The Integral Theory, Pelvic Floor Biomechanics, and Binary Innervation

Article information

Int Neurourol J. 2024;28(3):181-184
Publication date (electronic) : 2024 September 30
doi : https://doi.org/10.5213/inj.2448092.046
1Department of Urology, University of Antwerp, Edegem, Belgium
2Faculty of Medicine and Health Sciences, University of Antwerp, Edegem, Belgium
3Retired Pelvic Surgeon
Corresponding author: Jörgen Quaghebeur Department of Urology, University of Antwerp, Wilrijkstraat 10, Edegem, Belgium Email: jorgen.quaghebeur@telenet.be
Received 2024 February 9; Accepted 2024 March 18.

Abstract

The pelvic floor biomechanics and sphincter functioning are essential for understanding pelvic floor dysfunction and the pathophysiology of the pelvic organs. The pelvic floor consists of muscles, fascial connections and ligaments. The Integral Theory Paradigm (ITP) explains the musculoskeletal entity of the sphincter mechanism and the pathophysiology of pelvic organ function. The ITP explains the pelvic floor function determined by 3 directional muscle forces: forward, backwards and downward-acting muscle vector forces that form an anterior and posterior resultant. The resultant equilibrium is essential for urinary continence, voiding and defecation. Loose ligaments disturb the equilibrium of the pelvic floor’s muscular function with consequences for the organ function’s continence, evacuation, and sensory perception.

INTRODUCTION

The Integral Theory Paradigm (ITP) elucidates the biomechanics of the pelvic floor (PF) sphincter and the regulation of pelvic organ function. The PF muscles (PFM) are essential for organ support, voiding and defecation, continence, sexual function, delivery, and pelvic girdle stability [1]. The Integral Theory explains lower urinary tract symptoms (LUTS) and urogenital pelvic pain due to pelvic ligament injury and is based on the disruption of binary innervation of the pelvic organs [2-12]. The urethral and anorectal closure functions are controlled subconsciously [13-15]. Higher brain centres control the postponement of urination during the sensation of a full bladder and the voluntary opening of the sphincter when necessary [13-15]. We clarify the closure and opening of the female PF sphincter based on muscle vector forces that form an anterior and posterior resultant and enable the optimal function of the PF sphincter. We describe the dysfunction of this PF mechanism caused by weakened ligaments, disrupting the binary innervation system that regulates bladder function.

THE BIOMECHANICS OF THE PELVIC FLOOR SPHINCTER

The anterior portion of the pubococcygeus muscle (PCM), the levator plate (LP), and the conjoint longitudinal muscle of the anus (LMA) compose 3 directional muscle forces that accomplish the urethral and anal canal closure and support the pelvic organs [1,16,17]. The PCM is attached to the distal vagina and contracts forward against the pubourethral ligament (PUL). The puborectalis muscle (PRM) contracts only against the symphysis pubis. The LP attaches to the posterior wall of the rectum. The LP contracts backwards against the PUL and uterosacral ligament (USL). The LMA inserts proximal into the anterior portion of the LP and on the external anal sphincter distally. The LMA pulls only downwards against USLs [1,16-18]. Fig. 1 shows the PF sphincter mechanism and binary innervation model.

Fig. 1.

Binary innervation model and anatomical basis of the Integral Theory hypothesis. System in normal closed mode. Cortical control: Afferent impulses from stretch receptors ‘N’ are reflexly suppressed cortically (white arrows). When required, the cortex activates the micturition reflex. Peripheral control is by a musculo-elastic mechanism which responds to cortical efferents (small arrows). The 3 directional muscles (large arrows), forward, pubococcygeus muscle ‘PCM,’ backward, levator plate ‘LP,’ and downward, conjoint longitudinal muscle of the anus ‘LMA’ contract against the supporting ligaments, PUL (pubourethral) and USL (uterosacral), to stretch vagina tightly, much like the membrane of a drum. The stretched vagina supports the urine column, preventing activation of the stretch receptors ‘N,’ thereby decreasing afferent impulses to the cortex. Micturition central control (white arrows) relaxes, as does PCM (broken circle); this allows the posterior muscles LP and LMA to unrestrictedly open out the posterior wall of urethra (white broken lines) just before bladder evacuation by global detrusor muscle contraction. ATFP, arcus tendineus fascia pelvis; CL, cardinal ligament. Dysfunction weakness in the muscles PCM, LP, LMA, and/or the ligaments they contract against, PUL, USL, will affect the ability of the peripheral control mechanism to mechanically close urethra (incontinence), open it (obstructed micturition), or to suppress uncontrolled micturition by bilateral stretching of vagina by the 3 opposite muscle forces to support ‘N’ (urgency).

Forward-Acting Muscles Vector Forces

The PCM contracts against the PUL, and the PRM contracts against the symphysis pubis and act as forward muscle vector forces [1,16-18].

Backwards and Downward Muscle Vector Forces

Posterior and inferior directed muscle vector forces close the urethra by stretching the proximal urethra around the PUL [1,16-18]. The anterior vector closes the distal urethra pulling the suburethral hammock in a forward direction against the PUL and pubis. The posterior vectors, LP and LMA, open the proximal urethra during micturition when PCM relaxes and the anal canal during defecation when the PRM relaxes. These posterior vectors unlock the urethra and anorectum, exponentially reducing the internal resistance of the bladder and rectum to evacuation [1,17,18].

Resultant Equilibrium, Anterior and Posterior Vector Forces

Opposite muscle forces are at rest with zero resultant force at the level of the bladder neck. Weak PULs reduce the anterior-directed muscle force. The stronger backward muscles pull the equilibrium point zero posteriorly (broken blue lines) opening the urethra and causing SUI [8,10] (Fig. 2).

Fig. 2.

The mechanism of the pelvic floor sphincter. The figure shows zero resultant force at the level of the bladder neck. Weak PUL decrease forward muscle forces, so the stronger backward muscles pull the zero force backwards (broken blue lines). Weak USLs decrease the backward vector forces, so the stronger forward muscles pull the zero force forwards (broken red lines). CL, cardinal ligament; EAS, external anal sphincter; EUL, external urethral ligament; LMA, longitudinal muscle anus; LP, levator plate; N, bladder stretch receptors; PB, perineal body; PUL, pubourethral ligaments; USL, uterosacral ligaments; PCM, pubococcygeus muscle; PRM, puborectalis muscle.

Weak USLs reduce the backward vector forces, and the stronger forward muscles pull the vagina and equilibrium point zero forward (broken red lines) (Fig. 2). This may overtension the distal vagina and close the distal urethra more tightly, as reported in Fowler’s Syndrome [10,19]. In this situation, a larger bladder volume is needed to activate the afferent impulses to initiate the micturition reflex. This explains the larger bladder volumes at rest and retention reported in “underactive bladder.” [10,19].

LIGAMENT INJURY, BINARY INNERVATION, AND PELVIC FLOOR DYSFUNCTION

Loose USLs reduce the backwards directed contractile opening force. Consequently, the bladder and rectum empty against resistance with a nonopened urethra or rectum. Patients perceive this as obstructed voiding (e.g., hesitance, weak stream) or defecation (constipation). The external urethral and anal sphincters reinforce the urethra and anus closure [1,10]. If the PUL is weak, urinary incontinence occurs because the posterior resultant formed by the LP/LMA will pull open the posterior urethral wall [10,11,20].

The 3 directional muscle forces stretch the vagina comparable to the membrane of a drum supporting the stretch receptors in the bladder ‘N’ from below. Adequate support of the bladder (and other pelvic organs) is essential and prevents afferent proprioceptive impulses from activating the micturition reflex [17,18,20]. If the peripheral mechanism cannot stretch the vagina sufficiently, excessive afferent stimuli attain the cortex and are interpreted as urgency and frequency [10].

The muscular-ligamental system is the mechanical component of PF function, but ligament weakness or damage causes functional lesions and impaired proprioception. Uncontrolled proprioceptive stimuli, caused by ligament laxity or muscle tone, may cause LUTS [21]. Overactivity of the stretch receptors provokes a premature stimulation of the micturition reflex, with detrusor overactivity, bowel symptoms, cross-organ sensitization or sustained pelvic pain.

CONCLUSION

Muscular function, ligaments, and fascia determine the sphincter function of the organs in the small pelvis. The ITP interprets the PF function determined by 3 directional muscle forces: forward, backward and downward-acting muscle vector forces. These 3 directional forces form an anterior and posterior resultant that respectively maintain the closure and opening function of the PF sphincter. Loose ligaments disturb the PF’s muscular function with consequences for the continence, evacuation, and sensory perception of the organ function.

Notes

Grant/Fund Support

This study received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.

Conflict of Interest

No potential conflict of interest relevant to this article was reported.

AUTHOR CONTRIBUTION STATEMENT

· Conceptualization: JQ PP, JJW, SDW

· Writing - original draft: JQ PP, JJW, SDW

· Writing - review & editing: JQ PP, JJW, SDW

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Article information Continued

Fig. 1.

Binary innervation model and anatomical basis of the Integral Theory hypothesis. System in normal closed mode. Cortical control: Afferent impulses from stretch receptors ‘N’ are reflexly suppressed cortically (white arrows). When required, the cortex activates the micturition reflex. Peripheral control is by a musculo-elastic mechanism which responds to cortical efferents (small arrows). The 3 directional muscles (large arrows), forward, pubococcygeus muscle ‘PCM,’ backward, levator plate ‘LP,’ and downward, conjoint longitudinal muscle of the anus ‘LMA’ contract against the supporting ligaments, PUL (pubourethral) and USL (uterosacral), to stretch vagina tightly, much like the membrane of a drum. The stretched vagina supports the urine column, preventing activation of the stretch receptors ‘N,’ thereby decreasing afferent impulses to the cortex. Micturition central control (white arrows) relaxes, as does PCM (broken circle); this allows the posterior muscles LP and LMA to unrestrictedly open out the posterior wall of urethra (white broken lines) just before bladder evacuation by global detrusor muscle contraction. ATFP, arcus tendineus fascia pelvis; CL, cardinal ligament. Dysfunction weakness in the muscles PCM, LP, LMA, and/or the ligaments they contract against, PUL, USL, will affect the ability of the peripheral control mechanism to mechanically close urethra (incontinence), open it (obstructed micturition), or to suppress uncontrolled micturition by bilateral stretching of vagina by the 3 opposite muscle forces to support ‘N’ (urgency).

Fig. 2.

The mechanism of the pelvic floor sphincter. The figure shows zero resultant force at the level of the bladder neck. Weak PUL decrease forward muscle forces, so the stronger backward muscles pull the zero force backwards (broken blue lines). Weak USLs decrease the backward vector forces, so the stronger forward muscles pull the zero force forwards (broken red lines). CL, cardinal ligament; EAS, external anal sphincter; EUL, external urethral ligament; LMA, longitudinal muscle anus; LP, levator plate; N, bladder stretch receptors; PB, perineal body; PUL, pubourethral ligaments; USL, uterosacral ligaments; PCM, pubococcygeus muscle; PRM, puborectalis muscle.