Muscle tone, commonly referred to as muscle tension, is measured as stiffness; the change in resistance or force per unit change in length (∆force/∆dist ance) [18]. Clinically, the tone/stiffness of the pelvic floor muscles is assessed through palpation as the resistance felt when a passive stretch is applied to the muscles [36, 37]. In a normally innervated skeletal muscle, muscle tone comprises both passive (viscoelastic) and active (contractile) components [18]. Muscle activity is an active component of muscle tone and refers to the electrical activity generated by muscle fibers when the motor unit is active and propagation of action potentials is detectable by electromyography (EMG) [18]. The muscular contraction resulting from muscle activity (i.e., electrogenic contraction) contributes to muscle tone. During the measurement of muscle tone, close monitoring of EMG recordings can help identify the presence and relative contribution of electrogenic contraction. Both normal and abnormal electrogenic contraction (i.e., detectable by EMG) can occur [18]. Normal electrogenic contraction refers to contractile activity that occurs in a normal muscle because it is not completely relaxed, but can be controlled voluntarily, or due to reflex activation (e.g., myotactic stretch reflex) [18, 38]. On the other hand, muscle spasm is defined as an abnormal/pathological (involuntary) electrogenic contraction that may or may not be painful [18]. In the context of healthy normally innervated skeletal muscle, a muscle cramp can be considered to be a form of muscle spasm [18]. The pain associated with muscle spasm/cramp may be caused by the shearing forces between the “cramping” and normal (not cramping) parts of the muscle [18, 39]. In addition, pain can also occur if the muscle becomes ischemic and releases pain-producing substances, which can occur if the muscle contracts forcefully for too long, and compresses its own blood vessels [18]. Although the assessment of muscle spasm alone is challenging, its possible contribution to muscle tone must be acknowledged.

Endogenous contracture, defined as a contractile state within a muscle that is not accompanied by electrical activity (i.e., no EMG activity is detected) [18], is also considered to be an active component of muscle tone. In normal muscle, palpable taut bands that are often associated with myofascial trigger points (i.e., hypersensitive/painful spots found within the taut bands of muscle) [40], which are the hallmarks of myofascial pain syndromes, have been suggested to represent a form of endogenous muscle contracture [18]. Taut bands, within otherwise relaxed muscles, are devoid of action potentials (i.e., EMG-silent) although trigger points have been found to exhibit electrical activity at their loci [18]. To date, there is no conclusive evidence regarding the pathogenesis of trigger points and taut bands although research supports more local factors such as focal ischemia and the associated release of various biochemical substances rather than central processes [18, 38, 41]. Spinal cord mechanisms, however, are thought to mediate pain referral and local twitch responses associated with trigger points [42], and sensitization of central pain pathways is thought to play an important role in the conversion of episodic myofascial pain arising from taut bands and trigger points, to more chronic pain states [43]. It has also been suggested that muscle spasm can induce the development of trigger points, and vice versa [18]. Although trigger points and taut bands can be detected with palpation [40], their exact contribution to muscle tone, as with muscle spasm, is difficult to measure.

In a healthy skeletal muscle, an increase in muscle activity/EMG usually results in an increase in muscle tone due to the tension built-up from the contraction of muscle fibers. Hypertonic pelvic floor muscles, however, are not necessarily overactive. Muscle hypertonicity is a general increase in muscle tone that can be associated with either elevated contractile activity and/or viscoelastic stiffening in the muscle [18, 38] and may exist in the absence of muscle activity altogether. Figure 1.1 illustrates possible sources of muscle hypertonicity (measured as increased stiffness) in a normally innervated skeletal muscle.

Several passive (viscoelastic) structures are thought to contribute to the tone of skeletal muscles, including: the cross-bridges between the sarcomeric contractile proteins actin and myosin [44, 45], the extensibility of actomyosin filaments themselves [46, 47], the non-contractile proteins of the sarcomeric cytoskeletons (titin and desmin) and their filamentous connections [48–50], as well as the connective tissues (fascia) linking and covering muscle tissue [51–54]. An increase in muscle stiffness may occur due to changes in any of these passive structures, and in the absence of any detectable EMG. Both an increase (hypertrophy) and a decrease (atrophy) in a muscle’s size and mass are associated with increased muscle stiffness due to physiological adaptations of viscoelastic structures [51]. Since the sarcomeric proteins actin, myosin, titin, and desmin all reside within the muscle tissue itself, the increased stiffness that results from muscle hypertrophy [55] has been attributed in part to increases in these subcellular components [51]. Conversely, an increase in muscle stiffness seen with muscle atrophy due to disuse/immobilization is considered to primarily result from an accumulation and increased relative proportion of connective (fibrous) tissue within and surrounding the muscle [51]. Additionally, tissue adhesions (scars) resulting from injury to the muscle may also increase the viscoelastic stiffness of the muscle.

Although by definition OAPF implies a physical state of heightened activity within the pelvic floor muscles, individuals with OAPF are also commonly found to present with pelvic floor muscle hypertonicity from other sources, most notably myofascial trigger points [24, 31, 56], which are not associated with any detectable EMG. Emerging research also suggests that pelvic floor muscle hypertonicity in populations with OAPF symptoms and associated conditions may be in part due to changes in the muscles’ viscoelastic properties [57, 58]. Understanding and recognizing the various potential sources of pelvic floor muscle hypertonicity is particularly important for identifying the specific pelvic floor impairments affecting individuals with OAPF, and designing tailored treatment interventions; for example, in the case of physiotherapy, deciding whether to emphasize pelvic floor muscle awareness, control and relaxation exercises, and/or manual stretches and trigger point release techniques. In many cases, it is likely that OAPF symptoms are associated with various components of pelvic floor muscle hypertonicity and dysfunction, and a comprehensive treatment program involving a number of different techniques and strategies is usually applied to target all levels of dysfunction [32, 56, 59–61].

The relationships between the different sources of muscle tone (active and passive), and their contribution to muscle hypertonicity, remain under investigation. Although speculative, it is possible that in some cases there is a sequential pattern to the relative contribution of different elements to muscle hypertonicity. For example, a persistent lack of muscle relaxation and/or heightened (but “normal”) muscular activity may lead to involuntary muscle contraction (spasm), which may develop further into a myofascial pain syndrome involving taut bands and trigger points. Subsequently, the lack of movement/disuse of the muscles can lead to adaptive changes in their passive structures and result in viscoelastic stiffening. Given that the etiology of OAPF is poorly understood, the existence of relationships between the different components of muscle tone and a possible chronological nature to the development of muscle hypertonicity could be helpful in advancing knowledge on the pathogenesis of OAPF, as well as the duration and severity of impairments. Further research, however, is needed to elucidate these concepts, which for now remain hypothetical.

Of high relevance to the topic of OAPF, is the concept of “unnecessary” muscle tension [18]. In addition to the aforementioned active and passive components of muscle tone, Simons and Mense proposed that a type of muscular activity that is unintentional, but that is not a “spasm,” exists and is the source of what is often referred to clinically as “muscle tension” [18]. These authors note that this unnecessary/unintentional muscle activity, which is amenable to voluntary control with training (e.g., through biofeedback assistance), may arise from psychological distress or anxiety, overload from sustained contraction or repetitive activity, and/or inefficient use of muscles [18]. These sources of increased muscular activity, as they may pertain to OAPF, are discussed later in this chapter.

OAPF may well be “the organic substrate causing both different kinds of urethral, vaginal, and anal outlet obstruction and different kinds of [genital/pelvic] pain as well as sexual dysfunctions ” [23]. According to Van Lunsen and Ramakers this is supported by empirical evidence, including research demonstrating the effectiveness of physiotherapy interventions aimed at improving pelvic floor muscle relaxation on symptoms of conditions associated with OAPF (e.g., vulvodynia, prostatodynia, dysfunctional voiding, constipation) [23]. The mechanisms underlying the onset of OAPF, however, are not fully understood.

The coexistence of different kinds of urinary, anorectal, and gynecological problems, sexual difficulties, genital/pelvic pain, and psychological distress in individuals with OAPF suggests that, as per its clinical presentation, the etiology of OAPF is likely multifactorial. OAPF is thought to occur as a “conditioned response to threat” [23], which may come in different forms. A variety of risk factors or etiological determinants have been proposed to explain the onset and maintenance of OAPF.

Pelvic pain, which refers to pain located anywhere in the genital, pelvic, and lower abdominal region, which may itself result from OAPF, is also considered to be the predominant cause of OAPF [24]. Pelvic pain has several possible origins and perpetuating factors, including physical injury or pathology affecting any biological tissue (musculoskeletal, neural, visceral) within the pelvic area or distant structures with pain referral patterns to this region, as well as psychological, psychosocial, and/or psychosexual distress [33, 62, 63], which in turn are also risk factors for the onset of OAPF. Additional potential triggers for the development of OAPF include abnormal patterns of pelvic floor muscle use, direct trauma and/or pathology, and postural abnormalities resulting from faulty postures, sustained positions, repetitive activities and/or skeletal asymmetries. Identifying the underlying cause(s) and perpetuating factors of OAPF, although often challenging, may be of significant importance when attempting to break the “vicious cycle” of ongoing pelvic dysfunction and pain experienced by affected individuals.