing these

symptoms. Burning sensations are the most common, but the type and severity

of symptoms are highly individualized. Pain may be constant or intermittent,

localized or diffuse.

Vulvodynia

has been classified into the following subtypes: Dysesthetic vulvodynia,

Vulvar Vestibulitis Syndrome, and Vulvar Dermatoses. In addition, vulvar skin

disorders known collectively as “Vulvar Dermatoses” can also

cause vulvar pain. This article describes in detail dysesthetic vulvodynia,

vulvar vestibulitis, and the vulvar dermatoses in detail so that you can have

the knowledge to speak with your doctor about your particular symptoms.

Dysesthetic Vulvodynia

Dysesthetic vulvodynia is defined as vulvar burning, rawness, and irritation

without know cause. The pain is generally non-provoked- there is pain without

any contact. It is usually generalized to the entire vulva, but sometimes can

be located in one area (e.g. pain of the clitoris only called clitorodynia).

The cause of this disorder is unknown. Most experts believe that the pain of

dysesthetic vulvodynia is caused by a combination of nerve damage (with

central sensitization) and pelvic floor muscle dysfunction. What does this

all mean?

Nerve damage: The sensation of burning is almost

always neuropathic pain (nerve pain.) How can you get nerve damage? Many

ways. Back problems, allergic reactions, trauma, stretching the nerve,

persistent infections (however, infection is almost always overemphasized as

a cause of nerve damage).

Central sensitization: There are pain

nerve centers in the pelvis, spine, lower parts of the brain, and the cortex

(higher parts) of the brain. When these pain centers get persistent signals,

they get more sensitive, so almost all sensations are then perceived as pain.

This does NOT mean " it’s in you head " or " you’re

crazy. " This is a physiologic process and can be seen on brain scans

called PET scans. Women with central sensitization experience pain more

easily. Lastly, this is why stress and anxiety increase pain. The chemicals

(called neurotransmitters) that activate these pain centers are the same

neurotransmitters that are increased during stress/anxiety.

Pelvic muscle dysfunction: The muscles of

the pelvic floor become dysfunctional- too tight and weak. When there is an

increase in muscle tone then the blood flow through the muscles decreases. A

10% increase in muscle tone decreases blood flow by 50%. When there is

decreased blood flow there is decreased oxygen, decreased glucose, decreased

nutrients not just to the muscles, but to the rest of the tissue of the

vulva. Lactic acid builds up and the muscles become tight and weak and they

hurt. It is as if they are running a six-month marathon.

Treatments

for Dysesthetic Vulvodynia

We

must address all of the components above to treat DV. If you ignore one of these

you are much more likely to remain in pain. The concept of treating

neuropathic pain is very simple: “Numb the nerves.” If you limit

electrical signals going through the nerves, then the nerves can start to

heal. Healing only begins when you are out of pain. Secondly, nerves heal

very slowly over months not days/weeks.

So

which medicines numb nerves?

Tricyclic

antidepressants - amitriptyline, nortriptyline, desipramine do this (probably

the best), but they have side effects: sleepiness, dry mouth, constipation,

palpitation. Just because you may have a side effect (even palpitations) does

not mean that the medication is dangerous. I do not have a

“favorite” in this group. If one is not tolerated, then I try the

next.

Neurontin

(gabapentin) an anti- seizure medication, also “numbs nerves.” I

find that it works best for focal pain such as clitorodynia. There is a HUGE

range of doses that can work – from 100-4500mg. It is a relatively safe

medication. In my experience it sometimes works very well, other times not at

all. If I suspect that the pain may be from herpes (herpetic neuralgia) then

I will start with Neurontin first.

Venlafaxine

(Effexor). Dr. Wasserman and I

were awarded a large grant from the NVA to do a randomized study for these

two medications for DV. We have had excellent results with these medications

and are very excited about this study. I expect that we will start enrolling

patients in our study in October 2003. I will post more details about the

study when we have received the final OK from our investigational review

committee.

For

most diseases the general rule is to try to treat with one medication only.

This is NOT true of DV. Usually, I use at least two (sometimes three or four

medications). For example I often combine Effexor with Neurontin + an

anti-inflammatory (such as Celebrex or Bextra) + topical lidocaine. This has

proven to be an excellent combination.

It

is ESSENTIAL that the pelvic floor dysfunction is also addressed. A

combination of biofeedback and physical therapy often work the best. The

concept behind both biofeedback and physical therapy is that the muscles of

the pelvis become very tight and tender when a woman is in chronic pain. When

the muscles are tight, they constrict the blood vessels and nerves that run

through the muscles. This leads to decreased oxygen and nutrients going to

the pelvis and can help perpetuate vulvodynia. In biofeedback a machine with

vaginal sensors measures the activity of the muscles of the pelvis (a.k.a.

the “pelvic floor” muscles). By using the biofeedback machine a

woman is able to train the muscles of the pelvic floor to relax. Normally the

muscles of the pelvic floor are not under voluntary control; however, the

machine “teaches” you how to controls these muscles. There are

several different types of physical therapy including reflexology,

cranio-sacral therapy and myofascial release, and trigger point muscle

message. All of these modalities are used to relax overly tight and tender

muscles of the pelvic floor.

VULVAR VESTIBULITIS SYNDROME

Women

with VVS have pain only in the vestibule, and only during or after touch or

pressure is applied (see illustration above). Burning sensations are the most

common symptom and may be experienced with some or all of the following:

sexual intercourse, tampon insertion, gynecologic examination, bicycle

riding, and wearing tight pants. Traditionally, VVS is diagnosed using three

criteria established by Freidrich. These are: severe pain during attempted

vaginal entry, tenderness to pressure localized to the vulvar vestibule, and

erythema of the vulvar vestibule. In the last few years, increased awareness

of vulvar vestibulitis syndrome (VVS) has led to exciting new research. This

research focuses on many different aspects of VVS including possible genetic,

infectious or allergic etiologies, and on multiple treatment regimens. Even

basic assumptions of early researchers have been questioned, leading to a

greater understanding of VVS.

Two

studies question our assumptions that VVS has an infectious etiology. Until

recently, many physicians believed that VVS is a consequence of human

papillomavirus (HPV) infection. Using polymerase chain reaction (PCR)

amplification to detect HPV DNA, Morin and co-workers [3] showed, however,

that HPV is not more common in women with VVS. Another study, by Bornstein et

al. [4], questions the assumption that women with VVS have chronic candidal

infections. They showed that prolonged treatment with the oral antifungal,

fluconazole, was ineffective treatment for VVS. While both of these studies

do not eliminate the possibility that VVS is caused by an initial infection,

it appears that VVS is not a consequence of chronic infections of HPV or Candida.

Recent

studies from Sweden and Israel have

independently shown abnormalities in the vestibular mucosa of women with VSS.

Their conclusions showed that some women have ten times the area of nerve

fibers within their vestibular mucosa. These nerve fibers are called

nociceptors, which are “the pain” sensing endings. Therefore,

even very light touch is extremely painful. Other studies have shown a

possible genetic link that causes an exaggerated inflammatory or immune

response. Data also indicates that some women have increased pain perception

not limited to the vulvar area (such as fibromyalgia). [see Appendix A for

detailed information on these particular studies.]

Treatments

for Vulvar Vestibulitis Syndrome

Over

the past few years many studies have examined treatment options for VVS.

Several different treatment modalities have proven to be very successful in

treating VVS. To date at least 10 papers were published examining the

treatment of VVS with vestibulectomy (surgical removal of the mucosa of the

vestibule). Bornstein et al. [11] performed a meta-analysis of all the

published literature regarding vestibulectomy between 1981 and 1998 and

concluded that 89% of women who had a vestibulectomy experienced a

significant reduction in pain, and 72% of women had a complete resolution of

their symptoms. Schneider and co-workers [12] report

similar success and also present data showing that 83% of women who underwent

vestibulectomy would recommend it to others.

Several

papers have examined electromyographic (EMG) biofeedback for the treatment of

VVS. McKay and colleagues [13] report that

52% of women demonstrated markedly decreased vestibular pain after EMG and

69% of the women resumed sexual activity. Sarig et al. [14] reported that 43%

of women could have intercourse without pain after an average of 6 months of

EMG treatment. Lastly, Bergeron et al. [15] performed the first randomized

trial to compare EMG, group cognitive-behavior therapy, and vestibulectomy.

They reported that all three treatment modalities offered significant

improvement in the symptoms of VVS, but that women had a better outcome after

vestibulectomy than with either EMG or cognitive-behavioral therapy.

Several

studies have also examined interferon injections for the treatment of VVS.

While this treatment strategy was initially started to treat HPV infection

(which we now believe is not the cause of VVS), new data by Schernthaner et

al. [16] show that interferon inhibits mast cells. If our new hypothesis

about the cause of VVS is correct, this may explain why interferon has been

successful. Further evidence to support this theory is provided by Gerber and

team [17], who show that women with VVS are less likely to produce

interferon-beta when they were exposed to a lipopolysaccharide stimulus than

a control group of women. Marinoff et al. [18] report that 49% of women

experienced reduction in their pain after a course of interferon injections.

Vulvar vestibulitis – notice the

redness of the vestibule.

There

are many other treatments for VVS that have not well studied, but are being

used at various medical center throughout the country. As there have been no

randomized studies on any these medications, there usefulness cannot be

accurately discussed. A list of these experimental treatments would include:

Estrace cream, atropine cream, nitroglycerine cream, capsaicin cream,

lidocaine, desipramine and other tricyclic antidepressant medications,

antihistamines, and steroids.

VULVAR

DERMATOSES

There

are many dermatologic conditions that may cause pain in the vulva. The most

common include: lichen simplex chronicus, lichen sclerosis, and lichen

planus. These conditions may cause symptoms of itching and burning.

Scratching the vulva and overusing topical medications may inflame the

tissue, causing swelling and additional pain.

Lichen simplex chronicus: Lichen simplex

chronicus (aka: neurodermatitis, pruritus vulvae, squamous hyperplasia, and

hyperplastic dystrophy) is the end stage of an itch- scratch-itch cycle. The

cause of the initiating itching that leads to lichen simplex chronicus

includes atopic dermatitis, contact dermatitis, and eczema. Intense, chronic

itching from these diseases results in repetitive rubbing and scratching. The

skin responds by thickening, with increased skin markings called

lichenification.

Lichen Simplex

Chronicus

Lichen sclerosis: Lichen sclerosis is a chronic

skin disorder with a predilection for the vulva. The typical lesions of

lichen sclerosis are white plaques, often with areas of bruising and

ulceration. Often, there is destruction of vulvar architecture with scarring

of the clitoral prepuce, resorption of the labia minora, and narrowing of the

opening of the vagina. Symptoms of lichen sclerosis include: chronic itching

and soreness of the vulvar area. There can be splitting of the vulvar skin,

causing stinging, pain, inflammation and swelling. The skin becomes fragile

and pale and white in appearance and these skin changes often cause

difficulties with sexual intercourse. Historically, the treatment of lichen

sclerosis until the early 1990s was topical testosterone. Well-designed

randomized studies, however, demonstrated that clobetasol propionate, an

ultra potent topical corticosteroid, was significantly more effective in the

treatment of lichen sclerosis with fewer side effects. Lichen sclerosis must

be followed closely as 3-6% of women with LS develop vulvar cancer.

Lichen Sclerosis

Lichen Planus: Lichen planus is a skin condition

that can occur on the limbs, mouth, vulva and vagina. When it occurs on the

mucous membranes of the mouth or vagina it causes erosions or ulceration.

Lichen planus is an auto-immune disease- your own body starts to attack a

component of the skin causing breakdown of the tissue. Lichen planus may be

painful in the mouth and vagina and secondary infection may occur. If the

areas touch one another, scarring may occur resulting in a narrowing of the

vagina. Lichen planus is most often treated with topical steroid creams. If

scarring has occurred, vaginal dilators may be used to help prevent further

scar formation. Surgical separation of the vaginal scar tissue is sometimes

necessary.

Lichen Planus

While

the diagnosis and management of vulvodynia or the vulvar dermatoses is often

difficult, once an accurate diagnosis is made there are very effective

treatments. If one treatment does not work, do not hesitate to ask your

doctor to try something else. Remember, these are conditions that may take

months to relieve. Take heart that you are not alone. It’s not in your

head. Your determination to find relief can help the medical community

continue to develop treatment for millions of women.

Appendix

A

Although

some of our previously held beliefs about VVS have not survived scientific

scrutiny, several new ideas do have strong experimental backing. Bohm-Starke

and colleagues [5] used PGP 9.5 immunohistochemistry to demonstrate that the

number of intraepithelial nerve endings in the vestibular mucosa in women

with VVS is significantly increased. In addition, they showed that calcitonin

gene-related peptide, which is known to exist in nociceptive afferent nerves,

was the only neuropeptide detected in the superficial nerves of the

vestibular mucosa. Therefore, the increased free nerve endings within the

vestibular mucosa of women with VVS are nociceptors. Bornstein et al. [6]

confirmed these results and used computer-assisted histomorphometry to show

that women with VVS have ten times the area of nerve fibers than women

without VVS. Furthermore, they demonstrated the presence of increased mast

cells in the mucosa of women with VVS [6]. If we examine these results along

with data from Velangi [7] that shows that the skin of women with VVS is more

sensitive to chemical irritants than asymptomatic women, we can formulate a

new hypothesis about the cause of VVS. VVS may be initiated by an allergic

reaction to a chemical irritant in the vulvar vestibule. This irritation

– possibly to topical antifungal agents used to treat suspected

candidiasis (yeast infection) – causes mast cells to migrate to the

vestibule. If the irritation persists, activation of mast cells leads to an

uncontrolled proliferation of nociceptors in the mucosa. This hypothesis

explains why up to 80% of women with VVS complain of an acute onset of

symptoms that includes burning and itching, which then progress to severe

pain on touch. The pain on touch often then persists even after the initial

symptoms of itching and burning disappear. Of course, further studies should

be performed to assess the validity of this hypothesis.

Witkin

and associates [8] are the first to examine a possible genetic link to VVS.

They examined the relation between vulvar vestibulitis and polymorphisms in

the gene coding for the interleukin-1 receptor antagonist, a naturally

occurring down-regulator of pr-inflammatory immune responses. They

demonstrated a unique distribution of interleukin-1 receptor antagonist

alleles among women with vulvar vestibulitis. This suggests that polymorphism

in this gene may lead to elevated levels of interleukin-1 (IL-1), thereby

creating an exaggerated inflammatory or immune response. This hypothesis is

further supported by data from and Hasday [9], who showed that tissue

levels of IL-1 were 2.3-fold greater in women with VVS than in controls.

Several

articles have suggested that women with vulvar vestibulitis have increased

pain perception that is not limited to their genitalia. Pukall and colleagues

[10] used modified von Frey stimuli

to measure tactile and pain thresholds around the vulvar vestibule and in

five non-vestibular areas. Their data show that women with VVS had

significantly lower tactile and pain thresholds than controls in the vulvar

vestibule in non-vestibular regions such as the deltoid. This may imply that

VVS is part of a systemic pain syndrome (such as fibromyalgia) and not just a

genital condition.

09/2003

Copyright© Vibrance Associates, 2003-2004D

painkillers

I asked a question the

other day and had not received any replied

relating to pain killers such as Voltaren or Ibuprofen.

I was at one

point on a large dosage of these and I was

wondering if that could have

changed my vuvlar pain significantly. I was

feeling better at the time

and was on a treatment for vulvar pain

(guaifenesin). I was wondering

which one contributed the best to pain releif:

guai or pain killers.

I have never heard of Voltaren and Ibuprofen to

be used for this type

of pain. Does that mean that I should give

all the credit to guai

rather than painkillers?

Thanks

Anja