Biofeedback in the diagnosis and treatment of chronic essential pelvic pain disorders

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10 Biofeedback in the diagnosis and treatment of chronic essential pelvic pain disorders

Howard I. Glazer, Christopher Gilbert

Pain, relaxation and biofeedback

Changes in emotion and expectations have clear effects on level of pain. These underlying connections have been explored recently as part of research into the mechanism of the placebo effect (Wager et al. 2007, Zubieta & Stohler 2009). The conclusions go beyond mental constructs like distraction and endurance; pain intensity turns out to be modulated by specific chemical and neurological changes in a way resembling the gain control on an amplifier. Changes in synapses, in descending excitatory and inhibitory tracts, in specific brain site excitation and inhibition, in opioid receptor sensitivity, and positive and negative expectations about pain, all interact to enlarge or diminish the experience of pain. Evolution has apparently fine-tuned this set of mechanisms to maximize the chance of survival.

In the field of clinical biofeedback, chronic pain has been a frequent symptom of interest because it is common, distressing, and often seems unnecessary when the signal has little value for warning of body damage. Chronic pain seems to become detached from its origin, or spreads out so much (allodynia, spreading cortical representation; Flor 2002) that the mechanistically minded allopathic physician is without answers as to why something hurts so much. Medical imaging may offer little explanation as to pain sources, and blood tests may show nothing that would explain high pain levels not related or only loosely related to body use. Exercise sometimes improves and sometimes aggravates the pain. Decreased tolerance of the pain may be attributed to deconditioning, even though the original advent of the pain may have discouraged activity and thus led to deconditioning.

Biofeedback depends on providing continuous feedback of a signal to the person it is coming from. With pain, however, there is hardly any way to detect and feed back an actual ‘pain signal’. The closest thing to this is the work done by de Charms et al. (2005) using fMRI for continuous monitoring and display of activity in a brain region known for correlating with experienced pain (anterior cingulate cortex (ACC)). Investigating both chronic pain patients and normal experimental subjects, these researchers found that displaying the moment-to-moment fluctuations in amplitude from the ACC provided an opportunity to influence the signal, which would mean influencing the brain area generating the signal and therefore voluntarily adjusting pain intensity. Whether this pain relief came about via emotional modulation, attentional shifts, or neurological–biochemical changes awaits further research, but the question challenges the mind–body distinction which has oversimplified so much research in this area. Subjects felt their pain intensity reduce, and they felt they were controlling it by doing something to manipulate the graphic display on a video screen. However, the subjects were sitting inside an fMRI device in a research lab, and this would be impractical for large-scale application.

Other than the MRI route, a biofeedback approach generally concentrates on altering a system considered responsible for the pain, or at least correlated with it. Thus we can provide biofeedback from voluntary muscles, feedback from the autonomic nervous system (ANS) variables such as skin temperature, skin conductance, heart rate, heart rate variability (RSA, see below), breathing (rate, rhythm, tidal volume, CO₂ level) and EEG, including cerebral blood flow and slow cortical potential. For biofeedback overviews see Schwartz & Andrasik (2003) and Basmajian (1989).

Sometimes a specific system is the source of pain: muscles and low back or repetitive strain, for example, or hand temperature for Raynaud’s. But most often the pain, having turned chronic, becomes a distressing emotional experience regardless of its source, physical solutions have been exhausted, and long-term pain medication has become the solution. The usual pain patient rarely differentiates among these approaches and attributes to biofeedback a power to turn down pain by changing some correlate of it.

There is support (Arena 2002) for the non-specific use of biofeedback, however, and patients rarely question the lack of specificity. They may readily acknowledge that their pain seems responsive to variation in not only physical activity but emotional stress and depression. Thus the variables of effective or less effective coping, mood modulation in response to the pain, and the amount of co-occurring non-pain distress require consideration in pain management. It may seem that such complex emotional variables could not be detected and fed back via biofeedback devices. But emotions have biological correlates and teaching control over them amounts to gaining leverage over the feeling states themselves. And these feeling states (explored by the placebo researchers cited above) have neurochemical effects on pain intensity.

Pelvic floor biofeedback began with Arnold Kegel (1948), who designed a pressure perineometer to measure contractile force from inside the vagina, with pressure changes displayed on an external gauge. The intent was to improve strength of the pubococcygeus muscle, and it was usually successful. More modern use of biofeedback for pelvic pain usually relies on either manometric feedback (inflatable balloons with adjustable size, placed in the rectum) or surface electromyographic (SEMG) information gained via vaginal or rectal sensors. Information may also be gained from monitoring the external muscles of the lower abdomen, perineum, thighs, and buttocks. Pelvic pain can of course come from many sources, but if dysfunctional muscle activity is suspected, it is simple enough to feed back the continuous muscle amplitude to the patient, opening a channel for voluntary control.

Other approaches to pain in general and pelvic pain in particular are less specific than the EMG method, but capable of providing bodily information otherwise unavailable to consciousness. Below are descriptions of the main biofeedback instruments used in practice, followed by some applications of biofeedback to pelvic pain.

SEMG biofeedback

With adhesive surface electrodes and without skin penetration, this modality can measure muscle tension through skin just as EEG and EKG can, though the signal is attenuated compared with intramuscular electrodes. Monitoring small individual muscles is not very precise with SEMG, but for general muscle regions and groups such as the jaw, back of neck, upper shoulder, low back, or forearm flexors, this technique excels. Wider spacing of electrodes picks up a wider and deeper region of tissue.

Patients relate well to this variable because they can feel changes in muscle tension, and their perception can be validated by readings on a display or by audio feedback. For pelvic muscles, electrodes are in a special housing, but the electronics are the same as for external monitoring.

Skin temperature

A thermistor, usually a match-sized bimetallic junction encased in plastic, can be taped to the skin anywhere on the body to monitor local temperature. Biologically, what is monitored is a complex mix of cutaneous blood flow, blood vessel diameter, ambient temperature, gross shifts in regional allotment of circulation, and degree of emotional stress from moment to moment. Once the fight-or-flight response is triggered, blood is drawn away from the body surface, especially peripheral parts of the limbs, and as the blood vessels constrict, the skin temperature in that area drops. Pain is stressful, and this links skin temperature to pain and suffering via the emotional network and the sympathetic nervous system.

Hand temperature training has become a standard modality in biofeedback, regardless of where the pain is, because it tends to correlate with a reduction in perceived threat of some kind. Pain creates more distress at some times than others, and the state of distress can be reduced by focusing on hand-warming and peripheral circulatory increase in general, which by a kind of ‘upstream’ influence alters the ANS toward increased parasympathetic dominance.

Biofeedback thermometers are typically sensitive to at least 0.1°F, smaller than what the average person can perceive. As with muscle tension, tiny changes are amplified and displayed to the patient, who begins to feel some influence over this obscure body variable. Most uses of hand-temperature training for pain issues are non-specific, meaning the goal is general relaxation and shifting of autonomic dominance rather than warming of a specific body area. Hand-warming is often used for migraine prevention. Complex regional pain syndrome is sometimes approached from the self-regulation angle, especially when skin circulation is affected; the local area can be monitored and brought under temporary control via biofeedback principles.

Galvanic skin response

Galvanic skin response (GSR) is a variable that basically evaluates shifts in skin conductance, correlates well with sympathetic nervous system activity and can be used in a similar way to hand temperature, to lower the emotional stress related to pain. Two small electrodes are fastened to the palm or fingers and a tiny current passed between them samples the resistance of the skin. As eccrine sweat glands secrete more, skin resistance drops within seconds as part of the fight-or-flight response. Relaxation training can be enhanced by providing this indicator in either auditory or visual form. It is sensitive to various mental events such as surprise, apprehension, suffering or expectation of suffering, time urgency, confusion and recall of various stressors. GSR is less specific in pain treatment than hand temperature, but its value lies in fine-tuning the ability to self-calm and to reward emotional stability.

Breathing

Variables of breathing can be followed and fed back in several ways. Rate and rhythm can be monitored by a mechanical strain gauge around the torso, by changes in air temperature from the nostril, or by changes in tension of certain muscles in the neck and shoulders. Composition of exhaled air, primarily degree of CO₂, can be monitored and displayed by a capnograph. The relationship between breathing and pulse, often called RSA (respiratory-sinus arrhythmia), can be followed with a simple or complex analysis of how much the heart rate rises and falls with each breath.

Starting with yoga, breathing regulation has a long history in the field of voluntary self-regulation and every meditative tradition includes attention to breath regulation. Like the previous biofeedback variables, breathing is sensitive to the fight-or-flight reaction and is always subject to the central decision to accelerate breathing in order to prepare for exertion. Muscles need fuel in order to perform, and extra fuel must be delivered by the blood. When average individuals consciously attempt to reduce a state of alarm (perhaps responding to a general injunction ‘Calm down!’) they are not likely to think of keeping their limbs warm and their hands dry; they may attempt some muscle relaxation (fists, shoulders, face) but most likely they will try to control their breathing by means of one or more deep breaths. So the validity of breathing regulation is high for most people, though they may not see it as reversing their fight-or-flight reaction.

The five biofeedback-targeted variables of interest, then, in chronic pain treatment, are muscle tension, hand temperature, skin conductance, heart rate variability and breathing. These all in various ways reflect shifts in ANS activity, which is responsive to conscious and preconscious mental events related to current suffering and danger, as well as conditioned responses to cues associated with past or anticipated suffering and danger. Since pain is a prime signal of impending body damage, it is hard not to let pain perturb the nervous system toward emergency action even though the pain signal may not always be a valid warning.

Chronic pain creates a long-term ‘orange alert’ state which affects everyday functioning, including sleep quality, concentration, allotment of energy and resources, emotional stability, and resistance to depression and anxiety from other sources (Gatchel et al. 2007, Turk et al. 2008).

Research applications to pelvic pain problems

Hand temperature and pelvic pain

There is very little research using temperature biofeedback alone for pelvic pain problems. Hand temperature is a commonly used biofeedback modality, but is usually used in combination with others, for a variety of goals. But below is a study of hand temperature biofeedback and endometriosis.

In a small multiple baseline study (Hart et al. 1981) five women with pain from endometriosis were trained in hand-warming with individual sessions twice weekly over 2 months, with home practice in between sessions. The rationale was to reduce physiological arousal, and the intent was to have the skill generalize as a learned and perhaps automatic response to pain. All but one person learned to voluntarily increase hand temperature, and reports of pain relief were accompanied by decreases in life interference from pain, decrease in affective distress, and increase in ‘life control’. One person could not learn the hand-warming skill; her pain remained the same and some indicators got worse.

Muscle biofeedback and pelvic pain

In chronic pelvic pain (CPP) there is usually an interaction among pelvic muscle activity, negative affect, pain thresholds, and nervous system factors modulating pain. The average pelvic pain patient knows nothing of this interaction and considers the pain a direct readout of tissue damage. Bracing, avoidance of activity, and an often passive despair are common responses.

There are several ways that excess muscle tension can cause pain: prolonged ischaemia, accumulation of metabolites such as lactic acid and potassium; reduced intramuscular circulation, release of bradykinin and serotonin, and various aggravators of inflammation (Mense 2000). In addition, pain intensity is mediated by co-occurring emotional factors. Brain sites such as the anterior cingulate cortex are responsive to allodynia and are also involved in conscious mediation of ‘suffering’ (Yoshino et al. 2009). Therefore, negative affect from any source is likely to make pain worse because at some level different kinds of distress are not differentiated. The most reliable predictors of hyperalgesia seem to be varieties of anxiety, fear of movement, fear of injury, and the tendency toward catastrophic thinking (Boersma & Linton 2006a, 2006b).

Muscle tension is often elevated in chronic pain patients as part of an attempt to brace and protect the body from damage. Muscular rigidity is a primary defensive response to threat, pain and trauma, and this response can be triggered by both relevant and irrelevant sensory and emotional stimuli. SEMG monitoring can detect and quantify the degree of inappropriate pelvic muscle hypertonicity and instability (White et al. 1997, Glazer et al. 1998). Many chronic pain syndromes besides pelvic pain are associated with increased muscle tension (Flor et al. 1992) and can be alleviated in part by better muscle control.

Granot et al. (2002) studied pain sensitivity in a group of women with vulvar vestibulitis using a heated bar on the skin. A matched control group without pain was used for comparison. The researchers collected anxiety measures and estimates of pain intensity and unpleasantness, and blood pressure was also recorded. The pain patients had significantly more state and trait anxiety before the procedure began; they gave higher estimates for pain magnitude, unpleasantness, and had higher systolic blood pressure. The authors’ conclusions were that these subjects were more anxious and had higher systemic pain sensitivity.

The study of Bendaña et al. (2009) used a treatment sample of 52 women having problems with urinary frequency and urgency, interstitial cystitis, CPP, dysuria, and evidence of pelvic floor muscle (PFM) spasm. Initial determination of the levator ani muscle complex condition was done by manual vaginal examination. Subject criteria for selection were bladder dysfunction, including pelvic pain, and evidence of PFM tension. The therapeutic goal was to detect and reduce muscle tension and spasms in the PFMs using transvaginal SEMG and electrical stimulation. During six individual sessions the subjects observed computerized visual feedback which reflected their internal muscle tension from moment to moment. First isolating sensations of the relevant muscles from surrounding pelvic, abdominal and back muscles, they learned to increase control of the pertinent muscles in both tensing and relaxing directions.

Outcomes were good: reports of symptom improvement and reduced effect on daily life were in the range of 65–75% at 6-week and 3-month follow-up. The study’s authors concluded: ‘Patients gain a sense of which muscles in the pelvis they can control by manipulating feedback pathways and relaxing overall pelvic floor tone and afferent cross-stimulation, leading to symptomatic improvement’.

PFM biofeedback (neuromuscular re-education) has been found useful for men with pelvic floor dysfunction and prostatitis associated with pain.

The study of Heah et al. (1997) of men with levator ani syndrome (LAS) used manometric rectal balloon biofeedback. Average pain report after completion of biofeedback dropped to around 25% of that before biofeedback, with use of analgesics also significantly reduced.

Grimaud et al. (1991) also used a manometric technique to investigate patients with chronic idiopathic anal pain. In the 12 cases studied, the pressure in the anal canal was significantly higher than in a normal comparison group. After an average of eight biofeedback training sessions, in which patients learned voluntary control of the external sphincter, the pain disappeared, and the anal canal pressure dropped to normal or near-normal.

Cornel et al. (2005) reported treatment of 31 men with chronic prostatitis and CPP. They learned to control and relax PFM tension via biofeedback provided by a rectal SEMG sensor. Average muscle tension before treatment was 4.9 µv, and dropped to 1.7 µv afterward. Corresponding drops in symptom scores (NIH Chronic Prostatitis Symptom Index) went from 23.6 to 11.4.

Chiarioni et al. (2009) reports administering nine sessions of counselling plus electrogalvanic stimulation (EGS), massage or biofeedback randomized to 157 patients suffering from LAS. Outcomes were reassessed at 1, 3, 6 and 12 months. Among patients with LAS, adequate relief was reported by 87% for biofeedback, 45% for EGS, and 22% for massage. Pain days per month decreased from 14.7 at baseline to 3.3 after biofeedback, 8.9 after EGS, and 13.3 after massage. Pain intensity decreased from 6.8 (0–10 scale) at baseline to 1.8 after biofeedback, 4.7 after EGS, and 6.0 after massage. Improvements were maintained for 12 months. The authors conclude that biofeedback is the most effective of these treatments, and EGS is somewhat effective.

Jantos (2008) assessed vulvar pelvic muscle tension in 529 cases of vulvodynia, combined with psychological testing, to examine psychophysiological factors. The study also provided biofeedback-based intervention in the form of daily pelvic muscle exercises based on findings of SEMG using the ‘Glazer Protocol’ (Glazer et al. 1995) This involves use of progressively larger dilators to stretch and relax the vulvar and vaginal muscles, intravaginal EMG biofeedback, and brief psychotherapy aimed at improved psychological (anxiety, depression, fear of sexual activity) and sexual functioning. State and trait anxiety differentiated normals from vulvodynia patients, who also had lower sensory thresholds, more autonomic disturbances, and greater emotional responses. General outcomes after treatment included normalizing of muscle characteristics, capacity to accept larger dilators, and greater likelihood of resuming normal sexual activity. PFM improved in several ways, correlating with degree of improvement in the group as a whole, though not individually. Resting baseline and instability declined by more than 50%; maximum phasic and tonic contractions increased.

A unique finding in the Jantos study was the relationship between duration of symptoms and resting PFM EMG (subject characteristics at the onset of the study): severity of symptoms did not decline with time, but muscle tension did. The authors speculated that this could indicate development of contractures, which resemble muscle spasms upon palpation but are produced locally rather than by corticospinal input. As a result they are electrically silent and would not contribute to pelvic EMG. Such contractures could create pain by producing myofascial trigger points (Bornstein & Simon 2002). Trigger points produce a high local EMG signal that does not generalize to the whole muscle. These structures are sensitive to sympathetic nervous system activity (McNulty et al. 1994, Chen et al. 1998), and therefore can be aggravated by anxiety, apprehension and negative psychological states.

The psychophysiological perspective here gives a more complete understanding of how trigger points respond to physiological and emotional arousal by producing more pain (see also Chapter 4). For this reason, any arousal-reduction technique, including general relaxation methods, should be helpful for pain intensity that arises from trigger points.

Intrapelvic SEMG in the treatment of functional chronic urogenital, gastrointestinal and sexual pain and dysfunction

Biofeedback meets evidence-based medicine: The Glazer Protocol

This section of the chapter focuses on a specific methodology and protocol, the Glazer Protocol, for the diagnosis and treatment of essential CPP and dysfunction. The methodology involves the use of non-invasive intrapelvic (intravaginal or intra-anal) SEMG. The first factor differentiating this approach from the self-regulation biofeedback approach, discussed earlier, is the emphasis on the electrophysiology of the SEMG signal, rather than the psychophysiogy of self-regulation. This protocol relies more on the bioelectric information derived from the SEMG signal analysis, rather than the traditional biofeedback use of the SEMG signal to teach the patient voluntary self-regulation through enhanced interoceptive awareness. Unlike traditional biofeedback, this protocol is highly operationally defined, including diagnostic criteria (ICD), medical, psychological and sexual history, patient positioning and muscle use training, muscle activation and deactivation sequence, SEMG signal processing, recording and formatting, to create a standardized SEMG report and database. This approach facilitates the development of multicentre, multidiagnosis, multitreatment databases for statistical analysis. This operationally defined procedural and biometric/psychometric approach creates the foundation for evidence-based research and represents a substantial departure from past work in the field of clinical biofeedback (Glazer & Laine 2007).

Evidence-based medicine applies evidence from scientific methodology to health care practice. It assesses the quality of evidence relating to risks and benefits of treatments. The power of clinical evidence lies in its freedom from bias. The most powerful evidence for therapeutic efficacy comes from randomized, double-blind, placebo-controlled trials with operationally defined patient populations, diagnoses and treatment protocols. Patient testimonials, case studies, clinical experience and expert opinion have little value as scientific evidence. This in no way takes away from the importance of traditional clinical practice experience and thinking. Often clinical practice serves as an ‘incubator’ leading to ideas which are then transformed into more evidence-based hypotheses and subject to evidence-based medicine research. The completion of the cycle is the evidence-based research findings returning to clinical practice where their implementation can benefit clinical thinking and patient care (see Chapter 9).

The application of these scientific standards to biofeedback presents significant challenges because very little of the published literature in biofeedback reaches the higher levels of scientific evidence. The majority of biofeedback research is case histories, clinical experience and expert opinion, all subject to bias. This is largely due to the lack of standardization of technology and techniques, and failure to employ operationalized protocols, procedures and definitions.

A recent review article (Glazer & Laine 2007), summarizing the peer-reviewed literature in the use of PFM biofeedback for the treatment of functional urinary incontinence, exemplifies this. This review reports a total of 326 studies found in Medline between 1975 and 2005. Only 8.6% of these studies operationally defined independent and dependent variables, utilized prospective randomized trials with parametric statistical analyses, and used patient selection criteria to rule out organic causes of urinary incontinence. Among these 27 studies are six different operational definitions for the diagnosis, eight operational definitions for treatments, 12 operational definitions for biofeedback protocols, and six operational definitions for treatment outcome. In 30 years of peer-reviewed literature only seven studies reported a comparison of biofeedback to a matched, no treatment, control group. For these seven studies, differences in signal processing, biofeedback instrumentation, assessment and treatment protocols, biofeedback modalities, and multiple uncontrolled variables make each of these groups so different that there is no standardized definition of biofeedback. The same is true within each study, since the biofeedback groups are not comparable to their respective control groups due to non-randomized, uncontrolled variables between groups. This pervasive lack of standardization has hampered the scientific assessment of biofeedback by effectively precluding the application of evidence-based medicine standards to the field.

The hallmark of the Glazer Protocol is standardization in all aspects of clinical biofeedback research and practice. This includes the use of operational definitions for diagnoses (ICD, SEMG, history, medical exam, laboratory tests, etc.), biofeedback treatment (CPT, modality, instrumentation, signal processing, evaluation and treatment protocols, patient muscle identification training, positioning, etc.) and therapeutic efficacy (psychometrics, structural and functional organic changes, experiential self-report, lab reports, etc.). In addition, the protocol standardizes data measurement, collection, transmission and storage across multiple domestic and international site locations, languages, areas of study, etc. to produce large sample size, multinational, multidisorder databases. These databases serve as a standard to assist in diagnosis and treatment and can be statistically queried regarding the effects of variables on therapeutic outcomes. These intrapelvic SEMG readings help identify the variables which correlate with symptoms, and eventually may help to shed some light upon the pathophysiology involved in response to biofeedback and non-biofeedback interventions such as pharmacology, acupuncture, or surgery.

Applications

The Glazer Protocol is used in the diagnosis and treatment of a wide range of PFM-related disorder specialties as shown in Table 10.1.

Table 10.1 Disorders, categorized by medical specialty and ICD codes, treated with pelvic floor muscle SEMG biofeedback

Medical specialty	Diagnostic ICD-9/-10 code
Gynaecology/Dermatology/Psychiatry
1. Vulvar vestibulitis syndrome	625.71, 625.0
2. Dysaesthetic vulvodynia	625.70, 625.9
3. Vaginismus	F94.2, 625.1
4. Dyspareunia (introital N94.1, deep 302.76)	N94.1, 302.76

Female Urology/Neurourology
5. Dysuria	306.53, 788.1
6. Urinary stress incontinence	625.6
7. Urinary urge incontinence	N39.41
8. Urinary incontinence mixed	788.34
9a. Detrusor hyperactivity	N32.8
9b. Neurogenic bladder	N31.9
10. Urinary retention	N39.8
11. Interstitial cystitis	N30.1

Gastroenterology/Colorectal Surgery
12. Functional fecal incontinence	787.6 R15
13. Functional constipation	K59.00
14. Anismus (anorectal pain syndrome, levator ani proctalgia fugax)	K59.4
15. Irritable bowel syndrome	564.1

Male Urology/Neurourology
16. Mixed urinary incontinence	788.34
17. Prostatodynia	N42.81
18. Prostate cancer/prostatectomy	C61
19. Benign prostatic hypertrophy	600.0
20. Chronic pelvic or perineal pain	625.9 R10.2

Asymptomatic
21. Healthy male (controls)
Multiple codes limited to absence of specific organic pathology
22. Healthy female (controls)

Patient selection

Biofeedback is used in the treatment of functional or essential disorders. These are disorders which are diagnosed by first ruling out established anatomic and physiological pathology causing the reported symptoms. Therefore it is essential that all prospective biofeedback patients have medical assessment to identify and treat or rule out well-known medical conditions as the cause of the symptoms. In addition, the patient must have intact sensory and motor pathways. Finally, a major requirement for biofeedback candidates in general, and the Glazer Protocol in particular, is sufficient motivation and discipline to conduct daily biofeedback-assisted exercise sessions for a period ranging from 4 to 8 weeks up to a period ranging from 6 to 12 months. Non-compliance and drop out rates are high; clinicians should be cautious in prescribing biofeedback for patients expressing a preference for treatments involving less commitment of time and discipline. In the experience of the author, those patients being assessed for biofeedback who request a pharmacological or surgical approach to their problem are less likely to comply with home training prescriptions, and are therefore less likely to benefit from biofeedback as a primary treatment modality.

Assessment with the Glazer Protocol

The Glazer Protocol operationally defines both the intrapelvic SEMG assessment and rehabilitation of PFM. The assessment protocol starts by educating the patient on the structure and function of the PFM as they relate to their individual symptom presentation. This is accomplished with a scripted presentation, with responses to any questions the patient presents. The presentation includes instructions on private self-insertion of the intrapelvic sensor, body positioning as a critical factor in SEMG measurement, and teaching the patient the correct method for contracting and relaxing the PFM. This instruction focuses on creating the intravaginal lifting sensation associated with the correct use of PFM while permitting limited co-contractions, or overflow (Glazer & McConkay 1996) to offset fatigue during the initial stages of exercise.

The intrapelvic SEMG assessment consists of a fixed series of PFM contractions and relaxations, directed via an on-screen written script and simultaneous voice presentation. This assessment is a computer-controlled continuous process in which software (Biograph Infiniti with Glazer Protocol) directs both the instructions to the patient and the SEMG biofeedback signal processing device (Myotrac Infiniti), which continuously records raw SEMG data (2048 samples/s) and displays the integrated SEMG signal (20 samples/s) throughout the assessment. The SEMG screen presents a graphic and numeric presentation of the integrated SEMG signal as well as signal variability measures and a three-dimensional fast Fourier transformation power density spectral frequency display of the signal. This allows the clinician to view real-time changes in the spectral frequency distribution of the signal power throughout the conduct of the evaluation (Figure 10.1).

Figure 10.1 A screenshot from the Glazer Protocol as seen by the clinician and patient in real time showing the intrapelvic SEMG tracings and numerical values for signal amplitude, muscle activation onset and release times, variability, and power density spectral frequency

The engineering of the signal processor hardware and software is a critical element in the Protocol. Only by understanding the engineering details of the instrument (Differential Amplification, Common Mode Rejection Sensitivity, Impedance, Rectification, Bandpass and Notch Filtration, Analogue to Digital Conversion, Power Density Spectral Frequency Analysis via Fast Fourier Transformation, signal re-integration methods, etc.) can the clinician understand both the utility and the limits of the SEMG data which they are observing and interpreting.

The fixed sequence of muscle activity utilized during the protocol includes pre-baseline rest, phasic contractions, tonic contractions, endurance contraction, and post-baseline rest. This traditional series of PFM assessment contractions were originally intended to reflect sexual, sphincteric and support functions of the pubococcygeus muscle (Kegel 1948, 1952). In the Glazer Protocol, SEMG measures taken continuously throughout the protocol include average SEMG amplitude, muscle recruitment and recovery latencies, median power density spectral frequency, and two measures of SEMG variability: raw (standard deviation) and amplitude corrected (coefficient of variability). Upon completion of the protocol the data are stored in raw SEMG form (2048 samples/s).

The report is maintained in the patient’s electronic record and copies of the report are provided to the patient and to the referring and ongoing treating clinicians. The data derived from the raw SEMG are also exported into an SEMG database with each record categorized by diagnosis, patient demographic variables and therapeutic response variables. The database also includes data from asymptomatic volunteers to provide a matched or randomized control group for between-group statistical comparisons.

Comparing groups measured under standardized conditions is the first step in identifying SEMG characteristics associated with specific symptom patterns and diagnostic categories. This approach yields helpful data to confirm a diagnosis as well as develop hypotheses about the pathophysiology of symptoms and disorders. In addition, comparisons of SEMG measures within groups over assessment sessions can identify critical SEMG changes predictive of symptomatic and functional improvement. Once these findings have been replicated they can then form the basis of training protocols aimed at producing the SEMG changes known to be predictive of symptom reduction. Early published research findings will be reviewed later in this chapter along with a presentation of current, ongoing research and new advancements in which patients can be completely evaluated and treated via telemedicine technology over the internet.

SEMG is not a stand-alone diagnostic or therapeutic programme, no matter how well operationalized and defined its components may be. It is part of a comprehensive assessment process which often involves multiple specialists and diagnostic procedures. In CPP it is not at all unusual for patients to initially present with a history of many years of pain and visits to many physicians and non-physician healthcare practitioners (neurologists, anaesthesiologists, urologists, gynaecologists, urogynaecologists, gastroenterologists, mental health practitioners, holistic practitioners, psychopharmacologists, physiatrists, osteopaths, acupuncturists, nutritionists, physiotherapists, and many more). Satisfactory diagnosis and treatment of chronic pain is now well recognized by most practitioners as requiring an integrated biopsychosocial approach addressing organic, psychological, interpersonal and functional causes and consequences of complex pain syndromes. Biofeedback, like any procedure addressing chronic disorders, must incorporate a detailed review of medical history, systems review, medications and non-prescription agents, social and psychological status, diet, exercise and sexual functioning, in order to create a complete view of the patient. Collecting patient medical records, using standardized intake forms and acquiring input from significant others in the patient’s life is an integral part of the evaluation process, and ongoing communication and information exchange among multiple treatment resources is an essential part of treatment.

Levels of interpretation and applications of SEMG evaluation data include both empirical and pathophysiological perspectives

Empirical

This level of interpretation and application is purely empirical, utilizing operationally defined intrapelvic SEMG measures as independent variables and operationally defined symptom and function measures as dependent variables. Analysis at this level serves the functions listed below, without any deductions or assumptions concerning the underlying physiology reflected in these variables.

1. Descriptive statistics help develop normative SEMG database standards.

2. Identified symptom and disorder-specific SEMG patterns assist in differential diagnosis.

3. Consistent SEMG changes and associated symptom reduction and functional improvements help develop rehabilitation protocols.

Physiological

Electrophysiology data derived from SEMG is one manifestation of local and systemic integrated physiology. The functional integration of multiple physiological systems is necessary to understand disorders such as complex regional pain syndromes. It is this physiological integration which allows the use of striated muscle SEMG to better understand the multiple physiological processes contributing to dysfunction. There are several studies which have looked at the relationship between striate muscle fatigue, SEMG, blood flow, PO₂, subjective sense of fatigue, and pain (Alfonsi et al. 1999, Yoshitake et al. 2001, Hug et al. 2004, Tachi et al. 2004, Dimitrov et al. 2006). These variables show a complex, non-linear relationship to one another, but these studies basically report that subjective sense of muscle fatigue and localized nociceptive pain are correlated with the following: SEMG increased contractile amplitude, lower median power density spectral frequency, reduced microcirculation in local muscle and surrounding tissue, and hypoxia. On a neurochemical level these changes are associated with release of neurokines, cytokines, lactic acid, interleukin, and tumour necrosis factor-α, representing localized ‘defensive’ responses of ischaemia, inflammation and sensitization (Mense 2004). These markers are all part of an integrated response from the most molecular cellular level to the most molar level of cognition, affect and goal-oriented intentional behaviour.

In this integrated model, intrapelvic SEMG reflects not only myofascial phenomena such as chronic tension or chronic weakness, but also neurological, neurochemical, inflammatory, vascular, blood gas levels, hormonal availability, autonomic activity, and even cognition and affect. These are all components of a single integrated response. So, we no longer restrict ourselves to looking at SEMG as representing muscle tension or weakness or asymmetry. SEMG characteristics can now represent oxygen availability, blood flow, hormone levels, tissue inflammation, and even psychological processes such as thoughts and feelings. All such processes are a part of a single response, no longer seen in a sequential or causal model but as components of a single entity. For convenience of study we may divide these functions up by anatomy, physiology, function or medical specialty, but in doing so we must understand that this deconstruction process leaves us at risk for losing the ‘forest for the trees’.

If we see all responses at all levels as part of an integrated process, it now makes sense to look at the relationships which may exist among any of these components. An example of this is a recently recognized intrapelvic SEMG profile which represents atrophic vaginitis. This oestrogen loss condition may manifest as chronic, fluctuating vulvar dryness, irritation, tissue integrity compromise, dyspareunia, emotional changes, bone density loss, and pelvic organ prolapse (Mehta & Bachman 2008). There is also a highly reliable intrapelvic SEMG profile which correlates with this condition. This profile includes low-amplitude (hypotonicity), low-signal-variability resting tone, slow recruitment and recovery latencies to low-amplitude phasic, tonic, and endurance contractions. These contractions show low signal standard deviations and coefficients of variability, and a high median frequency power density spectrum on sustained isometric contractions. This SEMG pattern as a potential confirmation for oestrogen loss is still undergoing data collection to produce a sample size sufficient for parametric data analysis and publication.

Developing evidence-based biofeedback applications for pelvic pain

It is clear that the development of evidence-based biofeedback applications for pelvic pain is a major undertaking, well beyond the resources of any individual or small group of interested practitioners. Developing a structure of resources to meet this need became a major focus in the development of evidence-based biofeedback protocols for the diagnosis and treatment of CPP disorders.

Selected ongoing international collaborative research

The BFE/IREP team projects have led to collaboration with a team of colorectal surgeons in Nanjing, China, studying the use of intra-anal biofeedback in anal pain disorders. Urologists in Sao Paulo, Brazil, are completing a research project using the intra-anal SEMG protocol. Evaluations starting 30 days prior to patients undergoing radical prostatectomy are repeated every 3 months thereafter for a total of 12 months along with a control group. This group is also working on prediction and intervention in postpartum urinary incontinence. A second Sao Paulo group has initiated a study on a paediatric population suffering from polysymptomatic enuresis, employing a version of the Glazer Protocol. This project records simultaneous multiple SEMG measures and it is hoped that it will provide insight into this disorder and its pathophysiology.

Several recent technological and methodological advancements have also emerged from the Glazer BFE/IREP teams which have led to the introduction of clinical SEMG evaluation and treatment services via telemedicine, online, both domestically and internationally.

Research summary

The synergy between the goals of the BFE, to promote biofeedback, and the goals of Glazer, to develop evidence-based biofeedback applications for pelvic pain disorders, is clear. The BFE and Glazer have been working cooperatively for several years and the following selected studies exemplify peer-reviewed published research using intrapelvic SEMG biofeedback in diagnosis and treatment of PFM-related disorders. This representative group of studies includes SEMG diagnostic database studies, SEMG treatment studies, and protocol methodology studies.

SEMG diagnostic studies refer to the use of intrapelvic SEMG data using between-group comparison studies to determine which SEMG variable or combination of variables yield statistical significance in differentiating PFM-related disorders. The first study in this series, entitled ‘Establishing the diagnosis of vulvar vestibulitis’, was published in 1997 (White et al. 1997). This study compared intravaginal SEMG assessment findings from essential and organic vulvar pain patients. Six individual SEMG criteria differentiated vulvar vestibulitis patients from organic vulvar pain patients, with 88% of vulvar vestibulitis patients manifesting three or more of these criteria to a significantly greater degree than the organic vulvar pain patients. The single most statistically significant variable differentiating them was the resting baseline stability as measured by the coefficient of variability of the integrated intrapelvic SEMG. Vulvar vestibulitis patients showed significantly higher resting instability than organic vulvar pain control patients.

Another study ‘Electromyographic comparisons of the pelvic floor in women with dysesthetic vulvodynia and asymptomatic women’ compared SEMG PFM evaluation variables in dysaesthetic vulvodynia patients to matched asymptomatic controls (Glazer et al. 1998). Findings indicated that dysaesthetic vulvodynia patients manifest significantly greater intravaginal SEMG-sustained contractile weakness, resting hypertonicity and instability.

Two related papers (Glazer et al. 1999, Romanzi et al. 1999) studied reliability and clinical predictive validity of intravaginal SEMG. These papers reported the findings of a wide range of symptomatic patients undergoing both manual (digital) and SEMG intrapelvic repeated evaluations. At each administration, the order of procedure and clinician was randomized between a urogynaecologist and a gynaecologist conducting the digital exams and Glazer conducting intrapelvic SEMG evaluations. Reliability within and between evaluators and procedures was statistically significant but digital exam results could not significantly predict any clinical status. Intravaginal SEMG significantly predicts stress and urge incontinence, menstrual status and parity.

Hetrick et al. (2006) studied differences in intra-anal PFM SEMG readings between men suffering from chronic pelvic pain syndrome (CPPS) compared with a matched control group of pain-free men. CPPS patients were found to manifest overall greater PFM electrophysiological instability. This measure as well as chronic prebaseline resting hypertonicity and endurance contraction weakness were statistically significant in differentiating CPPS patients from their asymptomatic matched controls. It is interesting to note the similarity in these pelvic floor SEMG findings to those previously found in women suffering from essential vulvovaginal pain disorders (Glazer et al. 1995, 1998, White et al. 1997).

Intrapelvic SEMG treatment studies use intrapelvic SEMG data to develop PFM biofeedback treatment protocols. The earliest of these studies ‘Treatment of vulvar vestibulitis syndrome with electromyographic biofeedback of pelvic floor musculature’ (Glazer et al. 1995) was the first peer-review published study in the field. It reported a 50% rate of asymptomatic outcome on 6-month follow-up with overall self-reported improvement averaging 83%. Only the standard deviation of tonic resting periods showed significant predictive validity for pain reduction and improvement in sexual desire, arousal and orgasm. This study concluded that PFM electrophysiological stabilization through intrapelvic SEMG biofeedback-assisted exercise produces pain relief and improved sexual functioning for vulvovaginal pain patients.

Another study ‘Dysesthetic vulvodynia, long term follow-up after treatment with surface electromyography-assisted PFM rehabilitation’ (Glazer, 2000) reported on the 3–5-year follow-up status of 43 patients who were asymptomatic at the completion of their PFM rehabilitation treatment for vulvodynia. All 43 patients remained pain-free; recovery of sexual desire, pleasure and frequency, however, progressively improved but remained well below levels experienced prior to the onset of vulvar pain.

A doctoral dissertation from McGill University (Bergeron et al. 2001) described a prospective, randomized treatment design comparing vestibulectomy (surgical removal of a portion of the superficial tissue making up the vestibule of the vagina), Glazer Protocol biofeedback, and group cognitive behaviour therapy in the treatment of vulvar vestibulitis. Surgical outcomes were found superior to both the intrapelvic Glazer SEMG treatment protocol and the couples group cognitive behaviour therapy. When examining patient self-report measures, all three groups did equally well with a small, statistically non-significant, preference for surgery. Before biofeedback and cognitive behavioural therapy were included in the treatment of vulvar pain disorders, surgery was considered the primary treatment and ‘gold standard’ for many years, in spite of the significant adverse consequences as well as absence of patient satisfaction or long-term follow up.

In a study entitled ‘Treating vulvar vestibulitis with electromyographic biofeedback of pelvic floor musculature’ patients with moderate to severe vulvar vestibulitis syndrome underwent the Glazer intrapelvic biofeedback protocol (McKay et al. 2001). Patients received monthly in-office evaluation and daily home-trainer-assisted PFM rehabilitation. Eighty-three percent of patients demonstrated significant reduction in introital tenderness, with 69% resuming sexual intercourse and 48% reporting no discomfort during sexual intercourse.

Glazer & MacConkey (1996) published the first methodological paper ‘Functional rehabilitation of pelvic floor muscles: a challenge to tradition’. Traditional PFM biofeedback-assisted rehabilitation strongly emphasized the exclusive use of the pubococcygeus without the use of supportive or accessory muscles such as gluteal, quadriceps, adductor longus and particularly abdominal muscles. This study demonstrates that the traditional practice of excluding accessory muscles in PFM re-education is not always warranted. Subjects were trained and then tested either with or without abdominal augmented PFM contractions in a 2 × 2 experimental design. Results clearly demonstrated significantly greater contractile amplitude and reduced variability (strength and coordination) in subjects tested with exclusive pubococcygeus contraction after training with abdominals, compared to subjects both trained and tested without training abdominal muscles. Clearly, where up-training and coordination are the training goals, the co-contraction of abdominals during training of the pelvic floor should not be excluded.

Glazer et al. (2002) published the first methodological paper introducing the technology of telemedicine via videoconference over the internet. This paper reported a case history demonstrating the use of a newly developed telemedicine system permitting the remote, real-time use of SEMG of pelvic floor musculature. This browser-based version of the Glazer Protocol offers a reliable and convenient diagnostic and treatment tool that overcomes the barriers of distance and time. As this technology has become more readily available, it has greatly facilitated international education and research collaboration with the standardized procedures critical to research reaching the requirements of evidence-based medicine. It also permits direct patient assessment and treatment by those with most experience in fields just beginning to utilize SEMG intrapelvic biofeedback.

Brown et al. (2003, 2004, 2005, 2006) published a series of papers reporting on the use of botulinum toxin A injected into the pelvic floor musculature as a possible treatment for vulvar vestibulitis syndrome. These studies employed intravaginal SEMG to determine if any clinical findings correlate with this measure. Data suggested that only those patients with elevated resting tone, variability and spectral frequency benefited from the injection. This is consistent with the fact that botulinum toxin A is known to selectively block type II glycolytic fibre. This finding suggests that intravaginal SEMG would serve as a valuable tool in selecting patients who would benefit from this procedure.

Summary of Medline ‘biofeedback’ ‘pelvic pain’ literature search

A peer-reviewed literature search was conducted with the use of Medline, searching all languages, all ages, and both genders, from 1975 to the present and entering the search terms ‘biofeedback’ and ‘pelvic pain’. The search returned a total of 87 citations. Considered for inclusion in this review were only those citations reporting primary research in which at least one treatment condition was biofeedback alone, and at least one of the disorders treated had a component of chronic pelvic pain. Removed from consideration in this review were:

1. Review articles or meta-snalyses without original primary research reported;

2. Studies in which biofeedback was only one component of a protocol employing multiple treatment components (e.g. biofeedback+estim, biofeedback+neuromodulation, biofeedback+trigger point release, etc.). No subjects received a biofeedback alone treatment;

3. Studies in which there are no biofeedback treatments included (e.g. pelvic floor exercises without biofeedback);

4. Studies in which there are no pelvic pain disorders treated (e.g. disorders treated are urinary or bowel symptoms without a pain component or no pain components were measured or recorded).

Applying these criteria for inclusion/exclusion results in the inclusion of 13 and the exclusion of 74 studies. The 13 studies meeting inclusion criteria break down as follows.

Case study 10.1

J.A. is 44-year-old female, married, Caucasian, MBA, Corporate Executive, residing in northeastern USA with her husband of 17 years and their two teenage children. She is approximately 5’4” in height, 115 pounds and presented as neat, well-groomed, attractive, cooperative and well-spoken. Her husband, a neuroradiologist, was in attendance throughout the initial evaluation. Initial evaluation session is approximately 2 hours. She reports as follows on her initial intake form.

History and data review and integration with treatment(s) prescribed

Summary of findings

Generally healthy 44-year-old female reporting 17-month history of acute onset, post Cipro for UTI, vulvar pain with both spontaneous non-localized chronic burning (dysaesthetic vulvodynia) and 5 and 7 pm localized provoked sharp pain on contact with introital dyspareunia (vulvar vestibulitis syndrome). Notable history includes child abuse with PTSD, alcohol and substance abuse in remission. Allergies to Benadryl, elavil and trazadone, presently taking multiple prescribed pain medications and multiple non-prescription supplements. She reports a family history of cancer and substance abuse. Systems review reveals:

1. Easy bruising, splitting nails and warts.

2. Loss of appetite, nausea/vomiting/bloating and constipation with pain on bowel movements and greasy stool.

3. Urine retention, incomplete voids, kidney stones, vaginal/rectal sensation ‘like a ball pushing out from inside’ and SUI.

4. Dysmenorrhoea, irregular menses, vaginal discharge, dryness, dyspareunia, vulvar, vaginal and clitoral pain spontaneous unprovoked chronic and localized provoked.

5. Reduced sexual desire arousal and orgasms with 17 months abstinence and concerned over marital relations.

6. Psychological evaluation reveals generalized anxiety and a focus on somatic concerns and a predisposition to substance abuse.

7. Gynaecological exam and labs, including complete blood count, are normal. Well-established organic causes of vulvar pain (infections, dermatoses, neuropathies, anatomic changes, pelvic inflammatory disorder, pelvic congestion, etc.) have been ruled out on multiple gynaecological and imaging procedure evaluations.

8. Intrapelvic SEMG evaluation shows mildly elevated and unstable initial rest, slow recruit/recover latencies and low peak amplitudes on phasic contractions, low amplitude, stable, high median frequency for both tonic and endurance contractions, and low-amplitude, stable post baseline.

Interpretation of findings

• Well-established organic causes of vulvar pain have been ruled out.

• Symptoms meet criteria for diagnosis of both DV and VVS, commonly overlapping conditions.

• The role of multiple prescription pain medications and non-prescription supplements to both symptom relief and/or symptom contribution must be reviewed.

• Concurrent systems disturbances include lower gastrointestinal and urogenital symptoms, commonly co-occurring with essential vulvar pain disorders which may suggest a common pathophysiology.

• Psychological factors are consistent with secondary role rather than primary aetiology. Psychological, interpersonal and sexual consequences are significant factors leading to symptomatic maintenance and resistance to functional change.

• Intrapelvic SEMG shows a pattern of pelvic floor dysfunction consistent with menstrual changes (recent onset of irregular menses), voiding disorders (retention, SUI) and essential vulvar pain disorders (DV, VVS).

Treatment

Specialty pain neurology consultation results in titration to termination of all pain, anxiolytic and soporific medications originally reported, and initiating Cymbalta 60 mg along with maintenance of hydroxazine and a lowered dose of trazadone, all taken an hour before bed. Supplements are continued as originally reported.

The patient was also referred to an endocrinologist specializing in female hormone problems including menopause transitions with sexual dysfunction. She was prescribed both topical (estrace ×2 daily) and intravaginal (vagifem daily) hormone replacement therapy (HRT).

Urological and gastrointestinal evaluations were deferred for possible later use if the initial treatment regimen did not bring about therapeutic changes in urinary and bowel symptoms.

Initiation of manualized 10-session programme of couples group sexual therapy for women suffering from vulvar pain, and their partners. This is an informational, educational, support group conducted by a psychologist using cognitive behavioural techniques and specific home assignments (Bergeron et al. 2001). For those sufferers with more profound sexual disturbances of desire, arousal and orgasm (FSFI) which offer direct interference with compliance to sexual prescriptices, brief individual therapy may also be employed, which is the case with this patient who underwent a course of brief, 10-session, weekly eclectic prescriptive therapy with a focus on addressing her general anxiety (breathing retraining), PTSD (EMDR) from childhood abuse, somatic overconcern (systematic desensitization) and sexual avoidance (dilators, sensate focus, orgasmic restoration, etc.). Both the manualized group couples therapy and the individual therapy were conducted by the first author, who also conducted the intravaginal SEMG biofeedback.

As the patient is feeling vulnerable to relapse regarding alcohol and substance use she is encouraged to return to regular 12-step programme attendance upon completion of the manualized 10-session programme of group sexual therapy for couples in which women suffer from essential vulvar pain disorders.

The intrapelvic SEMG pattern most closely matches that pattern shown by perimenopausal women (Glazer et al. 1999, Romanzi et al. 1999). The age of the patient, recent onset of irregular menses, bowel and bladder changes, vulvar dryness, sensations associated with pelvic floor relaxation, and the findings of the endocrinologist all suggest atrophic changes may be contributory to her vulvar pain. The SEMG pattern is also consistent with the symptoms of urinary retention (elevated unstable baseline) and recent onset of SUI (slow and weak urethral closure) as well as functional faecal constipation. Intrapelvic SEMG biofeedback combined with topical and intravaginal HRT has, in my clinical practice, shown positive results with this symptom pattern.

Maintenance of collaboration with all treating resources and, as needed, availability to the patient for information and support is a key part of the ongoing treatment. The average treatment duration to maximize symptom relief and re-establish related functions is 6–12 months during which time the patient returns for office visits every 1–2 months for review of progress and modifications to treatments. The coordinating therapist is informed by the patient of upcoming appointment dates with collaborating physicians who are then asked to provide a summary of their office visit with the patient. These integrated records are, in turn, available to all members of the team, and the patient, who is encouraged to maintain a full set of her own records.