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Keywords:

  • female;
  • pelvic pain;
  • physical therapy

Abstract

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. DISCUSSION
  5. REFERENCES

The multisystem nature of female chronic pelvic pain (CPP) makes this condition a challenge for physical therapists and other health care providers to manage. This article uses a case scenario to illustrate commonly reported somatic, visceral, and neurologic symptoms and their associated health and participation impact in a female with CPP. Differential diagnosis of pain generators requires an in-depth understanding of possible anatomic and physiologic contributors to this disorder. This article provides a detailed discussion of the relevant clinical anatomy with specific attention to complex interrelationships between anatomic structures potentially leading to the patient's pain. In addition, it describes the physical therapy management specific to this case, including examination, differential diagnosis, and progression of interventions. Clin. Anat. 26:77–88, 2013. © 2012 Wiley Periodicals, Inc.


INTRODUCTION

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. DISCUSSION
  5. REFERENCES

Chronic pelvic pain (CPP) is defined as noncyclic pain for greater than 6 months located between the level of the umbilicus and above the knees (Paulson and Gor,2007). Female CPP is both a prevalent and costly condition. In a study by Mathias et al. (1996), 15% of surveyed women indicated CPP with these women indicating lower general health compared to those without CPP. In addition, the total annual direct costs for physician visits for this condition were estimated to be at $881.5 million US dollars per year.

Female chronic pelvic pain is considered a multisystem disorder, with symptoms arising from neurological, gynecologic, musculoskeletal, urinary, gastrointestinal, and/or endocrine conditions. In addition, CPP is further affected by behavioral and psychological factors (Gunter,2003; Apte et al.,2012). Thus, diagnosing and managing the contributors to female CPP can be quite challenging. Differential diagnosis of CPP requires the managing clinician to have a comprehensive knowledge of the anatomy and physiology of the musculoskeletal, gynecologic, urinary, gastrointestinal, endocrine, and nervous systems. In addition, understanding of psychological triggers of pain and their role in CPP is critical (Hilton and Vandyken,2011).

The purpose of this article is to describe, using a patient case scenario, the physical therapy (PT) management of female CPP. Particular attention will be directed toward the anatomical contributors to this patient's pain. Although this scenario does not represent an actual patient, it does reflect the PT management of numerous patients seen by the authors of this article.

Case Description: Patient History and Initial Data Collection

The patient was a 26-year-old female with a diagnosis of pelvic pain referred by her gynecologist to PT. She worked as a finance administrator at a local university. Her job required her to sit at her desk most of the day. Because her pain escalated during prolonged sitting, she indicated the need to take frequent “standing breaks” about every hour. When asked about other activities that exacerbated her pain, she indicated pain with intercourse.

She reported she had been suffering with the pain for over 2 years. On a pain scale and pain diagram (Farrar et al.,2001; Kahl and Cleland,2005), she noted 6/10 intensity of pain located in the lower abdomen, left groin area, and low back with radiation to the left and right buttock and left posterior mid-thigh.

Despite her pain, she exercised 6 days a week at a local health club. She faithfully attended Yoga classes and adhered to a rigorous abdominal strengthening program including “crunches and planks.” Because she had been active through college as a gymnast, she was reluctant to give up her exercise routine. She revealed little optimism that PT would help her pain. The only reason she pursued the appointment was because she recently began experiencing strong urges to urinate and was voiding every hour during waking hours. When asked about bowel habits, she indicated that she was only able to produce a bowel movement two to three times per week. Her bowel movements were hard, requiring a great deal of straining to evacuate. She also often sensed stools remained in her rectum following a bowel movement.

To further determine the health and participation impact of this patient's symptoms, she was asked to complete five questionnaires at the initial visit (see Table 1). Internal consistency, reliability, and validity of all of these measures have been reported (Brown et al.,1999; Fairbank and Pynsent,2000; Rosen et al.,2000; Varma et al.,2008). Data from these questionnaires revealed a moderate degree of bother associated with symptoms of urinary frequency and urgency; large impact of symptoms on the ability to enjoy intercourse and to achieve orgasm; a high level of pain with intercourse; bowel symptoms of obstructive defecation and poor colonic inertia; moderate level of pain with sitting and standing; and slight life impact on personal care ability, social interactions and ability to travel (Brown et al.,1999; Fairbank and Pynsent,2000; Rosen et al.,2000; Varma et al.,2008).

Table 1. Health and Participation Impact Questionnaires Scores at Initial and Discharge Examinations
  1. The Urge-UDI and Urge-IIQ measure the presence of urge-related urinary incontinence symptoms and perceived symptom-related bother and the impact of these symptoms on health-related quality of life, respectively. Urge-UDI scores range from 0-4 with a greater score indicating greater symptom-related distress. Urge-IIQ scores in each domain range from 0-6 with higher scores indicated greater symptom impact on quality of life (Brown, et al., 1999).

  2. The FSFI measures sexual function across 6 domains, including pain associated with intercourse. This patient was asked to answer only the FSFI Pain Domain questions. FSFI Pain Subscale Scores range from 0-6 with lower scores indicating greater pain associated with intercourse (Rosen, et al., 2000).

  3. The CSI includes 3 subscales (Obstructive Defecation, Colonic Inertia, and Pain) and measures the frequency, severity, and perceived bother associated with symptoms of constipation. CSI Total Score ranges from 0-73 (Subscales: Obstructive Defecation (0-28); Colonic Inertia (0-29); and Pain (0-16)) with higher scores indicating more frequent, severe, and bothersome constipation symptoms (Varma, et al., 2008).

  4. The ODI measures symptoms in persons with low back pain. It is scored on a 100 points (%) scale, with lower numbers indicating fewer symptoms. The minimally clinically important difference (MCID) is defined as 6 points (Fairbank and Pynsent, 2000).

 Urge-Urinary Distress Inventory (Urge-UDI)Female Sexual Function Index (FSFI)Constipation Severity Index (CSI)Oswestry Disability Index (ODI)
 Urge-Incontinence Impact Questionnaire (Urge-IIQ)
Initial ScoreUrge-UDI Score = 2.7Pain Subscale = 1.4Obstructive32%
Urge- IIQ Domain Scores defecation = 17 
 Activities = 2.3 Colonic inertia = 16 
 Travel = 1.5 Pain = 4 
 Physical activites = 1 Total = 37 
 Feelings = 2.25   
 Relationships = 1.75   
 Sexual function = 4   
Discharge ScoreUrge-UDI Score = 0.67Pain Subscale = 5.2Obstructive6%
Urge- IIQ Domain Scores defecation = 6 
 Activities = 0.57 Colonic inertia = 5 
 Travel = 0 Pain = 2 
 Physical activities = 0 Total = 13 
 Feelings = 0.50   
 Relationships = 0.33   
 Sexual function = 1.5   

Relevant Anatomy

The patient-identified problem list: pain with prolonged sitting, dyspareunia, urinary urgency and frequency, and constipation requires ordered examination of specific tissues, including those of the musculoskeletal, urologic, gynecologic, gastroenterologic, and neural systems. Such an extensive examination is vital to enable the clinician to differentiate between numerous possible pain generators. In order for the clinician to proceed successfully with the examination and subsequent diagnosis, a sound anatomical knowledge based is crucial.

Bony Pelvis, Supportive Ligaments, and Innervation

The bony pelvic ring contains three bones, including two innominate bones (comprised of the ilium, ischium, and pubis) and the sacrum (Williams et al.,1989). The symphysis pubis, a secondary cartilaginous joint, conjoins the ilia anteriorly and is innervated by branches of the iliohypogastric, ilioinguinal, and pudendal nerves (Standring,2008). The symphysis pubis promotes effective load transfer from one side of the pelvis to the other during gait. During sport and exercise, biomechanical strain increases due to magnified forces across the symphysis pubis and in this patient may play a role in her groin pain (Cunningham et al.,2007). In addition, it is important to note that the empty bladder and urethra is located posterior to the symphysis pubis (Standring,2008 p 1084 fig 63.3). Therefore, excessive symphysis pubis motion may contribute to her complaints of urinary urgency and frequency.

The sacrum consists of five fused vertebra creating the base of the vertebral column. It articulates with the two ilia through which load is transferred from the trunk to the limbs during upright movement (Snijders et al.,1993; Mens et al., 1996).The sacroiliac (SI) joints, modified synovial planar joints, consist of auricular-shaped synovial joints with hyaline cartilage on the ventral surface and interosseous ligament/fibrocartilage on the dorsal surface. Sacroiliac joint stability relies upon both form closure and force closure to maintain stability during weight bearing. Form closure is created by joint surface topography to resist shear forces along with ligamentous support. Force closure is created by dynamic muscle support generated across multiple joints. A dynamic relationship exists between the amount of form and force closure required to prevent regional pain (Pool-Goudzwaard et al.,1998).

Innervation to the SI joints is diverse creating the potential for varied pain-referral presentation (Slipman et al.,2000; Zelle et al.,2005, Simopoulos et al., 2012). Several researchers have reported that SI joint innervation stems from the dorsal rami of the lumbosacral region (Grob et al.,1995; Fortin et al.,1999; Murata et al.,2001). Murata's rat dissection study indicates that the ventral SI joints appear to be innervated from the upper lumbar (L1-3) dorsal root ganglia as well as the lower lumbar and sacral (L3-5 [L6 in rats] and S1-2) dorsal root ganglia; and dorsal SI joints appear to be innervated from the lower lumbar and sacral (L4-5 [L6 in rats] and S1-2) dorsal root ganglia. This L1-3 ventral SI joint innervation may contribute to groin pain in this particular patient (Murata et al.,2001). Fortin et al. (1999) pain mapped the SI joint capsule via intraarticular injection noting innervation most likely derived from S1-3 (S4) dorsal rami. This finding may explain the patient's complaint of low back pain with radiation into the thigh.

The pelvic ring is thought to be very stable with up to 4° of angular movement at the SI joints (Sturesson et al.,1989; Jacob and Kissling,1995). Form closure is assisted by the anterior and posterior sacroiliac interosseous ligaments, which resist shear forces in the SI joint. Cadaveric dissection of these ligaments has shown increased SI joint movement, supporting these ligaments are vital to form closure (Simonian et al.,1994). Key extrinsic ligaments, including the iliolumbar and long SI joint ligament assists form closure (Vleeming et al.,1996; Pool-Goudzwaard et al.,2003). Inferiorly, the sacrotuberous ligament, posterior sacroiliac ligament, and to a lesser degree, the sacrospinous ligament work to control sacral base motion (Williams et al.,1989). Ligamentous laxity can occur with joint hypermobility syndrome, hormonal and structural changes during and after pregnancy (Borell and Fernstrom,1957), and repetitive end range motion associated with sport (Standaert,2002). In this patient case, years of gymnastics most likely led to ligamentous laxity and could be a potential cause of her pelvic pain (Wilder et al.,1980).

The empty rectum rests on the pelvic surface of the sacrum and coccyx ending superior to the pelvic floor at the anorectal junction. Proximity of the SI joint and lumbosacral plexus to the sigmoid colon and rectum is significant in considering possible pain generators (Guvencer et al.,2009). The lumbosacral plexus lies dorsal to the rectum and ventral to the sacrum and piriformis muscle (Standring, 2008 p 1091–2 fig 63.9 and 63.10). Considering the patient's history of constipation, pressure from chronic hard stool storage in the rectum anatomically could contribute to neural, joint and soft tissue irritation around the SI joint (Guvencer et al.,2009).

Coccyx

The coccyx, often implicated in CPP (Howorth,1959), articulates with the 5th sacral vertebrae via the sacrococcygeal junction. It receives its innervation from the coccygeal plexus with contributions described as arising primarily from the L4-5 ventral rami and the coccygeal ventral rami. (Standring,2008; p 1092–3; Woon and Stringer,2012). The coccyx can be a common site of pain referral from soft tissues within the pelvis (Wise and Anderson, 2010). Ligamentous and muscular attachments add joint stability and neurovascular support during various sacrococcygeal stressors including repetitive movement, prolonged sitting, falls, vaginal delivery, and chronic straining associated with constipation.

Muscles of the Pelvic Floor

Key pain generating muscles within the pelvis include the coccygeus, levator ani, obturator internus, piriformis, and to a lesser degree, the muscles of the urogenital diaphragm (Bo and Sherburn,2005). These muscles are often grouped as the “pelvic floor muscles” (PFMS). Unfortunately, there is a lack of attention given to the unique actions that each muscle efficiently performs to support defecation, urination, sexual satisfaction, and postural support during gait (Pool-Goudswaard,2004; Peters,2006; Frawley,2007; Apte,2012).

The coccygeus (ischiococcygeus) originates from the pelvic surface of the ischial spine where it joins the sacrospinous ligament to insert onto the sacrum and coccyx (Williams et al.,1989). It is innervated by the sacral plexus (S3-4) (Standring,2008; p 1085) and can be implicated in isolation or along with the coccyx as a pain generator. Identification of impaired coccyx function from coccygeus irritation is key to determining the appropriate treatment intervention. The coccygeus is of particular relevance in cases of pain associated with sitting, vaginal delivery, or chronic constipation due to prolonged, repetitive, or traumatic irritation and compression of tissues.

The levator ani muscles (LA) comprise the deep pelvic diaphragm (Bo and Sherburn,2005). The LA is most commonly divided from medial to lateral into the puborectalis (PR), pubococcygeus (PC) (pubovisceralis), and Iliococcygeus (IC). The PR slings around the anorectal junction creating the anorectal angle below the coccyx, and functions to occlude the anorectal junction to maintain fecal continence. The pubococcygeus (PC) originates from the pubis with attachment into the perineal body, mid-urethral level of the vaginal vault, as well as intersphincteric groove and anoderm (Kearney,2004). The LA has numerous functions. It pulls the perineal body anteriorly and cephalad toward the pubis to support urinary continence (Retzky and Rogers,1995). It also elevates the mid-urethral vaginal vault and anus. It serves as an inner-core muscle to provide lumbopelvic stability, and it protects the pelvic girdle by resisting increases in intra-abdominal pressure (Mens et al.,2006). It also contracts during orgasm and to promote bowel and bladder continence. Of equal importance, is its ability to relax volitionally to assist normal urination and defecation (Rao et al.,2001; Fitzgerald et al.,2003). The IC originates from the tendinous arc of the levator ani and inserts into the iliococcygeal raphe creating a supportive diaphragm posteriorly (Kearney et al.,2004) to resist elevated intraabdominal pressures (Parks et al.,1962; Wei and DeLancey,2004).

Over the past decade, there has been much controversy regarding the innervation of the LA muscles (Barber et al.,2002; Grigorescu et al.,2008). Current cadaveric dissection (Grigorescu et al.,2008) supports the PR receiving equal innervation by the inferior rectal and perineal branches of the pudendal nerve (S2-4). Pubococcygeus innervation is primarily from the perineal branch of the pudendal nerve (S2-4) with secondary innvervation from the nerve to the levator ani (S3 and/or S4). The IC appears to be primarily innervated by the nerve to the levator ani (S3 and/or S4). Of the nerves responsible for deep pelvic diaphragm innervation, the pudendal nerve has the greatest potential for impingement. Compression can occur between the coccygeus and piriformis muscles, between the sacrospinous and sacrotuberous ligaments, or within Alcock's canal, medial to the ischial tuberosity (Popeney et al.,2007).

The superficial pelvic diaphragm assists the deeper pelvic diaphragm in its sphincteric and supportive roles. The superficial pelvic diaphragm is comprised of the urogenital triangle and includes the bulbospongiosus, ischiocavernosus, and superficial transverse perineal muscles. These muscles are a common site for trigger points as a potential source for nocioception (Pastore and Katzman,2012). Finally, the external anal sphincter (EAS), although embryologically distinct from the LA, works synchronously with the LA to coordinate fecal continence and defecation (Rassmussen,1994; Parker and Coller,2007). Because the functional history of the patient includes chronic bearing down, incomplete bowel movements, and constipation, a thorough examination of the muscles of the deep and superficial pelvic diaphragm and the EAS for incoordination, weakness, and/or spasm is critical.

Muscles of the Pelvic Wall

The patient's symptoms also require examination of the muscles of the pelvic wall. Of particular relevance is the obturator internus (OI) muscle. The origin of the OI includes the medial surface of the lateral wall of the pelvis (Standring,2008; Sinnatamby,2011, p 289–290). This is a more extensive description of the OI's origin than presented in other authors (Williams et al., 1987). The OI exits the pelvic bowl at a 90° angle posterior to the ischial spine with anterosuperior insertion onto the greater trochanter via a conjoint tendon with the piriformis (Solomon et al.,2010). It is innervated by the nerve to the obturator internus (Aung et al.,2001). The OI is known for its functional role as a hip lateral rotator and abductor when the hip is flexed. Its role as a femoral head stabilizer (Moore and Dalley,2006) is essential for posterior femoral glide during hip flexion (Sahrmann,2002) is underappreciated. This muscle has been implicated as a source of hip (Rohde and Ziran,2003; Cox and Bakkum,2005; Bushfield and Romero,2009) and pelvic floor pain including dyspareunia (Prather and Spitznagle,2007); a site of pudendal and sciatic nerve impingement (Rohde and Ziran,2003; Gajraj,2005; Murata et al.,2009; Weiss, 2010; Martin et al.,2011); and potentially mistaken as piriformis syndrome (Dalmau-Carolà,2005; Windisch et al.,2007). The OI may be implicated in this patient case given her symptoms of anterior groin pain (Busfield and Romero,2009) and dyspareunia (Simons and Travel,1983). In addition, her symptoms of urinary urgency may reflect the OI's close origin to the urethra (Standring,2008; p 1087 Fig. 63.5).

In this patient case, further investigation of the OI is needed to identify the relationship between this muscle and other local structures. For example, pain upon palpation of both the LA and OI muscles is a common clinical finding in women with CPP. These two muscles are linked anatomically as the tendinous arc of the LA is derived from the fascia of the OI. In addition, the OI's innervation, from the nerve to the obturator Internus (L5-S2) overlaps with the innervation of the LA (S2-S4), (Williams et al.,1989, p 1144).

Another important muscle coupling to consider involves the OI and piriformis muscle (PM). The PM, a pelvic wall muscle, is often misinterpreted as the primary source of pelvic pain. The PM functions as a hip lateral rotator with its origin arising from the anterior wall of the sacrum (S2-4) (Solomon et al.,2010) and exits the pelvis from the superior sciatic foramen to insert onto the greater trochanter of the femur. In cadaveric dissection studies, the IO and PM often share a common attachment into the superoanterior aspect of the greater trochanter (Pine et al.,2011). These muscles also have overlapping innervations from the dorsal rami of S1-2 (PM) and L5-S1-2 (OI) (Moore and Dalley,2006; p. 371).

Muscles of the pelvic wall may become symptomatic and overactive due to the failure of other regional muscles to provide lumbopelvic stabilization during movement. For example, muscles with origins external to the pelvic bowl, including the diaphragm, multifidus, internal obliques, and gluteus maximus, may exhibit altered activation during lumbopelvic load transfer (Hungerford et al.,2003). When this occurs, inefficient and ineffective load transfer through the pelvis and pain during gait or sport, as illustrated in this patient case, results.

Visceral Innervation

The patient has both musculoskeletal and visceral complaints. The relevant relationships between the musculoskeletal and visceral anatomy have been discussed previously. However, innervations of these systems differ substantially. Somatic structures are innervated according to segmental levels. Thus, when somatic structures are involved, pain is perceived in a localized area (Rogers, 1998; p. 31–58). Alternately, when autonomic nervous system (ANS) innervations to visceral structures are involved, generalized, or regional pain is sensed. This is due to the diffuse plexus-like vascular and neural supply of the ANS to the abdominal and pelvic viscera.

The sympathetic nerve supply to the abdominal and pelvic viscera is represented at spinal cord levels T6-L2. The sympathetic nervous system is responsible for nocioception of dull ache and generalized pain (Cervero and Tattersall,1986). The parasympathetic innervation to the abdominal viscera and ovaries descends from the brain stem through the vagus nerve (Cervero and Tattersall,1986). The parasympathetic system provides visceral sensations of hunger, nausea, bladder, and rectal compliance, and sexual sensation (Cervero and Tattersall,1986). The parasympathetic system also has the unique property of nocioceptive mediation from all organs except the uterus (McDonald,2001).

Afferent fibers of the ANS arise from the uterus, cervix, vagina, base of the bladder, proximal urethra, and the internal anorectal area. The efferent pelvic visceral innervation emerges from the spinal cord at S2-4 and intermingles with the somatic nerves on their way to their final innervations (Rogers, 1998; p. 31–58). They follow the same pathway back to the spinal cord as the afferent branches of the somatic system which leads to the convergence or neural cross-talk between the two systems. This crosstalk is necessary for normal regulation of sexual, bladder, and bowel function (Rogers, 1998; p. 31–58; Pezzone et al.,2005; Ustinova et al.,2010).

Any pathology involving these neural pathways can lead to the development of central sensitization, which is defined as a pathophysiological state characterized by generalized or wide-spread hypersensitivity (Devor and Seltzer,1999). Several published articles support this definition of central sensitization through the hypothesis of visceral/somatic convergence. This afferent convergence of impulses onto the dorsal horn at the spinal cord can result in muscle and visceral dysfunction. Muscle abnormalities may include myofascial trigger points, heightened resting tone, and decreased strength. Visceral dysfunctions may include diffuse pain and impaired bowel or bladder function (Markwell,2001; Weiss,2001; Butrick,2003; Tu et al.,2008). Thus, the widespread somatic symptoms and visceral complaints of bladder urgency/frequency in this patient case may be explained by convergence of aberrant or excessive afferent input into the dorsal horn from either or both visceral and somatic structures (Baker,1993; Glazer et al.,1999; Butrick,2003).

Clinical Examination and Results

Management of patients with chronic pelvic pain requires multidisciplinary care including timely referral to PT following adequate medical assessment. Prior to PT examination, the patient in this case had undergone recent examinations by her primary care physician and gynecologist. This was important to rule out other conditions with potential to cause pelvic pain including abdominal and pelvic masses, endometriosis, and urinary tract infection. In addition, the patient was seen by a urogynecologist who conducted urodynamic testing which confirmed normal bladder capacity, normal detrusor function during bladder filling, and coordinated PFM relaxation with voiding.

As noted previously, the complexity of the patient's symptoms required the physical therapist to conduct a comprehensive examination of multiple systems. Tests and measures, the rationale for selecting tests and measures, and examination findings for this patient are listed in Table 2.

Table 2. Physical Therapy Tests and Measures, their Rationale for Selection, Test Results and Selected Interventions
Tests and measuresRationale for testingFindingIntervention
Observation of Posture (Baker 1993; Montenegro et al., 2009)Pain in sitting• Forward head• Thoracokyphosis • Posterior Pelvic Ti4tPostural correction Work station ergonomics
Neurological Screen• Deep Tendon Reflexes (L3-L5; S1) • Sensation (Dermatomes L1-S1) • Strength (Myotomes L1-S1)Rule out spinal nerve impingement.(-) neurologic screen 
Tests for Pelvic and Sacral Asymmetry • Palpation of Pelvic and Sacral Landmarks (Cibulka and Koldehoff, 2009)○ Fortin's sign (Fortin and Falco, 1997; Levangie P, 1999)• Pelvic symmetry during motion testing (Cibulka and Koldehoff, 2009)○ Standing/seated forward lumbosacral flexion ○ Standing lumbosacral extension ○ Gillett's test: Standing unilateral hip and knee flexion (Meijne et al., 1999)Identify painful tissuesRule out pelvic asymmetry as cause of dyspareunia and anterior groin, low back and posterior thigh painPain over left posterior superior iliac spine (PSIS) (+ Fortin's sign) Increased mobility of left compared to right PSIS with lumbopelvic flexion Pain and limited mobility on left with lumbosacral extensionCorrection of Pelvic Asymmetry Manipulation of Sacro-iliac (SI) joint (Assendelft, et al., 2003)
Tests for load transfer• Balance on one leg○ Trendelenburg• Active Straight Leg Raise (ASLR)Drop/lateral shift of the hip can indicate hip/pelvic muscle weakness or inhibitionIdentify load transfer impairment in trunk or SI jointMaintained balanceLeft hip abductor weakness Patient indicated difficulty lifting left leg Manual compression to the iliac crests improves ASLRHip abductor strengthening in sidelying (static) and standing (dynamic) SI belt for weight bearing activities (Dreyfuss et al., 2004) Strengthen abdominal and pelvic muscles (see below)
Tests for SI joint pain provocation (Laslett et al., 2003; Laslett et al., 2005; Young et al., 2003; Petersen et al.,2004)• FABER • Posterior Thigh Thrust • Gaenslen's • Resisted Abduction • SI joint compressionTest clusters to confirm SI joint as pain generatorPain reported over left SI joint region on all testsSI joint manipulation SI beltPelvic and trunk strengthening exercises
Lumbar mobility Testing (Hicks, et al., 2003) • Lumbar extension ROM (weight bearing versus non- weight bearing) • Posterior to anterior (PA) segmental mobility • Prone instability testLow back pain (LBP) radiating to posterior thigh Compare trunk extension in weight bearing vs non- weight bearing to r/o lumbar instability (Hicks et al., 2003) Identify facet or discogneic irritability as cause of LBP and posterior thigh pain Standardized test to assess passive components of lumbar spineDecreased lumbar extension in weight bearing Full lumbar extension in non-weight bearing PA glides are non-painful with increased motion L4-L5 facets + prone instability testTrunk and Pelvic Stabilization Deep Muscles of the Core (Sapsford and Hodges, 2001; Richardson et al., 2002; Moseley et al., 2001)○ Multifitus○ Transverse abdominus○ Levator Ani○ Diaphragm Global Muscle Stabilization (Kavcic et al., 2004)○ Gradual progression to include high level exercise coordinated with deep muscles of the core
Hip Screen/Examination (Magee, 2006)• Hip ROM • Labral Tests • FABER Test : Supine • Hip muscle strength○ Abductors○ Extensors○ Lateral rotatorsLeft groin pain Test for labral tearTest for hip joint pathology Load transfer impacted by hip muscle weakness or SI joint dysfunction leading to hip muscle inhibition. (Laslett, 2003; O'Sullivan et al., 2002)Pain with end range left flexion; limited left hip medial rotation negative negative Left hip laterall rotator, gluteus medius and gluteus maximus weaknessMobilization of femoral head to restore pain-free flexion Gluteus Maximus activation Resolve OI trigger pointsProgressive hip muscle strengthening program.
Trunk Muscle Strength (Magee, 2006) • Abdominal Muscle Assessment○ Rectus Abdominus (RA) ○ Transversus Abdominus (TA) ○ Multifidus Muscle AssessmentRA strengthening may lead to increased abdominal pressure Altered RA activation and poor TA activation noted in women with urinary incontinence (Sapsford et al., 2008) Altered activation of Multifidus during load transfer through pelvis in the presence of SIJ pain (Hungerford et al., 2003)Normal RA strength Poor TA activation and RA over-activitation Multifidus underactivationSee above with trunk stabilization exercises
Soft tissue mobility of the abdomen, pelvis and thighs• Connective tissue mobility testing (Holey and Lawler, 1995) • Myofascial tender point and/or trigger point (Simons, Travell and Simmons, 1999)Pain with sitting and intimacy Habitual straining (Simons, Travell and Simmons, 1999)Soft tissue restriction Tender points (allodynia) Trigger pointsSoft tissue mobilization in the abdomen, hip and pelvic floor
Internal vaginal and rectal examination• Soft tissue palpation • Muscle○ Levator ani (LA) and external anal sphincter (EAS) strength (Laycock et al., 1994; Dorey, 2003)○ Activation and relaxation (coordination) of LA and EAS (Laycock and Jerwood, 2001) (Rao, 2001)(Rao et al., 2004)• Presence of Pelvic organ prolapse (POP) (Bump et al., 1996) • Sensation (external and internal) • SC joint mobilityIdentify painful and stiff tissues; and contributors to dyspareunia, constipation, and pain with sitting (Weiss, 2001; Fitzgerald et al., 2009) LA muscles support bladder, assist urethral closure (Clark et al., 2010). LA and EAS relaxation necessary to prevent straining with voids and bowel movements and to lessen risk of POP (Sapsford, 1998) Effects of bowel straining on pudendal nervePain response (allodynia) and muscle spasm to palpation of bilateral LA, OI at the anterior pubic ramus, Tendinous Arc (left > right), and EAS/ PR LA weakness Normal strength of EAS Inability to fully relax LA and EAS following muscle contraction and when asked to expel examiners finger from rectum Grade I rectoceleSensation Intact Normal SC joint mobilitySee above for soft tissue mobilization LA and EAS strengthening and coordination training after reducing muscle spasm with soft tissue mobilization (Anderson et al., 2001; Laycock and Jerwood, 2001)Toileting position and defecatory mechanics to improve constipation, and prevent POP and neural traction(Rao et al., 2006) (Chiarelli, 2002)
Bladder symptomsDifferential diagnosis of frequency/urgency vs. other painful bladder syndromes (Abrams et al., 2002)Bladder urgency (constant feeling to urinate) and frequency 20x/day (8x/day is normal) (Abrams et al., 2002)No pain is reported with urgency or voiding of urineUrge suppression strategies (Bø and Berghmans, 2000) Delayed voiding strategies to increase compliance of the bladder and decrease the frequency (Burgio and Borello-France, 2007)
Central Sensitization Symptoms(Nijs et al., 2010; Woolf, 2011) • Allodynia (exaggerated pain responses to low intensity mechanical stimuli) • Multisystem Involvement (visceral organ and somatic tissue symptoms)• Psychosocial changes (fear avoidance, catastrophization)Patient report of pain location, duration, and qualityPain > 6 months Allodynia Diffuse pain distributionStatements of decreased optimism Constipation and recent symptoms of urinary dysfunctionDown regulation of the nervous system–especially sympathetic system (Nijs et al., 2010; Woolf, 2011)• Diaphragmatic Breathing (Bush et al., 2011) • Paradoxical Relaxation (Anderson et al., 2011) • Behavioral techniques to reduce pain related fear (Vlaeyen et al., 2002)

Physical Therapy Diagnosis

This patient presented with a musculoskeletal pattern consistent with primary SI joint and PFM dysfunction, and secondary hip dysfunction. Her pain was unilateral, radiating to the groin and posterior thigh lower than L5, and occurred with sitting and rising from a seated posture. Decreased stability of the SI joint was demonstrated via testing of static and dynamic movements, poor load transfer, and pain provocation at the SI joint (Laslett et al.,2003, 2005; Young,2003; Petersen et al.,2004). In addition, PFM dysfunction was hypothesized to occur due to these muscles attempting to stabilize the unstable SI joint, and to support the load caused by increased intrabdominal pressure secondary to chronic constipation/straining and excessive rectus abdominus exercise. Pelvic floor muscle dysfunction was confirmed by the presence of muscle spasm, trigger points, and decreased medial hip rotation due to a tight/painful left OI and PM. Her symptoms progressed over time to a chronic pain classification with complaints consistent with central sensitization including allodynia, pain radiation into the thigh, groin and abdomen, connective tissue restrictions, and pelvic visceral involvement including recent onset of urinary urgency/frequency and dyspareunia (Devor and Seltzer,1999; Nijs et al.,2010; Woolf, 2011).

DISCUSSION

  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. DISCUSSION
  5. REFERENCES

Historically, the average duration of CPP is 2.5 years with inadequate consensus as to optimal management strategies to shorten this time-line (Reiter and Gambone, 1999). It is essential for the primary healthcare provider to recognize that musculoskeletal structures within the pelvis can be primary pain generators early in the evolution of CPP (Butrik,2009). In cases of visceral organ pathology, these same structures can be responsible for perpetuating pain long after the visceral pathology has been medically or surgically managed (Montenegro et al.,2008; Butrik,2009). Early multifaceted assessment and intervention by physicians, physician assistants, nurse practitioners, and PTs who are experts in both orthopedic and pelvic floor differential diagnosis is needed to expedite resolution of musculoskeletal impairments to avoid pathologic visceral somatic convergence with resultant hypersensitivity of the pelvic region (Montenegro et al.,2008; Ortiz,2008; Petersen and Giraldi,2008; Nijs et al.,2010; Kotarinos,2012). Unfortunately in this case, the patient initially received fragmented care that inadequately addressed emerging multi-system involvement. This progression into symptom chronicity allowed for visceral and somatic systems to evolve into a central sensitized CPP state, further compounding this patient's initial symptoms.

Interventions selected in this case were pain relieving and restorative in nature (see Table 2). Initial treatment focused on dampening the presence of central sensitization (Nijs et al.,2010; Woolf, 2011). Training in diaphragmatic breathing and paradoxical relaxation (Anderson et al.,2011) has been shown to decrease sensitivity of the sympathetic nervous system (Nijs et al.,2010; Woolf, 2011; Busch et al.,2012). With therapist direction, the patient was also encouraged to initiate a simple cardiovascular walking program aimed to lower her stress and anxiety regarding her condition and to improve her feeling of well-being (Hoffman and Hoffman,2008; Ströhle,2009).

Patient education was introduced early in the rehabilitation process. Habitual postural patterns common in CPP (Baker,1993; Montenegro et al.,2009) required patient self-correction to reduce symptoms attributed to abnormal tissue compression. The patient was instructed to apply correct sitting posture at her workstation (cervical and scapular retraction; thoracic extension with weight distributed on ischial tuberosities) to reduce pressure on the coccygeal region. To reinforce this behavior at work, the therapist suggested the patient set her computer to chime hourly to prompt self-postural correction and PFM relaxation. The patient was also educated to avoid activities that could cause further tissue compression, increase intraabdominal pressure, and contribute to trigger point development (Kotarinos,2012) including planks, sit ups, and straining with bowel movements (Hodges and Gandevia,2000).

Once the patient was independent with home management strategies to quiet global symptoms, the SI joint as a primary pain generator was addressed. Evidence for manipulation and joint oscillations to correct perceived pelvic asymmetries is not well supported in the literature. However, manipulation has been shown to reduce pain and hypothesized to increase activation of inhibited muscles surrounding the joint (Assendelft, et al.,2003). A SIJ belt was also recommended to decrease patient symptoms during progressive aerobic activities (Dreyfuss, et al.,2004).

Coccygeal, urological, and defecatory-based pain can be caused by myofascial tension, spasms, and trigger points in the LA, OI, and the tendinous arc of the LA (Fitzgerald et al.,2009; Anderson et al.,2011). External abdominopelvic, thigh, and internal vaginal and rectal soft tissue mobilization was implemented to identify and treat these painful structures. In this patient, the aim of systematic myofascial release (MFR) of trigger points was to increase local tissue mobility, LA, OI, and EAS muscle relaxation, and to reduce allodynia, dyspareunia, and defecatory dysfunction (Fitzgerald et al.,2009; Anderson et al.,2011). This musculoskeletal treatment approach is now recommended by the American Urologic Association (Hanno et al.,2011) and is gaining broader acceptance within the medical community. In a study of women with CPP, FitzGerald et al. (2009) found a 57% reduction in symptoms in the treatment group that received myofascial mobilization compared to only 21% improvement experienced by the sham group that received general massage therapy.

After resolution of trigger points within the pelvis, a LA muscle reeducation program was added to the patient's plan of care. Pelvic floor muscle training is one of several interventions to address urgency and urge urinary incontinence. Rationale for its use is based on studies that have shown that voluntary contraction of these muscles can inhibit detrusor contractions, reduce detrusor pressure and increase urethral pressure (Burgio et al.,2002; Shafik and Shafik,2003). In addition, several studies have shown PFM exercise to reduce incontinence episodes by up to 76–86% in women with urge UI (Burgio et al.,1985; Burgio et al.,1998). Once this patient improved her ability to contract her PFMs, she was taught to use these muscles to suppress urgency and delay voiding (Burgio and Borello-France,2007).

Home management to alter habitual straining with defecation was initiated as this deleterious practice leads to neural traction, LA strain, and pelvic organ prolapse (Engel and Camm,1994). To avoid tissue compression related to straining, the patient was educated to defecate while maintaining an open epiglottis. In addition, she was instructed to assume a squat-type position (hip flexion with knees higher than hips) on the toilet to minimize force required to expel stool. This position increases the anorectal angle and most closely mimics the evolutionary posture for optimal defecation (Sikirov2003).

Prior to return to sport and higher-level exercise, restoration of an optimal recruitment pattern of the deep core muscles including the transverse abdominis (TA) and the multifidus (MM) was important given this patient's history of rectus abdominis muscle overuse (Ferriera et al.,2010). It was also important to achieve consistently successful and pain-free load transfer from the lumbar spine to the pelvis during large trunk muscle activation (Hodges and Richardson,1997; Sapsford et al.,2001; Richardson et al.,2002). In normal subjects, the TA activates prior to movement regardless of direction of perturbation (Hodges and Richardson,1999). This preactivation trunk stabilization is often latent in subjects with LBP (Hodges and Richardson,1997, 1998).

In this patient case, the multifaceted plan of care outlined in Table 2 and further discussed above resulted in positive PT outcomes. Table 1 includes scores obtained at discharge on the same five questionnaires administered at the initial examination. The questionnaire scores reflect reduced urinary and bowel symptoms and symptom-related distress, and significantly reduced back and intercourse related pain.

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  1. Top of page
  2. Abstract
  3. INTRODUCTION
  4. DISCUSSION
  5. REFERENCES
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