Daniel Menkes, MD


 Botulinum toxin type A may be effective in reducing coital pain in  vestibulodynia with levator ani tenderness, but has little effect on  	vestibular allodynia. 


 To collect pilot data on the efficacy of intramuscular botulinum toxin type  	A (BTX/A) injection into the levator ani muscles to relieve coital pain,  	reduce pelvic floor tension and instability, and reduce vestibular  	hyperalgesia in vestibulodynia.
 
 


 Two subjects meeting diagnostic criteria for vestibulodynia were treated  	with 20 u and 40 u of BTX/A at 12-week intervals. Outcomes included a visual  	analogue scale (VAS), weekly coital pain diaries, surface electromyography (sEMG),  	and a vulvar algesiometer. 
 
 


 BTX/A modestly reduced coital pain in one patient and was ineffective in the  	other. Pelvic floor hypertonicity and variability were markedly reduced in  	both patients, but negligible changes occurred in vestibular hyperalgesia.  	The patient with greater pelvic floor tension had more reduction in  	diary-rated coital pain at 2 weeks post injection (29% v. 9%) and on the VAS  	at 12 weeks (15% vs. 3%). 
 
 


 BTX/A injections may be effective in reducing coital pain in vestibulodynia  	with levator ani tenderness, but has little effect on vestibular allodynia.  	The relationship between pelvic floor hypertonicity and decreased coital  	pain suggests vestibulodynia may be a variant of Chronic Regional Pain  	Syndrome. Dose and volume of BTX/A injected may be related to degree of  	relief. 

Vulvodynia is a complex  	disorder characterized by vulvar discomfort. Its classification is based on  	the pain’s location, whether it is generalized or localized, and whether it  	is provoked, unprovoked, or mixed.

 Provoked vestibulodynia,  	formerly known as vulvar vestibulitis syndrome (VVS), refers to discomfort  	from intercourse, clothing pressure, tampon insertion, or cotton-tipped  	applicator pressure on pelvic examination.

Although its etiology is  	unknown, vestibulodynia may be a variant of a chronic pain condition known  	as Complex Regional Pain Syndrome (CRPS). Complex Regional Pain Syndromes  	are painful conditions that usually affect the extremities and consist of a  	broad spectrum of sensory, autonomic, and motor features subdivided into two  	types.  Type I occurs in the absence of any identified peripheral nerve  	injury whereas Type II occurs in association with a known peripheral nerve  	injury.

   	Because vestibulodynia often occurs without an identifiable cause or a  	proven neurological injury, it is more likely to resemble Type I CRPS.   	However, one case report attributed equestrian dyspareunia to local pelvic  	trauma.

In CRPS, hypertonic pelvic  	floor muscles initiate a process by which local visceral afferent nerve  	fibers release histamine and prostaglandins. The resulting inflammation  	produces irritation of the vulvar tissue.  This results in tissue tenderness  	and leads to further reflex spasms of the

pelvic muscle resulting in  	positive feedback that exacerbates the condition. Two reports have  	demonstrated that biofeedback-induced pelvic muscle relaxation is associated  	with reduced vestibular pain in women with vestibulodynia.

  	These data support the hypothesis that hypertonic and unstable muscles in  	the pelvic floor are a contributing factor in perpetuating vulvar pain.   	Therefore, other interventions that would reduce muscle tone may also be an  	effective treatment for this condition.

Botulinum  	toxin type A (BTX/A) inhibits release of acetylcholine from the presynaptic  	region of the neuromuscular junction, producing chemodenervation that  	results in reduced muscle tone.

Thus, BTX/A  would break the  	cycle of hypertonic and unstable pelvic  	floor muscles stimulating nerve conduction and further spasm. Three case  	reports and one open-label study have reported reduced coital pain following  	BTX/A injection.

  BTX/A doses varying from 10-80 u produced  	pain relief in 2-14 days and lasted from 3-36 months. Vestibular pain was  	associated with levator ani tenderness in two of the case reports and in the  	open label study.

  Coital pain completely resolved in the  	three case reports.

  The open-label study reported similar  	findings of a significant reduction but incomplete resolution of coital  	pain.

Although these studies provide encouraging evidence of BTX/A relieving  	coital pain in women with vulvar pain, many methodological weaknesses were  	present.  Although vestibulodynia was diagnosed in three case reports,

  	only one confirmed the diagnosis with a cotton swab test.

    	The open label study enrolled women with chronic pelvic pain and dyspareunia  	but did not differentiate women with vestibulodynia.

 Needle  	electromyography (EMG) confirmation of  pelvic muscle placement was not  	performed in the open study

 None of the studies prospectively rated symptoms  	using a diary.  Direct measures of pelvic floor tension, such as surface  	electromyography (sEMG), and objective measures of vestibular tenderness  	were not performed in any report.

Prompted  	by the success reported in earlier studies treating vulvar pain, and a need  	for a more rigorous experimental design, we evaluated the effect of two  	different doses of BTX/A on relieving coital pain under EMG guidance in  	women who met diagnostic criteria for vestibulodynia using objective  	endpoints.


 Two women, with vestibulodynia underwent BTX/A injections into the pelvic  	floor. The University Institutional Review Board approved the treatment and  	subjects provided written informed consent. Each patient was seen over four  	visits, which included screening, baseline  and two separate BTX/A  	administrations spaced 12 weeks apart. Patients received 20 u BTX/A at  	baseline and 40 u 12 weeks later. They were evaluated 12 weeks  	post-injection of both doses for treatment response. 

diagnosis of localized, provoked vestibulodynia was  	confirmed by 1) moderate-to-severe pain during attempted penetration and 2)  	moderate-to-severe pain limited to the vulvar vestibule as confirmed by a  	cotton-swab test.

Symptoms of vaginitis, suspicious  	lesions on pelvic exam, a previous vestibulectomy, an active neurological  	disorder, significant ongoing medical conditions, current major depression,  	an abnormal physical exam or laboratory values were not present. 

One week after screening, baseline evaluations of patient-rated pain, muscle  	hypertonicity and vestibular tenderness were obtained and BTX/A was  	administered. Weekly diaries were collected, and the patients completed a  	Visual Analogue Scale (VAS) retrospectively documenting the “average” coital  	pain rating since the last visit. They were dispensed weekly diaries to take  	home, and instructed to return at 12 weeks for another BTX/A injection and a  	final follow-up visit at week 24.

Botulinum toxin A (Allergan,  	Irving, CA, USA) was prepared by adding 2 ml of normal saline to 100 u of  	freeze-dried drug giving a standard dilution of 5 u per 0.1 ml.

 	Injections were drawn up in a 1 ml graduated syringe. The site was covered  	with local anesthetic cream (EMLA, Astra Pharmaceuticals, Herts, UK) for  	approximately 30 minutes prior to injection. The pubococcygeal position of  	the levator ani muscle was palpated and the site was confirmed using EMG  	guidance through monopolar needle electrodes (SEI S.N.C., Cittadella,  	Italy). Depending on dose, the patients received a total of 20 to 40 u of  	BTX/A, with either a total of 0.4 ml or 0.8 ml solutions divided into two  	injections and injected transvaginally at the 5 and 7’oclock positions into  	the levator ani.

Electromyographic (EMG) Signals were recorded (Phasis ESAOTE Biomedica,  	Florence, Italy) and bandpass filtered at 20 Hz-5 kHz. The recording  	parameters were a sweep of 100 msec at a gain of 200 µV/div at a bandpass of  	20 Hz to 5k HZ on a commercial electromyograph (Phasis ESAOTE biomedical,  	Florence, Italy). BTX/A was injected into tissue with the highest  	electromyographic potentials using multiple injection points to enhance  	efficacy.

A weekly  	diary was used to prospectively evaluate the effectiveness of treatment by  	documenting pain severity after each coital episode using a 10 cm visual  	analogues scale (VAS) where 0 = no pain at all, at any time, during or after  	intercourse, and 10 = the worse pain ever experienced with intercourse. At  	the 12week follow-up visits patients completed a VAS scale using the same  	scale described in the weekly diary. Objective measures included surface  	electromyography (sEMG) to measure pubococcygeal 	muscle hypertonicity, and a vulvar algesiometer to measure vestibular  	tenderness.                       

Surface  	EMG has been shown to have diagnostic value in identifying women with  	vestibulodynia over normal controls if three of the four criteria are met:  	1) instability of muscle (>0.20 SD), 2) poor muscle recovery after  	contraction (> 2 seconds) and 3) elevated resting baseline (> 2 µV), and  	either 1) reduced frequency (< 115 Hz) or 2) reduced muscle contraction  	strength (< 17 µV).

Surface EMG assessment included one  	60 s resting baseline; 5 phasic, flicking, contractions with 10 s rest  	between each phasic contraction; five tonic, 10 s contractions with 10 s  	rest between each tonic contraction; one 60 s endurance contraction; and one  	60 s resting baseline (Myotrac3, Thought Technology, Montreal, Canada, with  	Glazer protocol software and bandpass filtration of 20-400 Hz).

  	Relaxation periods were measured with resting signal amplitudes, standard  	deviations and coefficients of variance. Recruitment and recovery times,  	amplitudes, standard deviations, and coefficients of variance and power  	density spectral frequencies measured contractions.

Vestibular  	tenderness has been objectively measured using the vulvar algesiometer.

  	Although there is no clear cutoff score between normal and abnormal scores  	on the algesiometer,

 significant treatment effects have been  	shown in women with vestibulodynia.

Lower readings  	correspond to decreased force exerted by the vulvar algesiometer and greater  	vestibular tenderness (e.g., the more tender the vestibule, the less force  	can be tolerated), with scores ranging from 4 (lowest threshold, worst pain)  	to 28 (no pain). Paraurethral and posterior vestibular areas are assessed by  	a vulvar algesiometer,

  starting with the minimum force and  	increasing the force by 1 reading until the patient reports pain similar to  	coitus, or to a maximum of eight force levels (in millinewtons).

VAS scores, sEMG, and  	algesiometer were obtained at baseline, 12, and 24 weeks post injection and  	weekly diaries were returned at each follow-up visit.

A 24-year  	old married Caucasian woman, gravida 0, presented with a 5-year history of  	insertion dyspareunia, which had recently worsened. Current medications  	included fluoxetine for generalized anxiety disorder, an oral contraceptive,  	and guaifenesin and calcium citrate for vulvar pain. She had observed no  	improvement with either guaifenesin or calcium citrate, and had previously  	observed mild improvement with topical lidocaine. On pelvic exam, she had   	moderate pain at the 1, 5, 7, and 11-oclock positions with a cotton swab  	test, levator muscle tenderness, and vestibular erythema. Cervical cultures  	and wet mounts were negative for candidiasis, chlamydia, gonorrhea,  	trichomonas, and bacterial vaginosis, and all laboratory values were normal.

Her mean baseline VAS  	coital pain scale was 8.9 cm, indicating severe pain (

). Mean VAS  	coital pain scores decreased by 10% over baseline at 12 weeks post injection  	of 20 u of BTX/A and by 15% post injection of 40 u. Weekly diaries showed a  	mean decrease of 17% after 12 weeks of BTX/A 20 u and 12% after BTX 40 u,  	but showed the greatest percent reduction after 9 days post injection of 20  	u (29% ) and 4 weeks post injection of 40u (21%) (

). Diaries  	revealed that coital frequency was higher at 12 weeks post injection after  	both 20 and 40 u of BTX/A (4 events/week) compared to 4 weeks (3  	events/week) and 8 weeks (2 events/week). Surface EMG showed progressive  	reductions in resting muscle tension (amplitude), muscle instability  	(variability), muscle recovery after contraction (average release), and  	spectral frequency (proportional contribution of muscle fiber subtypes to  	overall contractile amplitudes, ([Hz]) with higher doses of BTX/A (

).  	Pressure to vestibular touch decreased by 67% over baseline following 20 u  	BTX/A but increased by 33% over baseline following 40 u BTX/A injection. BTX/A  	was well tolerated with mild localized tenderness after the 1st injection  	and no other adverse events.


 A 43 year-old  	married Caucasian woman, gravida 1, para 1, presented with a 6-month history  	of insertion dyspareunia and introital burning with radiation to the  	abdomen  relieved by warm baths. Her gynecologic history was positive for a  	total abdominal hysterectomy and surgery for ovarian cancer. She had other  	co-existing illnesses (hypertension, fibromyalgia, dysthymia,  	osteoarthritis) that were stabilized with medications (metoprolol,  	hydrochlorothiazide/triamterine, meloxicam, meperidine, oxycodone, doxepin,  	clonazepam, trazodone, and paroxetine). The cotton swab test revealed severe  	pain at the 1, 5, 7, and 11 o’clock positions as well as levator tenderness  	on pelvic exam. All laboratory tests, cervical cultures, and wet mounts were  	unremarkable. Antifungal agents had improved her vulvar symptoms in the  	past, but diet, calcium citrate, biofeedback and topical lidocaine had been  	ineffective. Her baseline VAS coital pain score decreased by 3% twelve weeks  	after receiving 20u BTX/A. Weekly diaries showed the greatest pain reduction  	8 days post injection (9%), and pain progressively increased over time  	(

).  Coital frequency was higher at 8 weeks (5 events/week) than at  	4 weeks (4 events/week) and 12 weeks (2 events/week). Although she received  	40 u BTX/A at the 12-week visit, no follow-up evaluations were obtained  	because she prematurely discontinued due to family problems. Surface EMG  	showed reductions in resting muscle tension (amplitude), instability,  	recovery after contraction, and contraction amplitude, but not in spectral  	frequency. The amount of pressure tolerated to vestibular touch decreased by  	20%. No adverse events were reported at Visit 1 or at a follow-up phone  	call.


 BTX/A was modestly effective in one patient and ineffective in the other in  	reducing coital pain. BTX/A produced the greatest coital relief in both  	patients within 2 weeks post injection. At this time, Patient 1 demonstrated  	a 29% reduction from baseline values whereas Patient 2 showed a 9%  	reduction.  Patient 1 demonstrated a greater reduction on the VAS pain  	scores than Patient 2 twelve weeks after injection (15% vs. 3%). Coital  	frequency was highest at 8-12 weeks post-injection. 

Treatment  	onset and duration were consistent with the pharmacology of BTX/A, which  	typically creates muscle paralysis one to two days after injection, lasts  	for 2-6 weeks and gradually resolves over a similar interval.

    	Given that this was a pilot study of two patients, a discussion of these  	results will be restricted to the mechanism of action of BTX/A and plausible  	explanations for the different clinical responses reported by these  	patients.

The  	efficacy of BTX/A therapy is multifactorial and depends on variables such as dosing, concentration, injection  	techniques, use of concurrent therapeutic modalities, varying diagnoses, and  	chronicity of neurologic dysfunction.

   Gunter reported  	toleration to speculum insertion after 10 u BTX/A but pain free intercourse  	only after a vestibulectomy.

 Brin et al. reported improvement  	in spasms after administering 20 u of BTX/A, but 40 u were necessary to  	resolve dyspareunia in a women with vaginismus.

 Jarvis et al.  	reported a 65% decrease in dyspareunia on pain scores following 40 u of BTX/A  	in 12 women with chronic pelvic pain.

  Romito et al. found  	40-80 u of BTX/A  produced pain-free intercourse in two women with  	vestibulodynia.

While dosing is  	still rather arbitrary and based on a clinician’s experience, some studies  	have shown that the size of the denervation field is determined by dose and  	volume.

 Dose appears to be a stronger predictor of area of  	paralysis than volume, and the effect of BTX/A is greatest when injected  	closest to the motor endplate.

We confirmed localization of the  	injection site by observing a marked increase in interference pattern on  	EMG. However, we used a greater volume (5 u/ml) than reported by Jarvis et  	al. (10 u/ml, 20 u/ml and 100u/ml).

 Although Jarvis and  	colleagues found response was independent of dilution,

 it is  	conceivable that a “threshold” of at least 10 u/ml is necessary to maximize  	response. The combination of a low dose and large volume may have compounded  	the reduced effect by weakening the muscle and producing an overall  	“smoothing effect” as opposed to localizing the toxin and producing  	temporary muscle paralysis.

The reduced pain reduction seen on the VAS scores compared to the weekly  	diaries, may have been the result of measuring these outcomes after the peak  	drug effect, and thus failing to capture more significant changes.   	Alternatively, the patients may have demonstrated a partial treatment  	response due to insufficient doses of BTX/A.  It is also possible that the  	retrospective ratings used in previous studies over-rated the reduction in  	pain. Prospective diaries, as used in the present study, have been shown to  	be more accurate and reliable measures of changes in pain.

Regardless of  	timing, dose or volume, response was still higher in Patient 1 compared to  	Patient 2. Patient 1 showed greater pelvic floor hypertonicity than Patient  	2, characterized by elevated baseline resting amplitude and muscle  	instability. This hypertonicity is more characteristic of “pure”  	vestibuldynia.

 This may explain the failure of biofeedback to  	relieve symptoms in Patient 2, which is typically effective in classic  	vestibulodynia.

  Thus, Patient 1 may have experienced more  	pain relief because women with vestibulodynia and pelvic floor hypertonicity  	are more likely to respond to BTX/A. Moreover, three of the four previous  	reports observed success with BTX/A in women who had levator tenderness in  	addition to vulvar pain.

  In the remaining report where  	there was no levator tenderness,

 BTX/A produced a partial  	response, but complete symptom resolution required a vestibulectomy.

It is also  	possible that the efficacy of BTX/A may be due to selectively blocking fast  	twitch fibers, suggesting that only those patients with reduced spectral  	frequency in addition to hypertonicity, such as Patient 1, may benefit from  	this therapy, and that there may be more than one type of vestibulodynia.

Although significant muscle changes were found, it should be noted that  	BTX/A might have reduced pain in other ways besides inducing muscle  	paralysis.  In addition to inhibiting acetycholine release, BTX/A also  	inhibits the release of pain neurotransmitters such as glutamate, substance  	P, calcitonin gene-related peptide, and histamine.

Other patient  	factors that may account for the subjective differences  include  	co-morbidity and duration of disease.   Patient 2 had a greater number  of comorbid conditions and had experienced vestibulodynia for a longer  	duration.   Such patients are less likely to respond to any therapeutic   	intervention. 

Although it is  	possible that a placebo response accounted for the improvement in  	post-coital pain, it should be noted that neither of these women had a  	significant placebo response to previous interventions.  In addition, there  	are no placebo-controlled studies of any pharmacologic treatments in women  	with vestibulodynia.  Therefore, the likelihood of a placebo response in  	this population cannot be ascertained. Studies investigating the analgesic  	effects of BTX/A in populations with other musculoskeletal disorders, such  	as low back pain, have shown significant superiority over placebo.

With respect to  	adverse events, patient 1 experienced mild localized tenderness after the  	injection whereas patient 2 reported no adverse events, consistent with  	previous reports that BTX/A injections do not spread to surrounding tissues,  	resulting in urinary or fecal incontinence.

While  	findings were modest and reported in only two women, this is the first study  	to evaluate the efficacy of BTX/A under needle-guided EMG prospectively,  	using both subjective and objective measures in women meeting diagnostic  	criteria for vestibulodynia. The fact that the patient with the greater  	pelvic floor hypertonicity was more responsive suggests that the BTX/A-induced  	paralysis of the pelvic floor muscles may have removed a noxious stimulus in  	the cycle of events that led to further spasm and pain, providing  	preliminary support to the theory that vestibulodynia is a variant of CRPS.    	Based upon these data, a randomized, double-blind, placebo-controlled trial  	of BTX/A for vestibulodynia seems warranted.


 Presented at The International Society for the Study of Women’s Sexual  	Health (ISSWSH), Amsterdam, Netherlands, 2003 (October).

This research was supported, in  	part, by a General Clinical Research Center Grant M01-RR00211.

Figure 1. Mean weekly diary scores after 20 u (Week 0) and 40 u (Week  		12) post-injection of BTX/A in two patients. Patient 2 terminated  		therapy at Week 12.
   

Articles

Botulinum toxin type A may be effective in reducing coital pain in vestibulodynia with levator ani tenderness, but has little effect on vestibular allodynia.

Subjective and Objective Outcomes of Botulinum Toxin Type A Treatment in Vestibulodynia


     TeleVital Inc. has developed a browser-based software for the Glazer Pelvic      Floor Muscle Surface Electromography (sEMG) protocol for remote assessment      and treatment over the Internet. The initial application of this system is      being conducted between the Washington D.C. offices of the second author (SCM)      and remotely controlled in the New York City offices of the first author (HIG)      to determine the broad scale applicability of this system in office      practice. 
     
     


     Glazer has demonstrated that several characteristics of pelvic floor muscle      surface electromyography (sEMG) are statistically significant in      differentially diagnosing both dysesthetic vulvodynia (DV) and Vulvar      Vestibulitis Syndrome (VVS) from vulvar pain of organic origin.3,4 It has      further been demonstrated that normalization of these abnormal pelvic floor      muscle sEMG patterns, by use of sEMG-assisted rehabilitation, produces long      term treatment benefits.1 Digital palpation of pelvic floor musculature has      been demonstrated to have little clinical predictive validity while pelvic      floor muscle sEMG is highly clinically predictive.2 Instructions in the      conduct of unassisted pelvic floor muscle exercises have not been      demonstrated as effective. There is, therefore, a need to integrate pelvic      floor muscle sEMG into diagnostic workups and treatment regimens. The      browser-based pelvic floor muscle sEMG protocol offers a reliable and      convenient diagnostic and treatment tool that practitioners can easily      access when specialized assessment is needed. 
  


     A women with physical findings on gynecological exam, consistent with VVS      was shown to have elevated resting tension and contractile weakness of      pelvic floor musculature. The patient was monitored and her pelvic floor      muscles assessed remotely over the Internet using the browser-based Glazer      protocol software, with the option of communicating via real-time      videoconferencing, instant messaging, or plain old telephone service (POTS).      Video conferencing fully taps the capabilities of telemedicine by also      making the nonverbal components of communication available and allowing both      remote communication and observation to assure the correct use of pelvic      floor muscles. 
     
     The equipment used for this protocol included a minimally invasive sEMG      single-user vaginal sensor that was easily inserted by the patient in      private after receiving instructions from a nurse, and a portable sEMG      biofeedback instrument (Myotrac 3, manufactured by Thought Technology LTD,      Montreal Canada), which connects to the serial port of the patient’s      computer. Computerized sEMG data acquisition was transmitted, stored, and      retrieved with TeleVital’s browser-based software, VitalWeb.TM
     
     The patient completed an on-line intake form, including patient demographic      data and information concerning the current condition, onset,k prior      treatment, sexual activity and related symptoms, such as urinary frequency      and urgency, low back pain and gastrointestinal symptoms. Once the intake      form was completed, the remote clinician was notified and able to review the      information prior to conducting a remote assessment.
     
     After the patient had privately inserted the vaginal sensor, a session was      created from the patient location through the TeleVital website using a      secure login ID & password. The browser-driven software signaled when the      patient was on-line and ready to begin. By clicking the "live" button, the      remote clinician immediately viewed the patient’s real-time sEMG signals.      The remote clinician and the patient were able to communicate and      simultaneously view the real-time sEMG signals on the computer screen from      separate locations. Auditory and visual cues guided the patient through the      entire procedure, while The remote clinician controlled the advancement      through each segment of the protocol, and adjusted the gain for optimal      display.
     
     

Table 1: Pelvic Floor Muscle Surface Electromyographic Data at Initial      and Terminal Evaluations.


     
     Initial Evaluation Follow-up Evaluation 
     
     


     
     Average 6.0 2.5
     
     Standard Deviation 1.20 0.20
     
     True Standard Deviation 0.20 0.08
     
     


     
     Average Max 18.7 32.1
     
     Average Relax 6.8 2.8
     
     


     
     Average 7.5 1.8
     
     Standard Deviation 1.50 0.20
     
     True Standard Deviation 0.20 0.11
     
     


     
     Average 16.8 27.1
     
     Standard Deviation 3.02 2.44
     
     True Standard Deviation 0.18 0.09
     
     Average 80% Fire Time 0.67 0.20
     
     Average 20% Recovery Time 2.36 0.54
     
     


     
     Average 12.3 23.8
     
     Standard Deviation 2.34 2.37
     
     True Standard Deviation 0.19 0.10
     
     


     
     Average 7.3 2.6 
     
     Standard Deviation 1.60 0.26
     
     True Standard Deviation 0.22 0.10
     
     


     
     The patient was initially asked via instant messenger to tighten her pelvic      muscles to verify accurate sensor placement, signaling and to make sure that      she was able to voluntarily contract the correct isolated muscle group. Once      this was determined, the remote clinician advanced to the beginning of the      protocol, starting with the one minute pre-baseline. The automated data      collection for evaluation of the pelvic floor muscles was gathered for the      following segments:

One minute resting EMG baseline period. 
       
       Five quick muscle contractions, one every 10 seconds for 5 repetitions
       
       Five repetitions of 10-second periods alternating between rest and        contract, starting with a 10-second rest followed by 10-second contracts.       
       
       Ten seconds of rest. 
       
       One 60-second contraction (endurance)
       
       One minute post-baseline

Consistent with sexual, sphincteric and support functions of the pelvic      floor musculature, and in order to look at recruitment and endurance, there      are three phases to the assessment that consisted of contracting the muscles      for different durations (1, 10 and 60 seconds). The contraction and      intervening relaxation, maximal amplitude, minimal amplitude, mean amplitude      and signal standard deviation were recorded. 
     
     After conducting a real-time, remote assessment, an auto-generated graphical      and statistical summary report was displayed, which includes data fields for      adding patient data, clinical notes and treatment recommendations. This      report can be printed both at the protocol administrator’s and patient’s      location. 
     
     The patient was given remote follow-up evaluation to ensure continued      compliance with the home exercise regimen, and to assess improvement.
     
     Data shown in Table 1 demonstrated improvement from initial assessment to      follow-up session. The results indicate after an average of 24 weeks of      practice, pelvic floor muscle contractions increased 61.3%. resting tension      levels decreased 58.3%, and the instability of the muscle at rest decreased      by 60%. Subjective reports of pain decreased 100%
     
     


     In conclusion, a woman suffering from VVS was remotely assessed and      demonstrated elevated resting tension and contractile weakness of pelvic      floor musculature. Remote training of pelvic floor musculature with      twice-daily exercises resulted in stronger, more relaxed and more stable      pelvic muscles accompanied by a decrease in subjective pain reports. 
     
     Pelvic floor muscle instability is a critical factor in pain associated with      VVS.1 A remote sEMG assessment was able to demonstrate the state of the      pelvic floor. An sEMG-assisted exercise program significantly stabilized the      patient’s pelvic floor muscles, and reduced the symptoms of vulvar      vestibulitis as indicated by remote follow-up evaluations.
     
     Telecommunication of electrophysiological data is already well established      in some applications such as electrocardiography. Recent advances in      technology provide an easy and effective way to incorporate pelvic floor      muscle sEMG into a routine diagnostic evaluation or treatment plan that can      be done remotely, and in real-time, over the Internet using the      browser-based Glazer protocol software developed by TeleVital Inc. The      browser-based pelvic floor muscle sEMG protocol offers a reliable and      convenient diagnostic and treatment tool that will help practitioners      overcome the barriers of distance and time, and improve continuity of care.

    Glazer HI, Rodke G, Swencionis C, Hertz R, Young A: Treatment of Vulvar Vestibulitis Syndrome wit h Electromyographic Biofeedback of Pelvic Floor Musculature. J Reprod Med 1995;40: 283-290

    Glazer HI, Romanzi, L, Polaneczky, M: Pelvic Floor Muscle Surface Electromyography; Reliability and Clinical Predictive Validity. J Reprod Med 1999;44: 779-782.

    Glazer HI, Jantos M, Hartmann EH, Swencionis, C: Electromyographic Comparisons of Pelvic Floor in Women with Dysesthetic Vulvodynia and Asymptomatic Women. J Reprod Med 1998;43: 959-962.

    White G, Jantos M, Glazer HI: Establishing the Diagnosis of Vulvar Vestibulitis. J Reprod med 1997; 42: 157-160.

The Web-enabled Glazer Surface Electromyographic Protocol for the Remote, Real-time Assessment and Rehabilitation of Pelvic Floor Dysfunction in Vulvar Vestibulitis Syndrome: A Case Report

The Web-enabled Glazer Surface Electromyographic Protocol


 Biofeedback is a self regulation training technique derived from well      established principles of human learning. Biofeedback is a technique, not a      stand alone treatment, which is one component of a behavioral training      program to facilitate acquisition of pelvic floor muscle control and other      continence skills. The purpose of this chapter is to familiarize the reader      with various methods of biofeedback training for urinary and fecal      incontinence or retention and their practical implementation in the office      practice setting.

 With the use of biofeedback, physiological change can be achieved by means      of operant conditioning, a type of learning which occurs as a result of      feedback, or the experience and awareness of the consequences of one’s      behavior. The first step in using biofeedback as a therapeutic tool is to      understand the anatomy and physiology underlying the symptomatic      dysfunction. This allows the selection and measurement, and ultimately      voluntary control, of a physiological response. In this chapter we are      dealing with urinary and defecatory dysfunctions, primarily incontinence, or      involuntary loss, but also disorders of retention or inability to void.      Bowel and bladder storage and voiding are both complex physiological events      with many controlling factors as described in the following sections. While      it is possible to measure the pressure changes that result from the activity      of the bladder and bowel using intravesical or rectal manometry      respectively, these procedures are not well adapted to office practice,      particularly by non medical biofeedback practitioners. Therefore we will      restrict ourselves in this chapter to dealing with external urethral and      anal sphincter surface electromyography (sEMG) biofeedback using      intravaginal and intraanal probes with embedded electrodes. These devices      are particularly well suited to office biofeedback as they produce reliable      measures, can easily be inserted and removed by the patient privately with a      minimum of discomfort and can be used on a daily basis for home training      with a portable take-home sEMG trainer designed for this purpose. Once the      appropriate physiological measurement has been selected, in this case      external sphincter sEMG, the measured response undergoes electronic      processing including analog to digital conversion, amplification, filtering      and mathematical reintegration to immediately form a visual, auditory or      other sensory signal which is fed back to the patient. In this way      biofeedback makes it possible to learn control over physiologic responses of      which, ordinarily, we have little or no awareness and consequently are      unable to control. 

 In order for biofeedback to be effective several prerequisites must be met.      There must be a measurable response functionally related to the symptoms      under treatment, in this case the sEMG response of the external      urethral/anal sphincters. This response must have variability and a      perceptible sensory cue associated with this variability, in this case the      ability to sense changes in the activity level of the sphincter muscle. The      ability on the part of the patient to voluntarily change the status of the      measured response, that is in this case the ability of the patient to      voluntarily contract and relax the external sphincters. These last two      requirements also involve an intact nervous system permitting afferent      sensory awareness and efferent motor control. Finally, since biofeedback is      an active process of learning, in this case sphincter neuromotomotor      control, it requires an attentive and motivated patient. The goals of      training will vary according to the specific symptoms of the patient. For      example, disorders of retention, including urinary retention and      constipation, are often associated with chronic or situational excess tone      or hypertonicity of the external sphincters. In this case the goal of      training is to voluntarily relax the sphincter during elimination. For      disorders of incontinence the goal of training is to inhibit bowel or      bladder sensory urgency and to voluntarily contract external urethral/anal      sphincters to prevent involuntary loss associated with voiding urgency or      episodes of elevation of intraabdominal pressure which could lead to      involuntary expulsion of urine or feces. Patients acquire these self      regulation skills in outpatient training and home training sessions. Through      repeated practice and implementation of the learned skills they improve      control over the responses that affect continence.





Anatomy and Physiology of Micturation and Defecation



 The lower urinary tract includes the distal portions of the ureters and      their ureterovesical junction at the detrusor muscle. The detrusor is smooth      muscle and forms the bladder wall. It provides the propulsive force that      expels urine through the urethra. The prostate in the male and the smooth      and striated muscle of the urethra are also part of the lower urinary      system. The pelvic floor muscles connect to and support the bladder neck,      the vaginal and the anal canal. The pelvic floor muscles have significant      influence on bladder control. A complex set of learned and reflexive control      mechanisms govern the functions of urine storage and micturation. At      maturity micturition is coordinated at several levels of the nervous system      extending from the frontal lobe and sensorimotor cortex to the peripheral      nervous system. Normal bladder function depends upon the integrative      functions of the frontal lobes, the sensorimotor cortex, the thalamus, the      hypothalamus, the basal ganglia, the cerebellum, specific centers in the      brain stem, the spinal cord, nerve roots and the peripheral nerves. The      process of urine storage and micturation also involves efferent and afferent      activity from the sympathetic and parasympathetic branches of the autonomic      nervous system. When experiencing a need to urinate the sympathetic and      somatic activity diminish and parasympathetic activity increases. This      causes detrusor contractions. The brain stem and cortical centers mediate      these peripheral processes. With learning, the cerebral and cerebellar      influences become the predominant inhibitory control over bladder      contractions. 

 Hald and Bradley (1982) reviewed the components that interact to maintain      normal bladder functioning. These factors help understanding the      pathophysiology of various types of voiding dysfunction. To maintain      continence during filling the pressure within the bladder must remain low      compared to urethral pressure. Disruption of the low intravesical pressure      by bladder noncompliance can lead to urine overflow. The base of the bladder      is the bladder neck or trigone which is flat during urine storage and forms      a funnel during voiding. The integrity of the vesicourethral angle during      storage provides a barrier to urine loss when pressure is transmitted to the      bladder and the bladder neck through activities which increase intra      abdominal pressure, such as laughing, coughing, sneeing, standing and      lifting. The proper functioning of the bladder neck depends on urethral      pliancy, anatomic placement (Tanagho, 1991) of the bladder neck and      sufficient support of the levator ani muscle. Smooth muscle comprises the      innermost layers of the bladder neck and the proximal urethra. Appropriate      functioning of the urethra depends on the integrity of these smooth muscles.      Striated muscles in the distal one third of the urethra, periurethral area      and levator ani complex are critical for bladder support and urethral      closure. Collagen and elastin connective tissue within the urethral tissue      are critical in maintaining the compliance of the urethral lumen for      purposes of closure. Vascular, epithelial and hormonal factors also play an      important role in the compliance of the urethra. Finally, all of these      peripheral factors are interdependant with both central and peripheral      nervous system factors that control their functions. 





 The rectum is the most distal portion of the colon. It extends from the      sigmoid colon to the anal canal, is approximately 12-15 centimeters in      length and consists of circular and longitudinal smooth muscle layers. When      gas or feces move into the rectum it expands to accommodate the larger mass      and sensory nerve cells within the rectal walls provide a subjective      sensation of fullness and the urge to defecate. Contraction of the colon and      rectum provide the propulsive force to move stool toward and through the      anal canal. The anal canal pierces the levator ani posteriorally. The      levator ani, or pelvic floor muscles form the floor of the bony pelvic and      surrounds the urethra, vagina and anal canal providing support for all these      lower abdominal organs and interdigitating with fibers of the external      urethral and external anal sphincters. The puborectalis portion of the      levator ani forms a sling that extends from the pubis around the junction      between the rectum and the anal canal and back to the pubis. This muscle is      normally in a state of contraction during the storage phase and maintains an      acute angle between the rectum and anal canal and is a critical factor in      stool continence (Henry & Swash, 1985). The terminal portion of the rectum      narrows into the anal canal. The anal canal is approximately 3 cm in length.      It consists of the internal anal sphincter, a thickening of the smooth      muscle extending down from the distal portion of the rectum, which is      maximally contracted during storage, and the external anal sphincter,      consisting of bundles of striated muscle fiber, including the deep ,      superficial and subcutaneous bundles. The external anal sphincter and      levator ani maintain minimal activity during the storage phase. The internal      anal sphincter relaxes several times an hour allowing small amounts of stool      into the anal canal. The walls of the anal canal are densely packed with      receptors allowing for the discrimination of gas, liquid and solid. When the      internal anal sphincter relaxes for the passage of stool into the anal canal      the external anal sphincter must contract to prevent fecal incontinence.      This contraction is so highly learned it is often believed to be an      unconditioned reflex. However it has been demonstrated that this response      does not occur if the individual does not sense rectal distension even when      the distension produces internal anal sphincter relaxation, showing this to      be a learned response (Whitehead, Orr, Engel and Schuster, 1981). When      defecation is desired the puborectalis, internal anal sphincter and external      anal sphincter relax in a coordinated fashion and completely for the      unrestricted passage of stool.





 Anatomy of the human pelvic floor musculature has been extensively has been      extensively studied and described (Pernkopf, 1964, Critchley, Dixon and      Gosling, 1980).

 The bilateral muscles of the levator ani meet in the midline to form the      pelvic diaphragm across the floor of the pelvis. The urogenital hiatus and      the anal hiatus pierce through the pelvic diaphragm. The levator ani muscle      includes the more anterior and inferior pubococcygeus and the more posterior      and superior iliococcygeus. The pubococcygeus attaches to the dorsal surface      of the pubic bone and laterally to the arcus tendonius levator ani, or      muscle white line. It forms a sling around the anus, prostate or vagina, and      urethra. The most anterior fibers are the pubovaginalis, and the more      posterior fibers are the puborectalis. The posterior of the levator ani, the      iliococcygeus muscle, anchors above the tendinous arch of the levator ani      muscle and to the spine of the ischium and below attaches to the      anococcygeal body and to the last two segments of the coccyx. The coccygeus      muscle, also referred to as the ischiococcygeus, lies adjacent to, and forms      a continuous plane with, the iliococcygeus. Laterally the coccygeus is      anchored to the spine of the ischium and the fibers of the sacrospinous      ligament. Medially it fans out to end on the margin of the coccyx and on      thie side of the lowest piece of the sacrum. The Internal obturator muscle      forms the muscular sidewalls of the pelvis and narrows down to a tendinous      band which exits the pelvic below the ischial spines to attach to the      greater trochanter of the femurs. The bulbospongiosis, ischiocavernosus and      transversus perinei superficialis muscles on each side of the body form a      traingle. The medial leg of the triangle is the bulbospongiosus, also known      as the bulbocavernosus or the sphincter vagina which surrounds the vaginal      opening. This muscle attaches anteriorly to the copora cavernosa clitoridis      with a muscular fasciculus that also crosses over the body of the clitoris      and compresses its deep dorsal vein. Posteriorly the bulbospongiosus anchors      to the perineal body where it interdigitates with the external anal      sphincter and the transversus perinei superficialis. The ischiocavernosus,      also known as the erector clitoridis, is located along the lateral boundary      of the perineum next to the bony ridge of the anterior pubic ramus between      the pubic symphysis and the ischial tuberosity. The ischiocavernosus      anteriorally blends with the sides of the crus clitoridis and posteriorly it      anchors to the surface of the crus clitoridids and to the ischal tuberosity.      The trasversus perinei superficialis muscle spans the perineum laterally      between the ischail tuberosities joining the sphincter ani and the      bulbospongiosi in the midline at the perineal body.


 Inferior to superior view of the pelvic floor musculature as seen from below      in the supine female
  



 Urge incontinence is the involuntary loss of urine associated with an abrupt      and strong desire to void. Urge incontinence is usually associated with the      urodynamic findings of involuntary detrusor contractions. Urgency in the      absence of detrusor contractions is often referred to as sensory urge      contrasted with detrusor hyperactivity or motor urge. Ideopathic detrusor      hyperactivity is referred to as detrusor instability while detrusor      contractions caused by neurologic deficits are referred to as detrusor      hyperreflexia or neurogenic bladder (Abrams, Blaivas, Stantan and Andersen,      1988). In patients with neurogenic bladder urge is often accompanied by      external urethral sphincter dyssenergia or an inappropriate contraction of      the external sphincter which can cause some degree of urinary retention.      Urge may also result from involuntary urethral relaxation, known as urethral      instability. Urgency can also occur with detrusor hyperactivity with      impaired bladder contractility (Resnick and Yalla, 1987) which leads to urge      incontinence and elevated post void residuals (PVR’s).

 Stress incontinence is the involuntary loss of urine associated with      coughing, sneezing, laughing or other physical activities which increase      abdominal pressure. This symptom may be confirmed by observing urine loss      coincident with an increase in abdominal pressure, in the absence of a      detrusor contrction or an overdistended bladder. Most commonly the abdominal      pressure causes hypermobility or significant displacement of the urethra and      bladder neck during exertion. Stress incontinence can also result from      urethral sphincter deficienty (ISD) due to congenital weakness or acquired,      most often associated with multiple anti-incontinence surgeries (Blaivas,      1985). 

 Overflow Incontinence is the involuntary loss of urine associated with      overdistension of the bladder. This may present as constant dribbling or may      have urge and stress incontinence symptoms. Overflow incontinence may result      from an acontractile bladder due to drugs, spinal cord injury, neuropathy,      or fecal impaction or may be due to bladder outlet or urethral obstruction      leading to an overdistended bladder and overflow.

 It is not unusual for patients to present with a combination of both urge      and stress incontinence. When symptoms of both types of incontinence are      present it is referred to as mixed incontinence.

 Finally it should be noted that male urinary incontinence is most often      associated with prostate surgery, primarily a radical prostatectomy for      prostate cancer. 




 There are five major types of deficits associated with fecal incontinence.      First, with loss of rectal sensation due to sensory nerve damage or repeated      rectal hyperdistension from chronic constipation, the external anal      sphincter does not contract with internal anal sphincter relaxation leading      to fecal incontinence. Second, a weak external anal sphincter, often      resulting from prolonged second stage labor, surgery, radiation or rectal      tearing during childbirth can lead to fecal incontinence because the      descending stool pressure cannot be offset by the pressure of the external      anal sphincter. Third, weak internal anal sphincter tone often resulting      from rectal surgery or chronic dilation from constipation. Individual with a      weak internal anal sphincter but adequate external anal sphincter may      experience leakage of liquid stool or gas which in small amounts will not      produce a distension stimulus and therefore will not lead to an offsetting      external anal sphincter contraction. Fourth, reduced capacity of the rectum      results from rectal noncompliance. This will result in frequent, loose bowel      movements often associated with strong bowel urge and involuntary loss or      explosive bowel movements. Fifth is a pattern of uncoordinated or      paradoxical striate muscle contractions (i.e. external anal sphincter or      puborectalis) often referred to as sphincter dyssenergia in the external      anal sphincter or paradoxical or nonrelaxing puborectalis in the      puborectalis muscle. Failure of appropriate relaxation in these muscles      leads to obstructive constipation. Although this is a disorder of retention,      not incontinence, this condition can lead to pelvic floor nerve damage      through straining which can cause incontinence. Also chronic constipation      can lead to rectoceles, prolapse, and hemorrhoids often corrected by      surgeries which lead to fecal incontinence. Finally patients can present      with both sphincter weakness problems and disordered defecation patterns      leading to both fecal incontinence and incomplete evacuation with      postdefecation seepage.






 Patient evaluation should start with a history of the patient’s urinary and      bowel patterns and symptoms. Any pertinent medical history should be      reviewed including hospitalizations, surgeries, family history, chronic      illness, medication and allergies. Urinary and/or bowel symptoms should be      evaluated in the following areas:

 Symptom onset, duration and course of symptoms.

 Precipitating events

 Frequency and volume of voluntary and involuntary voids (voiding diary)

 Patterns of straining during voids, pain, and incomplete voids with      incontinence after voiding

 Food and fluid intake as a factor in voiding

 Occurrence of urgency and control of voids or flatus

 Timing of incontinence, e.g. nocturnal, diurnal, food/fluid ingestion,      activities, emotional state, etc

 Type and number of protective pads used

 Medication being used such as bladder stabilizing medications or laxatives

 Pelvic floor, penile/vaginal or rectal pain

 Suprapubic or abdominal cramping






 Clinical practice recommendations for identifying and evaluating urinary      incontinence have been made by the United States Department of Health and      Human Services (Agency for Health Care Policy and Research Pub. No. 92-0038,      1992). The physical examination should include andominal exam to detect      masses, suprapubic tenderness or fullness and estimation of urinary flow and      post void residuals or fecal matter retained. Genital examination in men to      detect abnormalities of foreskin, glans penis and perineal skin. Pelvic exam      in women to assess perineal skin, atrophy, prolapse, pelvic mass,      paravaginal muscle tone, urethral hypermobility and bladder beck angle. A      rectal exam should be conducted for perineal sensation, sphincter tone,      bulbocavernosis reflex, fecal impaction, rectal mass and prostate status in      men. If indicated a general exam should be conducted to detect edemetous      conditions and neurological abnormalities.





 Additional Urinary testing may include post void residual (PVR) estimation,      provocative stress testing, urinalysis, urine cytology, testing for blood      urea nitrogen (BUN), voiding record, evaluation of environmental and social      factors and observation of urination to detect hesitancy and straining.      Specialized testing may include uroflow, cystometry, urodynamics, urethral      pressure profilometry (UPP), endoscopy and upper and lower urinary tract      imaging. In addition, pelvic floor muscle sEMG has been demonstrated to be      clinically reliable and predictively valid in identifying subtypes of      urinary incontinence (Glazer, Romanzi, and Polaneczky, 1999, Romanzi,      Poleneczky, and Glazer, 1999) and therefore should be a standard part of an      initial evaluation for voiding dysfunctions.

 Additional testing for fecal incontinence or retention is most often      conducted using a Schuster probe, which is a type of anal manometry or      pressure reading. This type of assessment provides information on rectal      sensation, integrity of reflexes such as internal anal sphincter inhibitory      reflex and rectosphincteric reflex response to rectal distension as well as      external anal sphincter squeeze pressure and maladaptive abdominal pressure      associate with voluntary contraction of the external sphincter. Imaging of      the lower gastrointestinal tract can also be conducted using defecography.


 In the office practice of biofeedback it is important that patients be fully      medically evaluated prior to initiating treatment so that by history and      examination all physiological, anatomical, pharmacological, neurological,      etc factors can be identified and appropriately treated or ruled out. It has      been claimed that external urethral and anal sphincter surface      electromyography and biofeedback is a noninvasive, benign intervention, and      therefore cannot be contraindicated and does not require prior medical      consultation. However, this author strongly believes in requiring patients      to undergo appropriate medical evaluation prior to initiating biofeedback as      failure to do so may lead to delay in the identification and appropriate      treatment of medical conditions including degenerative neurological diseases      such as diabetic neruopathy or multiple sclerosis, a wide range of      infectious diseases, or even the identification of potential malignancies,      all of which may manifest as voiding disorders.



Surface Electromyography Apparatus and Signal Analysis



 The sEMG signal is the electrical activity associated with the neuromuscular      activation of a voluntary muscle. This signal is highly complex and multiply      determined by phenomenon such as anatomical and physiological properties of      the striate muscle, central and peripheral nervous system control over the      muscle, and the instrumentation and signal processing used to measure the      activity. It is imperative that the practitioner of surface      electromyographic biofeedback have an understanding of sEMG instrumentation      and signal processing (Basmajian, and DeLuca, 1985). In selecting      electrodes, instrumentation and signal analysis characteristics for pelvic      floor muscle sEMG the user must be familiar with all of the following:

Characteristics of surface electrodes including material, shape, size,      spacing of sensor plates, orientation relative to muscle striations, signal      stability, response to environmental noise, response to tissue impedence      factors and sensor maintenance factors for repeated usage.

 Analog to digital conversion rates when using computer based equipment.

 Factors relating to electronic pre-amplifiers and amplifiers including        noise characteristics, signal to noise ratio, gain, common mode-rejection        ratio, input impedance and bias, and bandwidth

Signal rectification preferably by full-wave rectification.

 Signal integration of rectified digitized signal preferably by the Root Mean      Square (RMS) method.

 Frequency domain analysis of the sEMG signal by zero crossing or Fast      Fourrier Power Density Spectral Frequency Analysis.

To summarize the important characteristics of instrumentation and signal      processing the reader should look for intravaginal or intra-anal sensors      constructed with longitudinal sensor plates embedded in a probe which      assures the locational stability of the sensor plates relative to the pelvic      floor musculature. This will reduce the low bandpass filtering effects      associated with the physical relationship between the active bipolar sensors      and the active striate muscle. The electrode-electrolyte interface should be      consistent over measurements to reduce the high pass filtering effects of      this interface. Therefore patients should be told not to introduce any      chemical into the vagina or anus for 24 hours prior to the sEMG evaluation.      With regard to signal processing, rectification should be full wave. Analog      to digital conversion should be at 2000 samples per second per channel.      Reintegration should utilize the true Root Mean Square (RMS). Sensor gain      should be X500 and input impedance should be greater than one million      MegaOhms. Common Mode Rejection Ration (CMRR) should be greater than or      equal to –140db from 20 to 500Hz with a 50Hz or 60Hz line filter (depending      on the power source of the country in which the instrument is being used).      Input bias current should be less than 1 picoAmp and noise less than 0.1uv.      Bandwidth should utilize wide bandpass settings of 20Hz +/-5Hz to 500Hz      +/-50Hz. These signal processing characteristics will assure accurate,      reliable, high quality sEMG readings which will permit meaningful      comparisons both within patients over sessions and between patients. The      instrumentation selected should have two sEMG channels so the user can      measure both pelvic floor muscle and selected accessory muscles which may be      helpful in teaching the patient the correct activation of the pelvic floor      muscles. In the selection of equipment the user must also keep in mind the      necessity of using assessment protocols for meaningful data comparisons and      thus the instrumentation used must either permit the user to program      protocols or must have application software protocols available for pelvic      floor muscle assessment.


 Myotrac3 for in-office sEMG pelvic floor muscle evaluation shown above with      vaginal sensor and serial port connector with fiber optic cable.



 A protocol is a fixed sequence of events and operationally defined      measurements of those events. An sEMG protocol defines a fixed sequence of      muscle contraction and relaxation and includes statistical measurements      derived from segments of the sEMG signal. The following sequence of activity      and measurements are recommended for assessment of the pelvic floor muscle:

Sixty second preliminary resting baseline with measurements of average      integrated sEMG rms amplitude, standard deviation and coefficient of      variance (i.e. signal standard deviation divided by signal amplitude). This      permits an initial assessment of the resting amplitude and variability of      the pelvic floor muscle.

 A series of 5 rapid contractions or "flicks", each contraction preceded by a      ten second rest period. Measurements include rest period average amplitude      and standard deviations and flick average peaks and average onset time. This      protocol segment assesses both the maximum amplitude and speed of onset of      the phasic or fast acting muscle fibers and their effect on resting      potential. 

 A series of 5 ten second contractions, each contraction preceded by a ten      second rest period. Measurements include for rest and work periods the      average signal amplitude, standard deviation and coefficient of variance.      For contractions, measurements also include either median power density      spectral frequencies or zero crossings as well as average contraction onset      and release times. This protocol segment is referred to as the tonic muscle      fiber activity. It helps define the type of muscle fibers participating in a      contraction and to what degree, as well as the effects of tonic contractions      on the resting potential. 

 A single 60 second sustained contraction preceded and followed by a 10      second rest period. Measurements include for both rest periods and the work      period the average signal amplitude, standard deviation and coefficient of      variance. For contractions, measurements also include median power density      spectral frequencies or zero crossings as well as signal amplitude decline      during the contraction. This protocol segment is referred to as the      endurance muscle fiber test. It helps to assess the type of fibers      participating in a sustained endurance contraction, the effects of this      contraction on the resting potential, and the degree of muscle fatigue which      occurs during the endurance contraction.

 Sixty second post baseline resting period with measurements of signal      average amplitude, standard deviation and coefficient of variance. This      segment defines the resting amplitude and variability of the muscle after      the series of protocolized contractions have been conducted.

This protocol was first described in 1997 (Glazer and Marinoff) and is known      as the Glazer Protocol. This protocol not only provides a fixed sequence of      muscle actions and their measurements but also provides a database of sEMG      readings for normal subjects and those with a range of pelvic floor muscle      related dysfunctions. 



Conducting the Surface Electromyographic Pelvic Floor Muscle Assessment:



 Prior to the conduct of the pelvic floor muscle surface electromyographic      assessment it is important to first educate the patient on the procedure. A      description of the gross anatomy of the pelvic floor muscle structures and      the lower abdominal viscera is provided to the patient. The functions of the      pelvic floor muscles; sexual, sphincteric, and support, and their      relationship to fiber types are then discussed. Basic mechanisms of      urine/stool storage and elimination are reviewed. It is critical for the      patient to understand the structures and functions of the pelvic floor      musculature and how they relate to their clinical symptoms in order to      achieve maximum therapeutic benefit. Next the patient is provided      information on surface electromyography and given information on the types      of measurements that will be conducted. It very helpful to provide patients      with normative readings for each of the measures which will be conducted so      that they are able to see, along with the clinician, any deviations from      normal readings which appear during the conduct of the evaluation. Normative      readings will vary depending on the type of hardware, signal processing and      software which is used. In general both pre baseline and post baseline      average resting tone is 2uv, with a standard deviation of .2uv, peak flicks      average 30-35uv with onset times of .2sec. Tonic contractions average      20-25uv with standard deviations of 2.5uv, median spectral frequencies of      120Hz, and onset and recovery times of under one second. A general rule is      that the resting amplitude during the tonic contraction phase should average      no more that 10% of the average tonic contraction amplitude. Endurance      contraction amplitude should be 20uv with median spectral frequencies of      125Hz and should show little to no amplitude decline throughout the 60      second endurance contraction. At this point the patient is shown the vaginal      or anal sensor and given detailed instructions on the insertion of the      sensor including the orientation of the sensor and the appropriate use of      lubrication.


 sEMG anal sensor (top) and vaginal sensor (bottom) with grounding patches.

The patient then privately self -inserts the sensor as instructed and      returns to the procedure room fully clothed with the sensor wire available      to be connected to the electromyograph. Both the clinician and the patient      must be able to simultaneously view the sEMG tracing on the screen. This can      most easily be accomplished by using two screens, one for the patient and      one for the clinician.


 Patient with correct placement of intravaginal sEMG sensor with ground pad      attached.

Positioning of the patient for evaluation and      instructing the patient on the correct manner to contract and relax the      pelvic floor muscles is important as this can substantially alter the sEMG      readings. Initial readings are best made with the patient in a reclining      position with the top half of the body at approximately a 135 degree angle      to the bottom half. The legs should be rotated outward with the heels      slightly separated. Degree of rotation will vary amongst patients and should      be set to the patients’ comfort. While determining the best position for the      patient the sEMG should be monitored as it may significantly vary across      different positions. For example, the greater the degree of hip rotation the      higher the pelvic floor muscle sEMG as hip rotation induces activation of      the internal obturators which in turn connect to the anterior portion of the      pubococcygeus where they share a fascial connection at the archus tendonius      levator ani or muscle white line. While adding activity in this manner to      the pubococcygeus muscle may enhance the patients’ sensory awareness of      pelvic floor contractions it can also produce a falsely elevated resting      tone leading to an incorrect diagnosis of resting hypertonicity. Patients      may also be tested and may conduct a portion or all of their home exercises      in varying positions including reclining, sitting and standing. This will be      determined by the nature of the patient’s symptoms. Type II stress      incontinence, in which involuntary urine loss is associated with acute      episodes of intra-abdominal pressure such as that produced by laugh, cough,      sneeze or lift, occurs almost exclusively in the standing position.      Therefore, at least part of the assessment and rehabilitation of the pelvic      floor muscle in these patients must be conducted in the standing position.      Urge incontinence, involuntary urine loss associated with a strong urge to      void, can occur in any position and therefore these patients must be      assessed and trained in all positions.


 Patient positioned correctly with sEMG intravaginal sensor inserted. Note      the 
 position of the legs slightly rotated externally and the elevation of      the back. 
 Also note the presence of two screens, one for the patient to view the sEMG      and the 
 laptop computer from which the clinician controls the protocol      administration.

Once the patient has been correctly      positioned the process of teaching the patient the correct use of the      levator muscles begins. While the activation of most striate muscles can be      accomplished by instructing the patient to perform a certain movement, this      is not true for the pelvic floor musculature. Furthermore, the instruction      to "contract your pelvic floor muscles" is of little value as most patients      will have no idea how to do this. It is best to start with an instruction      such as "hold in as if you are experiencing and urge to urinate and have a      bowel movement at the same time". This instruction is most likely to lead to      the simultaneous contraction of both the anterior and posterior aspect of      the pubococcygeus muscle, thus providing the most accurate sEMG measurement      of the contractile capacity of the muscle. Training the correct use of the      pelvic floor muscles is a highly variable phenomenon, much like teaching a      child to ride a bike. Some get on and ride off in minutes while others      struggle and never truly attain the skill. Acquiring pelvic floor muscle      control is neither an intellectual/cognitive task nor one which simply      requires maximum undifferentiated muscle effort. It is a refined      neuromuscular skill, which, like bicycle riding, or playing tennis can be      acquired only by diligent and reliable practice. Much like controlling the      bicycle or the tennis ball for the first time, patients are usually aware of      correctly activating the pelvic floor musculature. The usual description      spontaneously offered by patients is a sensation "lifting" or "sucking up"      of the sensor. This sensation may be very subtle at first and hard for the      patient to produce on command. With training patients become reliably able      to contract the pelvic floor muscle correctly. The clinician can use the      sEMG pelvic floor muscle signal to aid the patient in learning the correct      activatin pattern of the muscle. The correct use of the muscle will result      in an elevation and stabilization of sEMG which can be quickly recognized by      both clinician and patient. It is the essential change which the muscle      undergoes during this learning process which permits the patient to use the      muscle in a manner which can control dysfunctional urogenital symptoms. In      the initial evaluation we simply start the learning process.

 In most patients first asked to activate their pelvic floor muscles you will      likely see significant co-contractions occurring in other muscle groups.      This phenomenon may be restricted to the pelvic region, including gluteal      maximus, transverse abdominals and leg adductors, or it may involve more      pervasive whole body tension, including breath holding. Creating the correct      balance of muscle usage for each patient is critical for the initial      evaluation and to get the patient started correctly in the conduct of their      home exercises. Not surprisingly, it is patients who have weak pelvic floor      muscles and/or poor ability to sense pelvic floor muscle contractions who      are most likely to engage in this excessive contractile pattern. In teaching      patients the correct muscle usage pattern, a balance must be struck.      Excluding all co-contractions will lead to submaximal contractions of the      pelvic floor and will therefore limit the muscle rehabilitation, which is      best achieved with maximal contraction force. On the other hand, excessive      undifferentiated recruitment of large muscles will overwhelm any sensory      awareness of pelvic floor muscle contractions and prevent the patient from      learning appropriate control patterns over the target muscle group. In a      balanced approach the patient is taught to focus on a maximum force pelvic      floor muscle contraction while permitting natural overflow or      co-contractions in a limited manner (Glazer and MacConkey, 1996). In this      fashion patients can best engage in rehabilitation of pelvic floor      musculature while limiting co-contractions. In order to facilitate this      learning the clinician can use sEMG measurements of co-contracting muscles      or can simply manually palpate to help the patient limit any excessive      overflow.

 The patient is provided only enough instruction and education to permit the      conduct of a valid pelvic floor muscle assessment protocol. This process      should take no more than five minutes. At this point, although the patient      remains far from reliable in their use of the pelvic floor musculature, the      clinician should proceed with the protocol. The patient should be told in      advance exactly what series of muscle activity they will be asked to      perform. Patients should also be instructed to limit any movement as this      may lead to artifacts in the sEMG recordings. In order for a protocol to      produce data for reliable within patient over sessions, and between patient      comparisons, the protocol must be run in exactly the same manner every time.      Excessive pauses between segments to conduct discussions with the patient      should not occur. Patients should be told to hold any questions until the      completion of the protocol. The entire Glazer protocol, described earlier,      takes approximately five minutes to conduct. Upon completion of the protocol      the clinician should immediately complete any information, including      clinical notes, required by the software, in order to print out a complete      report. The instrumentation and software which you choose should have the      capacity to print out a complete report, including sEMG tracings,      statistical summaries and clinical notes. An example of such a printout      follows.

 A complete copy of such a printout should be provided to the patient on      each office evaluation. At this time the clinician should review all the      findings with the patient and compare the findings to those of previous      sessions when appropriate. Findings reviewed should include interpretations      of "flick" peaks and onset time, "tonic" rests and resting variability,      contractile onset and recovery times, contractile amplitude, variability and      spectral frequency, and "endurance" contraction amplitude, variability,      spectral frequency and fatigue. In this manner all the sEMG muscle      abnormalities can be identified for the patient and changes in these      measures can be followed over time. These readings are used by the clinican      to modify any patient home exercise instructions so that the patient can      clearly understand the purpose of all exercise modifications.


 Sample sEMG tracing showing resting hypertonicity and instability, low      amplitude contractions with slow onset and recovery with poor control and      low spectral frequencies




 Sample sEMG tracing showing stable low amplitude resting potential with high      amplitude contractions and rapid onset and recovery with good control, no      fatigue and high spectral frequencies.


 Following the initial evaluation, assuming sEMG muscle abnormalities      consistent with patient symptom reports are found, the clinician will then      demonstrate the use of the sEMG home training device and prescribe the home      training regimen. All patients are initially prescribed home training of 10      second maximum pelvic floor muscle contraction followed by 10 seconds of      relaxation for a total of 60 repetitions, that is twenty minutes, twice a      day, preferably morning and evening. All exercises are initially prescribed      to be performed in the reclining position. Some elderly, frail, or weak      patients may be initially unable to complete the full prescribed number of      repetitions and may need to build up to the full twenty minute exercise      periods. It is also important for the clinician to assess the likelihood of      compliance with home exercise. Approximately 25% of patients undergoing      initial evaluation and prescription of home training will drop out of      treatment. Thus, patients should be thoroughly assessed for their motivation      and ability to reliably comply with the home training protocol to minimize      therapeutic failures due to noncompliance. It is best to see patients once a      week for the conduct of an office evaluation. This helps to support patient      compliance with home exercises and allows the clinician to follow the      patient’s sEMG muscle changes and symptomatic progress.


 U-Control sEMG biofeedback home trainer pictured here with vaginal sensor      and grounding pad.



 Modification of prescribed home training is done on an individualized basis.      It is rarely advisable to change the basic prescription of 10sec work/10sec      rest with 60 repetitions, twice a day. However, many other exercise      parameters and factors may be modified based on office assessment findings      over the course of treatment. For example, intentional use of acessory      muscles may be used for persistent weakness. Having the patinet focus on      rapid initiation of voluntary contractions can be used to address patients      reports of leakage even while initiating a pelvic floor muscle contraction.      The patient may instructed to focus on reducing the variability of the      contraction if small amounts of loss occurring with sustained contractions.      Home training position may be altered, as the patient gains contractile      amplitude and control more of their home training can be conducted in the      standing position.

 Pelvic floor muscle rehabilitation is only the first step. As the patient      increased their contractile speed, amplitude, and control they will need      instruction in the application of the external sphincter to control      involuntary loss. Patients with stress incontinence must be told that they      need to initiate a voluntary contraction of the pelvic floor muscles just      prior to the occurrence of acute intra-abdominal events such as a laugh,      cough, or sneeze. Urge incontinence patients must be instructed to remain      still when they experience a strong urge and to contract and hold the pelvic      floor muscles until the urge goes away. This can be quite difficult for      patients as it is counterintuitive to the natural desire to quickly get to      the toilet in response to an urge. This will increase the likelihood of      involuntary loss because patients cannot effectively contract their pelvic      floor muscles while walking or running to the toilet. Using pelvic floor      muscle contractions to inhibit the detrusor activity associated with voiding      urgency can be used to progressively increase the time between voids in      those who suffer urinary urgency and frequency. In such patients voiding is      conducted on a timed basis, slowly increasing the inter-void intervals. Also      voiding patterns, diet, fluid consumption, straining, and dysfunctional      muscle use patterns must be addressed at each follow up session. Symptom      changes must be assessed with voiding diaries and pad test. 





 In disorders of functional urinary retention or constipation a complete sEMG      evaluation can assist in identifying any sphincteric component of the      problem. Most commonly chronic essential hypertonicity, episodic      hypertonicity of external sphincters, or learned dysfunctional voiding      habits, with or without an identifiable precipitant, can lead to disorders      of retention. Excessive pelvic floor muscle activity associated with voiding      dysfunction is referred to as sphincter dyssenergia. The sEMG training for      pelvic floor muscle dyssenergia is similar to training for incontinence but      during the conduct of prescribed muscle exercises greater emphasis is put on      improving the patient’s discrimination of low levels of pelvic floor muscle      activity. As with other forms of progressive muscle relaxation the clinician      seeks to lower the pelvic floor muscle activity by having the patient      contract to maximum amplitudes followed by a period of relaxation. The      resting tone of the muscle will likely be reduced after a series of maximum      contractions allowing the patient enhanced awareness of levels of      relaxation. The same home prescription of 20 minutes twice a day of 10      second contract/10second relax is used. The patient is focused on quickly      and completely releasing the maximum contraction and becoming aware of small      differences in post contraction pelvic floor muscle relaxation. As with      incontinence treatment these exercise can advance from reclining to sitting      and to standing position. Finally the patient must learn to maintain the      greatest levels of relaxation while bearing down with a gentle Valsalva      maneuver. This helps the patients ability to generalize the pelvic floor      muscle relaxation response to the actual voiding situation. 



Application of Pelvic Floor Muscle Surface Electromyography to Urogenital      Pain



 Within the past decade Glazer and his colleagues have demonstrated the      application of pelvic floor muscle surface electromyography in the diagnosis      and treatment of a broad range of essential urogynecological pain disorders.      This includes conditions such as urethral syndrome, vulvodynia, vulvar      vestibulitis syndrome, chronic abacterial prostatitis, or prostatodynia, in      men, and levator ani syndrome. The etiology of these disorders is most often      associated with tissue irritation or trauma related to infections and/or      substances used locally to treat these infections, hormonol changes,      dermatologic irritants, surgery, or accidents, but fail to self resolve once      the provocation has been resolved. The majority of these patients show      significant pelvic floor muscle hypertonicity and resting instability often      accompanied by slow recruitment and recover times, contractile weakness and      instability with low spectral frequencies. These sEMG abnormalities have      been shown to diagnostically differentiate essential vulvar pain patients      from both vulvar pain of acute medical origin (White, Jantos and Glazer,      1997) and from normal asymptomatic females (Glazer, Jantos, Hartmann and      Swencionis, 1998). The application of sEMG pelvic floor muscle      rehabilitation has also been demonstrated to be effective in the treatment      of essential vulvovaginal pain disorders (Glazer, Rodke, Swencionis, Hertz      and Young, 1995). Long term follow up conducted on patients successfully      treated with this protocol has shown the maintenance of therapeutic benefit      for three to five years (Glazer, in press). For further information on the      application of sEMG to the treatment of pelvic pain disorders visit Dr.      Glazer’s website located at 

Name: ___________________________________________________________

Date: ____________________________________________________________

INSTRUCTIONS: Place a check in the appropriate column next to the time      you urinated

In the toilet or an incontinence episode occurred. Note the reason for      the incontinence and describe your liquid intake (for example, coffee,      water) and estimate the amount (for example, one cup). 
  

Number of pads used today _______________ number of episodes      _________________

 Comments ______________________________________________________________

 _______________________________________________________________________

 - Sensory signals from the somatic and autonomic nerves that carry        information to the spinal cord.



 - The anal canal is surrounded by the voluntary external        anal sphincter and the involuntary internal anal sphincter. The internal        sphincter is continuous with the smooth muscle lining the colon and the        external sphincter is continuous with the puborectalis portion of the        levator ani. Discoordination of the two sphincters leads to voiding        dysfunctions including constipation and incontinence.



 - A procedure involving the use of balloons to measure        how much pressure can be generated within the anal canal and rectum.



 - A discoordinated voiding pattern in which        the bladder and sphincter contractions happen simultaneously rather than        the sphincter relaxation for urination. This can occur as a learned        voiding dysfunction as well as for neurological reasons.



 - A behavioral program to increase intervoid intervals and        enhance bladder capacity, usually involving timed voids as a treatment for        urge incontinence.



 - This is a relflex contraction of the anal        sphincter mediated by the pudendal nerve and produced by squeezing the        clitoris or the glans of the penis.



 - Three to five small fused ridimentary vertebrae forming the lower        extremity of the veterbral colum extending from the sacrum



 - Fibrous nonsoluble protein in connective tissue.



 - A urodynamic evaluation of the bladder volume/pressure        relationship assessed by filling the bladder while measuring presure and        perineal muscle activity.



Detrusor hyperactivity with impaired bladder control

 - A neurologic        disorder in which uninhibited detrusor contractions occur with bladder        contractions that are inefficient in emptying the bladder without the aid        of abdominal straining.



 - Involuntary detrusor contractions in the absence of        neurological disease.



 - Smooth muscle making up the wall of the bladder that        contracts to expel the urine.



 - The essential part of the yellow elastic connective tissue made        up of protein.



 - Anaerobic striated muscle fiber that provides        strong fast contractions as compared to aerobic slow sustaining striate        muscle fiber.



 - Involuntary bladder contractions resulting from        neurological disease



 - The large muscle which forms the floor of the pelvis        and supports the pelvic viscera. The levator ani is made up of the        pubococcygeus, puborectalis and iliococcygeus muscles. The levator ani        interdigitates with the external urethral and anal sphincters for        continence.



 - A number of conditions including coccydynia,        proctalgia fugax, prostatodynia, characterised by idiopathic pain in the        anal and perianal region.



 - Coexisting stress and urge incontinence. 



 - The puborectalis muscle maintains the        angle between the rectum and anal canal and prevents stool from passing        out of the rectum for continence. This muscle should relax with        defecation. Failure of the puborectalis to relax during defecation leads        to stool retention or constipation.



 - A test used to measure urine leakage in which the patient        records the use of pads which are weighed before and after use.



 - Prolapse means to move forward, down or out and subsumes several        specific conditions including rectocele, cystocele, urethrocele        andcystourethrocel involving the movment of the rectum, bladder and        urethra. The degree of movement is graded with fourth degree being most        severe and involving the extrusion of the organ through the vagina or        rectum.



 - Urge incontinence without unhibited bladder        contractions.



 - Pertaining to the ureters and the bladder.



 - A thin sheet of striated muscle stretching between        the two sides of the pubic arch.



 - A diagnosis applied to symptoms of urethral discomfort        after ruling out identifiable anatomic defect and infectious conditions.       



 - A bearing down conducted as a forced exhalation effort        against occluded nostrils and closed mouth. This maneuver increases intrathorasic and intra-abdominal pressure.

    Hald, T., & Bradley, W.E. The urinary bladder: Neurology and dynamics. 1987, Baltimore: Williams & Wilkins.

    Tanagho, E.A. Retropubic surgical approach for correction of urinary stress incontinence. In D.R. Ostergard and A.E. Bent (Eds.), Urogynecology and urodynamics: Theory and practice (3rd ed.), Baltimore: Williams & Wilkins, 1991

    Henry, M.M. and Swash, M., Fecal Incontinence, defecation and colorectal motility. In M.M. Henry & M. Swash (Eds.) Coloproctology and the Pelvic Floor: Pathophysiology and management, pp 42-47, 1985, London: Butterworths.

    Whitehead, W.E., Orr, W.C., Engel, B.T., and Schuster, M.M., External anal sphincter response to rectal distension: Learned response or reflex, Psychophysilogy, 19: 57-62, 1981.

    Critchley, H.O.D., Dixon, J.S., and Gosling, J.A., Comparative study of the periurethral and perianal parts of the human levator ani muscle. Urol Int 35: 226-232, 1980

Biofeedback is a self regulation training technique derived from well established principles of human learning. Biofeedback is a technique, not a stand alone treatment, which is one component of a behavioral training program to facilitate acquisition of pelvic floor muscle control and other continence skills.

Surface Electromyographic Biofeedback of Pelvic Floor Musculature

hirty-three women diagnosed as suffering from vulvar vestibulitis syndrome, marked by a significant history of long-term moderate to severe chronic introital dyspareunia and tenderness of the vulvar vestibule, were selected for treatment. Patients were given a computerized electromyographic evaluation of the pelvic floor muscles and were then provided with portable electromyographic biofeedback instrumentation and instructions on the conduct of daily, at-home, biofeedback-assisted pelvic floor muscle rehabilitation exercises. They received intermittent evaluations of pelvic floor muscles to ensure compliance and monitor their progress and symptom changes. The results show that after an average of 16 weeks of practice, pelvic floor muscle contractions increased 95.4%, resting tension levels decreased 68%, and the instability of the muscle at rest decreased by 62%. Subjective reports of pain decreased an average of 83%. Twenty-eight patients had abstained from intercourse for an average of 13 months. Twenty-two of these 28 patients resumed intercourse by the end of the treatment period. Six month follow-up indicated maintenance of therapeutic benefits. (J Reprod Med 1995;40 283-290) 
 Keywords: vulvar diseases, electromyography, vulvar vestibulitis syndrome.  

atients with vulvar vestibulitis syndrome constitute an identifiable subset of patients with vulvodynia. Aside from "focal vestibulitis vulvae," 

 this condition has also been referred to as "erythematous vulvitis en plaque,"

 A task force set up by the Tenth World Congress of the International Society for the Study of Vulvar Disease 

 replaced the term burning vulvar syndrome with the term vulvodynia and defined the condition clinically. Vulvar vestibulitis is typically marked by a history of intermittent, then continuous discomfort in the vulva and introital dyspareunia. Examination reveals significant focal tenderness of the vestibule on contact or pressure in the absence of vulvar lesions or identifiable vulvovaginal infection. Macular erythematous patches may be noted along the hymeneal sulcus, at the openings of the major and minor vestibular glands. The paraurethral glands are also frequently involved. The erythema may vary in intensity and may not be apparent in all cases or at all times. Histology may reveal a chronic inflammatory cell reaction surrounding the vestibular glands. 
 
 

he typical patient is white, upper middle class, sexually experienced and in her 20s or 30s. The etiology is unknown, and although attempts have been made to explain the mechanism of pain, 

 all therapeutic approaches utilized to date have been empirical. Most are based on their success in treating other conditions presumed to be of similar origin and are aimed at reducing the secondary symptomatology, with varying degrees of success. Studies have not been able to demonstrate etiologic involvement of any of the more common infections, but patient reports indicate that the onset is frequently associated with vulvovaginal infection or trauma and exacerbated by application of topical medications. Tovell and Young l suggested that the high incidence of reports of vaginitis preceding the onset of this condition (85¡o) may indicate misdiagnosis; however, the possibility of misdiagnosis is difficult to differentiate from infection as the etiologic agent or from the possibility that the topical agents used in treatment for these conditions may have elicited a hypersensitivity response. Vulvar vestibulitis may well be multifactorial. Local inflammation or infection with bacteria, Candida and human papillomavirus (HPV) have been implicated in some cases. However, a study attempting to associate vulvodynia with HPV proved to be unproductive. 

 Association versus causation is difficult, if not impossible, to prove in retrospect. In the acute setting, the major differential diagnoses to be ruled out include herpes simplex virus (HSV), HPV, squamous papillomatosis, 

 vulvovaginitis, traumatic injury, and vulvar dystrophy or dysplasia, all of which have been associated with burning pain and/or acute tenderness in this area. 
 
 

pontaneous remission may occur but is uncommon, and generally those cases of sufficient duration to result in referral to our service are past the usual duration for spontaneous resolution. Although surgical resection of the affected tender vestibular area has been the "gold standard" of therapy, it is not uniformly successful, and success is variously defined as degree of improvement and postoperative function. 

 Patients with an underlying component of burning pain or those with associated urinary symptoms have had even less success with surgical therapy since it does not address these symptoms. Medical therapies include antihistamines, tricyclic antidepressants, compresses, topical anesthetics and lubricants. Topical remedies do not cure the condition, but soaks of Burow's, Aveeno-oilated or aqueous lidocaine solution have been reported to produce temporary and partial relief of symptoms in some patients. Steroids have been tried for their anti-inflammatory effect. Peckham 

reported that neither topical nor systemic steroids were effectual. Laser surgery is not recommended due to prolonged and painful healing time. Local injections of alpha interferon (r-alpha IFN) in selected patients have not proven entirely successful, but immunotherapy may be beneficial in some cases.

 Dietary restrictions and reduction of irritants in the urine or in topical agents are reported as being successful in some cases.

o reports are found in the literature regarding any relationship between pelvic floor muscles and focal vestibulitis vulvae. Our rationale for studying pelvic floor muscles is that patients with focal vestibulitis often show hyperirritability of pelvic floor muscles, which, when compressed are locally tender. Pelvic floor musculature is not responsive to general states of muscle tension; standard progressive muscle relaxation techniques are not effective. Travell

 reported that this myofascial hyperirritability can be activated by localized tissue disturbance. In the case of vulvar vestibulitis syndrome, we believe that cutaneous vulvar disturbances destabilize pelvic floor muscles. (Note that the principal motor and sensory nerve fibers to both the vulva and the pubococcygeus are branches of the pudendal nerve plexus containing fibers from S3 and 4.) Travell and Simons

reported that such muscle disturbances, reflected in discoordination of the electromyography (EMG), are prone to develop in muscles that lie within the pain reference zone of disturbed tissue and in turn reflex back through a dorsal root spinal cord mechanism to perpetuate tissue disturbance via its effects on local autonomically (sympathetic) mediated activity, including vascular changes and histamine release. To the extent that destabilization of pelvic floor muscles is a factor in perpetuating the vulvar skin disturbance and accompanying pain described above, restabilization of pelvic floor muscles should allow this condition to resolve. Since Travell and Simons 

reported that this type of muscle disturbance is reflected in EMG records, EMGs were used to objectively measure that status of the pelvic floor muscles in the present study.

atients for this study were drawn from the Cutaneous-Vulvar Service of St. Luke's Roosevelt Hospital Center, which currently manages vulvar vestibulitis as follows. The patient is examined in detail to exclude any contributing bacterial vaginosis or vaginitis or concurrent dermatologic problem. A gynecologic examination and inspection of the glabrous skin are both necessary. Initial therapy, depending upon the predominant symptomatology, commences with antihistamines: terfenadine, 60 mg twice daily, or hydroxyzine, 25 mg, h.s.; or tricyclic antidepressants, amitriptyline or nortryptaline, 10-25 mg, h.s. Dosages are evaluated in two to four weeks and are adjusted accordingly. The patient is also prescribed a colloidal oatmeal (Aveeno-oilated) solution to be used in dilution as a cold compress two or three times a day for 10 minute periods. Patient education and psychological support are also provided. Even with successful therapy, the symptoms are slow to resolve, averaging six weeks to several months until relief. Patients whose response to the above treatment regimen was partial or suboptimal were advised to participate in the present study. 
 
 

he patients were 33 Caucasian females, 19 married, 14 single, 29 nulliparous and 4 multiparous, ranging in age from 21 to 45 years, with a mean of 31.5. Duration of experiencing vestibulitis symptoms ranged from 2 to 6 years, with a mean of 3.4. The self-reported symptoms varied from only introital dyspareunia to chronic, intense pain without any provocation. Twenty-eight of the 33 patients were abstinent from intercourse at the time of evaluation, and for them the average duration of abstinence was 13 months. The diagnosis of vulvar vestibulitis syndrome was confirmed by physical examination; in addition, tension and/or sensitivity to palpation of pelvic floor muscles was present. Other coexisting vulvovaginal conditions were excluded; if intercurrent vaginitis was present, it was specifically diagnosed and treated, and reevaluation of the diagnosis was performed prior to proceeding with the protocol. None of the patients selected for this study had prior surgery for the condition. All reported the previous use of topical treatments, and 27 took amitriptyline (range, of 5-85 mg) during the course of the treatment.

nce referred for pelvic floor EMG biofeedback, the patient underwent a brief history review, the initial pelvic floor muscle EMG assessment and training in the use of the portable EMG home trainer. 
 
 

The instrumentation employed in this study consisted of:

. A surface EMG single-user vaginal sensor (model SUP-V, PerryMeter Systems, Division of Biotechnologies, Inc., Dallas, Texas). This single-user sensor eliminates concerns about adequate sterilization; is easily inserted by the patient in private, with minimal instruction and without the need to completely disrobe; minimizes discomfort; and produces EMG data that correlate 99% with data produced by invasive fine wire stainless steel electrodes.

 The portable EMG biofeedback instrument was used by the patients for daily, in-home practice. The sensor described above can be used with any brand of EMG instrument, though some require a simple plug adapter. This study used a portable EMG biofeedback instrument specifically developed for use with the above sensor for rehabilitation of pelvic floor muscles (

, Farrall Instruments, Inc., Grand Island, Nebraska, for Biotechnologies). This instrument provides visual feedback in the form of a circle of 20 lights; each light representing 0.25, 0.5 or 1.0 ,microVolt, according to the amplification setting selected. Two lights in the center of the circle alternate illumination for 10 seconds each, instructing the patient to alternately contract and relax the pelvic floor muscles. 
 
 

 Computerized EMG data acquisition equipment was used in the office for initial and periodic follow-up assessments of pelvic floor musculature. This study used 

Thirty-three women diagnosed as suffering from vulvar vestibulitis syndrome, marked by a significant history of long-term moderate to severe chronic introital dyspareunia and tenderness of the vulvar vestibule, were selected for treatment.

Daniel Menkes, MD

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