For ESHS, the ITB complex is often involved and is typically the focus of clinical testing if this condition is suspected. Movement tests often include femoral rotation of a flexed hip, rotation of an extended and adducted hip, or flexing and extending the hip.3,18 No specific test is mentioned in the literature. In addition, with these movements, no reports have measured the clinometric properties of these movements. Other tests that may yield information include the Thomas test and the Ober test.
Currently, no specific patient outcome tools are related to SHS. The clinician may have to use related hip outcome questionnaires (e.g., Lower Extremity Function Scale) that will yield valuable information related to the patient’s function, preferred activity, and rehabilitation goals.
Differential Diagnosis
Differential diagnosis often involves a good patient history to determine whether the “snapping sensation” is felt in the anterior hip (ISHS) or lateral hip (ESHS), followed by reproduction of the sensation. This is considered one of the most important diagnostic indicators for differentiating SHS from other potential disorders.3 For ISHS, other disorders that should be considered include iliopectineal bursitis, rectus femoris tendinitis, and, to a lesser extent, intraarticular disease (e.g., FAI). For ESHS, other pathologic processes to consider include trochanteric bursitis and gluteus medius tendinitis. These pathologic conditions may accompany SHS and should be ruled out during the examination.
Imaging
Different types of imaging are commonly used to rule out other disorders and to confirm involved structures. Radiographic findings are often normal in patients with SHS but may be used to check for fractures, small femoral neck angle (coxa vara), or developmental dysplasia, which have been linked to SHS.3,5,19 Radiographic imaging often includes anteroposterior and frog-lateral views.5
Magnetic resonance imaging (MRI) is often used to evaluate possible intraarticular causes such as FAI, acetabular labral tears, osteochondral fractures, and loose bodies. MRI can also be used to evaluate possible extraarticular causes including iliopsoas tendon disorders (ISHS), trochanteric bursitis (ESHS), and soft tissue tumors.3,5
Ultrasound is also used to detect tendinopathy, bursitis, and synovitis. Dynamic ultrasound has been used to detect the pathologic movement of the iliopsoas tendon in ISHS and the gluteus maximus and ITB in ESHS during provocation movements.3,5
Postinjury Considerations
As mentioned earlier, SHS may have an insidious onset and may eventually worsen with prolonged repetitive movements. These patients may seek medical consultation if the condition begins to reduce their ability to function or becomes painful. The physician may impose activity restrictions, prescribe oral medications, administer a cortisone or anesthetic injection, and order imaging as needed (e.g., MRI, ultrasound).3,4 Physical therapy is often prescribed with a focus on decreasing pain with modalities (e.g., ice) and restoring myofascial mobility, muscle length, strength, and function of the lower kinetic chain.3,4
Rehabilitation Considerations
Patient Education
Patient education should include education to avoid painful movements, proper training techniques, early injury recognition, and restorative techniques after activity (e.g., stretching, foam rolling). These patients may tend to ignore the “snapping” sensation, which could eventually lead to discomfort during activity. The patient should be symptom free with activity. Proper warmup and cool-down activity should be reinforced, especially stretching after activity.
Rehabilitation Programming
Rehabilitation interventions must address the musculoskeletal impairments that are contributing to the syndrome. The literature on SHS rehabilitation is sparse, containing only case studies and clinical commentaries.2–7,10,14,17,20 The primary strategies that are discussed are manual therapy, myofascial release, stretching, and strengthening exercises.
Manual Therapy
Each type of SHS may have specific soft tissue restrictions that contribute to the problem. For ISHS, the iliopsoas is often tight and is the primary muscle involved.3 Soft tissue mobilization may be used to release the iliopsoas muscle (Fig. 3-2).10 Mobilization or manipulative treatment of the pelvis has also been cited as an effective intervention.5,10,20 For ESHS, similar soft tissue mobilization techniques targeting the gluteus maximus, tensor fasciae latae (TFL), and ITB complex may be effective interventions. Secondary soft tissue restrictions in the hamstrings, hip external rotators, and adductors may be present and will need to be addressed during treatment.
Stretching and Self-Myofascial Release
For ISHS, stretching of the iliopsoas and rectus femoris muscles has been found to be an effective intervention, along with self-myofascial release techniques such as foam rolling to the anterior hip muscles.10,14,17,21 For ESHS, the gluteals, hip abductors, and external rotators may need stretching and myofascial release techniques.3,22 Specific stretching techniques, such as static stretching and proprioceptive neuromuscular facilitation (PNF), stretching may be effective in achieving increased muscle length.23,24 Dynamic stretching may also be beneficial but should be done with caution.23,25 Certain dynamic stretching patterns require multiplane hip movements that could elicit the “snapping” sensation of the inner or outer hip. It is recommended that the client perform symptom-free activity.
During the initial postinjury phase, consistent daily stretching should be emphasized, to promote tissue lengthening. The stretching and myofascial mobility program should first address the tight tissues and then progress to a global maintenance program once the desired mobility is obtained.
Strengthening and Functional Activity
For both ISHS and ESHS, specific strengthening exercises should be prescribed that help restore proper strength and control. As mentioned earlier, early hip control appears to have a strong influence on lower kinetic chain alignment. For the internal snapping hip, strengthening of the gluteals, hip external rotators, and iliopsoas should be the focus, with the other major muscles of the hip strengthened as needed. For the external snapping hip, the gluteals, external rotators, hip abductors, and adductors should be the focus, with strengthening of other muscle groups as needed. Clients with SHS should be progressed slowly to avoid any discomfort. Any activity that elicits the “snapping” should be avoided. Basic closed kinetic chain progression is advised, beginning with sagittal plane movement, then frontal plane movements, and last transverse or multiplane movements. Caution should be taken with multiplane movements because they can elicit an internal or external snapping. As the patient improves, more advanced movements can be performed. Table 3-1 provides some examples of closed kinetic chain activities in various planes of motion.
TABLE 3-1
Suggested Closed Kinetic Chain Progression for the Lower Extremity
| Plane of Motion | Exercise Progression (Easy → Difficult) |
| Sagittal plane | Leg press machine → wall squats with ball → forward lunges → stair walking → bilateral squats on foam → bilateral squats on air-filled disk or BOSU → single leg squats on ground → single leg squat on foam → single leg squats on air-filled disk or BOSU |
| Frontal plane | Side stepping on level surface → side stepping up onto a step → side stepping with bands → side stepping (fast) with ball passing → slide board |
| Combined planes | Multidirectional lunges → single leg balance with multidirectional toe touch → Single leg cone reach → multidirectional hops (bilateral) → multidirectional hops (single leg) |
Surgical Intervention
If conservative management fails, then surgical intervention is an option for both ISHS and ESHS. For ISHS, an arthroscopic or open iliopsoas tendon release is conducted at the level of the hip joint or at the insertion at the lesser trochanter.26 Khan and colleagues13 conducted a systematic review looking at the success rate of both open and arthroscopic procedures for ISHS. These investigators found that 100% of patients reported a resolution of symptoms after arthroscopic release, and 77% had a resolution of symptoms after open procedures. The complication rate was 21% for the open procedure compared with 2.3% for the arthroscopic.13 For ESHS, the arthroscopic or open technique is meant to release the ITB by producing a diamond-shaped defect lateral to the greater trochanter that allows the trochanter to move freely without snapping, or a Z-plasty is conducted to lengthen the ITB.26–28 The research on outcomes of both procedures is still emerging. Preliminary investigations of the Z-plasty for ESHS have shown good short-term outcomes.27–30 A comprehensive discussion on these surgical interventions is beyond the scope of this chapter. The reader is referred to the reference list for related articles on this topic.
Summary
Both ISHS and ESHS are commonly caused by repetitive overuse activity and are usually diagnosed through the clinical examination. Imaging is often used to rule out other potential pathologic processes. The management of SHS frequently includes a multimodal program consisting of patient education (e.g., reducing risk factors), manual therapy, therapeutic exercise, and modalities.
Meralgia Paresthetica
MP is a nerve entrapment resulting in any combination of pain, paresthesias, and sensory loss within the distribution of the lateral femoral cutaneous nerve or lateral cutaneous nerve of the thigh (LCNT).31,32 The reported incident rate is 4.3 cases per 10,000 patient-years in the general population and 247 cases per 100,000 patient-years in patients with diabetes mellitus.33–35 MP is most prevalent in 30- to 40-year old persons and in male patients more commonly than female.32,36 MP has been associated with various sports and physical activities including gymnastics, baseball, soccer, body building, and strenuous exercise.32,37–42
Anatomic Review
The LCNT is part of the lumbar plexus and functions primarily as a sensory nerve that innervates the anterolateral thigh. The nerve may have a variable orientation among persons with several different combinations of lumbar nerves that originate from L1 to L3.31 The LCNT emerges from the lumbar plexus at the lateral border of the psoas major muscle and crosses the iliacus, to the anterior superior iliac spine. The nerve then passes under the inguinal ligament and over the sartorius muscle and enters the thigh as it divides into anterior and posterior branches.37,44 Individual variations may be seen in the anatomic course of the nerve as it exits the pelvis. Five different types of variations have been reported through cadaveric investigations (Table 3-2).44–46 This variation is important for clinical practice because compression of the LCNT most commonly occurs as it exits the pelvis. Patients may present with different signs and symptoms that reflect their own unique anatomy.47
TABLE 3-2
Variations in Anatomy of the Lateral Cutaneous Nerve of the Thigh
| Types* | Percentage (%) | Anatomic Location |
| A | 4 | Posterior to the anterior superior iliac spine, across the iliac crest |
| B | 27 | Anterior to the anterior superior iliac spine and superficial to the origin of the sartorius muscle but within the substance of the inguinal ligament |
| C | 23 | Medial to the anterior superior iliac spine, ensheathed in the tendinous origin of the sartorius muscle |
| D | 26 | Medial to the origin of the sartorius muscle located in an interval between the tendon of the sartorius muscle and thick fascia of the Iliopsoas muscle, deep to the inguinal ligament |
| E | 20 | Most medial and embedded in loose connective tissue, deep to the inguinal ligament, overlying the thin fascia of the iliopsoas muscle, and contributing to the femoral branch of the genitofemoral nerve |
Patient Profile
Patients diagnosed with MP may present with one or more of the following symptoms: pain, burning, numbness, muscle achiness, coldness, lightning pain, or buzzing (like a cell phone) in their anterolateral thigh.31,48,49 Patients may experience a mild onset with spontaneous resolution or more severe symptoms that limit function.31,48 Prolonged standing and walking may also cause pain, and sitting may alleviate pain as a result of hip flexion, which theoretically reduces or changes the tension in the LCNT.32,48,50
Each patient has a unique clinical presentation and distribution of symptoms. Seror and Seror51 conducted an investigation using neurophysiologic studies in a sample of 120 patients diagnosed with MP. These investigators found that the lateral thigh was solely involved in 88 (73%) cases, and the anterolateral thigh was involved in 32 (26%) cases. The right thigh was involved in 62 (51.6%) cases and the left in 58 (48.3%) of cases.51 Thus, patients may have unilateral or bilateral symptoms that occur in the lateral or anterolateral thigh.
Prevalence and Mechanism of Injury
MP can be classified as either idiopathic or iatrogenic.48 Idiopathic MP is often related to mechanical factors that result in the compression of the LCNT along its anatomic course as it exits the pelvis. Related mechanical factors include direct trauma, obesity (body mass index ≥30 kg/m2), tight garments such as jeans, military and police uniforms, pregnancy, seat belts, muscle spasm, spinal scoliosis, leg length changes, and iliacus hemotoma.34,52–63 MP has been linked to several metabolic factors such as diabetes mellitus, alcoholism, and lead poisoning.48
MP has also been reported as an iatrogenic complication after hip joint replacement. Goulding and associates64 examined the occurrences of injury to the LCNT in 192 patients, 85 of whom underwent anterior-approach total hip arthroplasty (THA) and 107 of whom had hip resurfacing.32,64 As their outcomes measures, these investigators used self-administered questionnaires including the following: neuropathic pain scores; visual analog scale (VAS), to quantify pain; 12-Item Short Form Health Survey (SF-12), to quantify overall health; University of California Los Angeles (UCLA) activity scale, to quantify activity level; and the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC), to quantify pain, stiffness, and physical function. The investigators found that 170 patients (81%) had reported LCNT neurapraxia with a mean severity score of 2.32 out of 10 and a mean neuropathic pain score of 2.42 out of 10 1 year postoperatively. Despite the presence of severity and pain, the subjects reported an absence of functional limitations with the SF-12, UCLA activity scale, and WOMAC.64 Patients who underwent anterior approach hip resurfacing (91%) had a higher incidence than those who had anterior approach THA (67%).32 Bhargava and colleagues65 reported similar findings in a retrospective case review of 81 patients who underwent anterior approach THA. These investigators also found similar symptoms among patients with no apparent functional deficits.
MP has also been reported as a complication in patients after surgical procedures of the spine. Gupta and colleagues66 reported on the incidences of MP in 110 patients (66 male and 44 female; 15 to 81 years old; mean age, 46.9 years) who underwent posterior lumbar spine operations.32 Thirteen patients (12%) had MP postoperatively. The investigators hypothesized that when the patient is prone, the anterior hip becomes compressed from the surgical equipment during surgical procedures, and this leads to the onset of MP.66 Other investigators have reported equipment-related incidents in patients who underwent direct lateral and posterior lumbar spinal surgery.67–70 MP has also been reported as a postsurgical complication in iliac bone harvesting, open and laparoscopic appendectomy, cesarean section with epidural analgesics, and other obstetric and gynecologic surgical procedures.71–75
Clinical Examination
Patients with MP may present with a cluster of symptoms that can mimic the more common hip and lumbar disorders. Diagnosis of MP often includes a clinical examination and, if necessary, neurophysiologic and imaging tests. The clinical examination often includes common test and measures such as active range of motion (AROM), passive range of motion (PROM), palpation, strength testing, function, and special clinical tests. This section discusses special clinical tests that are commonly used to diagnose MP. The reader is also referred to Chapter 2, which provides a comprehensive discussion of the hip examination.
Pelvic Compression Test
The pelvic compression test is based on the premise that the LCNT is compressed by the inguinal ligament and that a downward force to the innominate will slack the ligament and temporarily alleviate the patient’s symptoms.76 Thus, a positive test result consists of alleviation of symptoms. With testing, the patient is positioned in the side-lying position with the symptomatic side facing upward. The examiner applies a downward, compression force to the pelvis (Fig. 3-3) and maintains pressure for 45 seconds. If the patient reports an alleviation of symptoms, the test result is considered positive.32,76 The test has a sensitivity of 95% and a specificity of 93.3% for diagnosing the condition as MP when compared with electromyography (EMG).76
Tinel Sign
The Tinel sign test is based on the premise that tapping over the LCNT as it exits the inguinal ligament region will elicit symptoms reported by the patient.77 Currently, no published studies have investigated the diagnostic utility of this test. The Tinel sign has primarily been used in the diagnosis of upper extremity disorders such as carpel tunnel syndrome.78,79
Neurodynamic Testing
Neurodynamic testing is based on the premise that adverse mechanical tension of the LCNT is a contributor to the patient’s reported symptoms.80 With testing, the patient is in the side-lying position with the symptomatic side upward and the bottom knee bent.80,81 The examiner stabilizes the pelvis with the cranial hand and grasps the lower extremity at the knee with the caudal hand. The examiner then bends the knee and adducts the hip to tension the LCNT (Fig. 3-4).80,81 A positive test result consists of reproduction of the patient’s neurologic symptoms versus feeling tension in the soft tissue structures of the hip. Neurodynamic testing of the LCNT has not been assessed in the literature for its diagnostic ability.32 This lack of evidence should be considered when using this test as part of the clinical examination.
Differential Diagnosis
MP is often a considered a potential pathologic condition once the more common hip disorders have been excluded. MP can be challenging to diagnose because it has neurologic symptoms (e.g., numbness, paresthesias) similar to those that accompany the more common causes of anterolateral thigh pain such as lumbar stenosis, disk herniation, and nerve root radiculopathy.82–85 One clinical method of differential diagnosis is the nerve block test that is commonly done by physicians. With this test, the physicians injects an anesthetic (e.g., 1% lidocaine) at the site where the LCNT exits the pelvis at the inguinal ligament to see whether the patient’s symptoms change.81,82 The test is considered successful if the patient has immediate symptom relief that lasts 30 to 40 minutes after injection.81,82 This is often a more economical confirmatory test before ordering more expensive neurophysiologic tests or imaging. The nerve block may also be used as a treatment.
Neurophysiologic Studies and Imaging
Physicians may also order neurophysiologic tests or imaging to confirm or deny their clinical diagnoses further. Common neurophysiologic studies include somatosensory evoked potentials and sensory nerve conduction tests, which are often considered the gold standard in diagnosing MP and may be less expensive than imaging studies.86–88
Magnetic resonance neurography (MRN) has been used to capture direct images of the nerves of the body (Fig. 3-5). MRN produces a detailed image of the nerve from the resonance signals that come from the nerve itself.89 Chhabra and colleagues90 investigated the intrarater reliability between two blinded raters in the diagnosis of MP using MRN in a sample of 38 persons (11 with MP, 28 controls). The sensitivity, specificity, positive predictive value, and negative predictive value of MRN for MP diagnosis were 71% or higher and 94% or higher for both raters, and the diagnostic accuracy was 90% or higher for both raters.90 The physician may elect to order either neurophysiologic testing or MRN to confirm the diagnosis of MP further.
Postinjury Considerations
Postinjury management often includes a period of conservative nonsurgical care. If the condition is recalcitrant to treatment, then surgical interventions are an option. Nonsurgical and surgical interventions for MP are currently underinvestigated. Khalil and associates91,92 conducted a systematic review in 2008 with a follow-up in 2012 and found no quasi-controlled or randomized controlled trials for either nonsurgical or surgical interventions. The weakness in the literature must be considered by the clinician when integrating these techniques into the plan of care.
Nonsurgical Interventions
Nonsurgical treatments may include medications (e.g., nonsteroidal antiinflammatory drugs [NSAIDs]), protection of the area, avoidance of compression activities, and rehabilitation.31,48 Rehabilitation interventions for MP are underreported in the literature, with only case reports and a few clinical trials.38,42,58,74,93–97 To date, no comprehensive study has assessed the efficacy of physical therapy interventions for the treatment of MP. The available literature on rehabilitation interventions is discussed later in this section.
Manual Therapy
The available literature on manual therapy is sparse, with only two chiropractic case studies describing the management of patients with chronic MP and one chiropractic case study describing the management of a pregnant patient with MP.93,97,98 The treatments reported among the three case studies included active release techniques, mobilization or manipulation for the pelvis, myofascial therapy for the rectus femoris and iliopsoas, transverse friction massage of the inguinal ligament, stretching exercises for the hip and pelvic musculature, and pelvic stabilization or abdominal core exercises.93,97,98 Based on the successful outcomes reported, the combination of interventions described may be effective in treating MP. However, the clinician must keep in mind that case studies fail to offer a high level of evidence. More controlled trials are needed to validate these interventions further. As for negative outcomes, only one previous study cites a case in which chiropractic manual treatment of the hip and pelvis resulted in MP.99
Kinesio Taping
The effectiveness of kinesio (Kinesio Precut, Albuquerque, NM) taping for various orthopedic conditions has seen a growing amount of evidence. Currently, only one pilot study is investigating the effects of kinesio tape on relieving symptoms of MP. Kalichman and colleagues94 investigated the effects of kinesio taping (Fig. 3-6) in a group of 10 patients (6 men and 4 women; mean age, 52 years) with a clinical and neurophysiologic diagnosis of MP over a 4-week period (8 treatment sessions). The investigators used the VAS, VAS global quality of life (QOL) instrument, and the size of the symptomatic area as their outcome measures. On conclusion, the investigators found significant improvements in all measures, including a decrease in the patients’ reported symptoms and symptomatic area after kinesio taping.94 Despite the small sample size, this pilot study suggests that kinesio taping may be a good intervention in the treatment of MP. Further studies will be needed to confirm these findings.
Acupuncture
Acupuncture treatment (e.g., needling and cupping) for MP has elicited interest among Eastern and European researchers, although most of the publications are in Eastern journals. A systematic review found 21 studies on acupuncture treatment for MP that have been published in Eastern journals since 1956.100,101 Among the case studies, one particular case report from German researchers described the successful treatment of MP with acupuncture in two patients who did not respond well to conventional physical therapy.102 Another study, by Wang and colleagues,103 reported the successful acupuncture treatment of 43 patients diagnosed with MP who underwent an intervention of needling and cupping. The available literature suggests that acupuncture may be effective in the treatment of MP. However, the exact physiologic mechanisms are still under investigation.104,105 Further studies are needed in general to develop a broader understanding of the efficacy of acupuncture in the treatment for MP.
Other Nonsurgical Interventions
Pulsed radiofrequency ablation is an emerging treatment for MP when conservative treatment fails. Pulsed radiofrequency uses a high-frequency alternating current. The heat generated from the high-frequency alternating current ablates the nerve fibers or dysfunctional tissues without damaging the surrounding tissue.106 Currently, no clinical trials have been conducted, and only case reports describing the intervention have been published.106–108
As mentioned in the previous section, physicians may also use a nerve block as a diagnostic test or as nonsurgical treatment. For treatment, LCNT blocks use a combination of lidocaine and corticosteroids.65 Tagliafico and associates50 reported their experience conducting an ultrasound-guided nerve block in 20 patients (7 male, 13 female; age range, 23 to 66 years) with a diagnosis of MP confirmed by EMG. These investigators used the pain VAS and VAS QOL scales as their outcome measures. At 1 week after injection, 16 patients (80%) experienced progressively decreased symptoms, and 4 patients (20%) required a second injection for continued pain. At the 2-month follow-up, all patients experienced complete resolution of symptoms and significant improvements on the QOL scale.50 Other researchers have found similar outcomes.109,110
Surgical Interventions
If nonsurgical interventions fail, then surgical interventions may be an option. LCNT neurolysis and resection are optional interventions. Neurolysis is destruction of the nerve, and a resection is removal of the nerve or a section of nerve. Neurolysis has shown favorable outcomes in patients up to 4 years postoperatively, and resection has also shown favorable results despite the complete loss of sensation in the anterolateral thigh that occurs after the surgical procedure.111–114 The overall consensus on which procedure is the best is still unknown.111 Emamhadi115 compared neurolysis with resection in the treatment of 14 patients diagnosed with MP, with a follow-up within 18 months. This investigator found that the resection group (n = 9) reported complete relief, whereas the neurolysis group (n = 5) reported a recurrence of symptoms within 1 to 9 months.115 de Ruiter and colleagues111 also found higher success rates with resection than with neurolysis.111 These comparison studies suggest that LCNT resection produces better outcomes; however; both procedures are still underinvestigated. The success of LCNT resection may be caused by the complete resolution of symptoms and the acceptance of permanent changes (e.g., numbness) by the patient.111 Neurolysis may provide symptom relief, but with a probability of recurrence.115 Thus, neurolysis procedures may be considered first and resection considered if the nerve has been severely damaged.115
Summary
MP is challenging to diagnose and should be considered once the more common diagnoses are excluded. The diagnosis and nonsurgical and surgical management of MP are currently underinvestigated. The available evidence does provide some guidance for clinical practice. These limitations should be considered when using the information for clinical practice.
Adductor-Related Groin Injuries
Groin pain in the athlete has traditionally been classified as a pathologic condition of the adductor muscle group.116,117 Most often, the adductor longus is involved as a single source of groin pain or in combination with abdominal injury (sports hernia) or intraarticular hip disorders.118,119 Despite the traditional definition, the recent literature examining sports-related injuries has expanded the definition of “groin pain” to other disorders such as FAI, sports hernia, osteitis pubis, inguinal hernia, and obturator neuropathy.120–123 For this section, adductor-related groin pain is used to differentiate adductor muscle injury from other potential pathologic conditions.124
Anatomic Review
Among all the groin muscles, the adductor group (brevis, longus, and magnus) has a unique role in stabilizing the hip during sports activity.125,126 This muscle group is susceptible to injury resulting from the demands it undergoes with both open-chain and closed-chain hip movements, with the adductor longus the most involved.116 The anatomic architecture of the adductor longus and its relationship with athletic pubalgia (see Chapter 5) have garnered interest among researchers. Athletic pubalgia is commonly classified as a distal rectus abdominis injury at the pubic symphysis, conjoint tendon injury, and injury to the proximal adductor longus.116,120,127 Norton-Old and colleagues128 investigated the anatomic relationship of the adductor longus with this disorder by using cadaveric dissection. The investigators found that the adductor longus attached to the anteroinferior aspect of the pubis, with the superficial fibers tendinous and the deep fibers muscular.128 Other researchers have confirmed this anatomic variation.129,130 Norton-Old and associates128 also found that the adductor longus had secondary communications with the following structures: contralateral distal rectus sheath, pubic symphysis, anterior capsule, ilioinguinal ligament, and contralateral proximal adductor longus tendon. The investigators also simulated a mechanical load across one of the adductor longus muscles and measured the strain in the ipsilateral and contralateral rectus sheath with a strain gauge. They found that the strain experience was varied among cadavers and concluded that the proximal attachment of the adductor longus plays a role in withstanding high forces across the pubic symphysis during multidirectional athletic activity. These investigators concluded that this finding may explain the vulnerability of the anatomic relationship of the rectus abdominis and adductor longus.128
Biomechanical Considerations
The actions of the adductor longus muscle during lower extremity motions such as kicking and skating has been a topic of interest because of the high prevalence of injuries among soccer and ice hockey players. Charnock and colleagues131 examined adductor muscle length and activation during a soccer kick in male collegiate soccer players. Their investigation revealed the following: maximum hip extension occurred near 40% of swing phase, the maximum rate of stretch of the adductor longus occurred at 65% of the swing phase, activation of the adductor longus occurred between 10% and 50% of the swing phase, and maximum hip abduction occurred at 80% of swing phase. The investigators concluded that the adductor longus could be at risk for injury during the transition from hip extension to flexion.131
Chang and associates132 examined the role of the hip adductors during forward skating in ice hockey players. These investigators used surface EMG to measure adductor muscle activity at three different skating velocities: slow, medium, and fast. They investigators found that with increased skating velocity, the adductor magnus exhibited an extremely large increase in peak muscle activation and prolonged activation.132 They also found that with increased skating velocity, lower extremity stride rate and stride length increased despite a lack of significant increases in hip, knee and ankle total range of motion (ROM). To accommodate for the increased stride rate with higher skating speeds, the rate of hip joint abduction and adductors muscle activation increased together, a finding indicating a substantial eccentric contraction.132
The available research suggests that the adductor muscle group may be susceptible to injury because of the unique anatomy and high demands experienced during various sports such as soccer and ice hockey. In the presence of pain, adductor muscle activation may be inhibited, resulting in weakness and a potential risk for further injury. Crow and colleagues133 found decreased adductor muscle strength with the onset of groin pain or injury in Australian football players. Tyler and associates134 also found that adduction strength was 78% of abduction strength in injured ice hockey players compared with 95% adduction strength in uninjured players.
Prevalence and Mechanism of Injury
The prevalence of groin injuries represents 2% to 5% of all sports-related injuries and 5% to 9% of high school injuries in the United States, with the adductor group most commonly involved.135,136 The incidence of groin injuries in soccer can be as high as 10 to 18 injury incidents per 100 players.135,137,138 Hagglund and colleagues139 found that 56% of adductor injuries occurred in the kicking leg in a sample of professional soccer players from 2001 to 2010. In professional ice hockey players, 10% to 11% of all injuries are groin related.116 Previous data from the National Hockey League (NHL) showed that groin and abdominal injuries occurred at a rate of 12.99 injuries per 100 players per year during the 1991 to 1992 season, with an increase to 19.87 injuries per 100 players per year during the 1997 to 1997 season; 90% of injuries were not contact related.140 Adductor-related groin pain has also been reported in other sports such as rugby, swimming, water polo, and cricket.141–145 Among all the sports, adductor-related groin injuries are most prevalent in ice hockey and soccer and may occur in 10% to 20% of players.116
Common mechanisms associated with adductor-related groin pain have been reported in the literature.127,141,146–148 Athletes who participate in sports involving repetitive kicking and multidirectional movements such as ice hockey may be susceptible to adductor-related groin injuries.149 The most common reported risk factors include hip muscle weakness, abdominal core muscle weakness, delayed transversus abdominis recruitment, poor off-season conditioning, years of experience, age, and earlier groin injury.* Other risk factors include decreased hip ROM,151,152 adductor strength less than 80% of abductor strength,126,134 reduced muscle activation of the abductors and adductors with groin pain,133,153 poor preseason lower extremity flexibility,154 pelvic instability,155 and poor adductor flexibility.156
Patient Profile
Patients may report a general “groin pain” that is mechanical in nature. Adductor-related groin pain is typically localized along the adductor longus belly, the proximal musculotendinous junction, or the origin at the inferior pubic ramus.157 The pain often is exacerbated with physical activity or contraction of the muscle, depending on the extent of the injury. With mild adductor strains, the proximal pain may slightly decrease initially with activity, but if the injury is untreated, the pain may persist during activity.143 With more severe strains, the pain may affect function. If groin pain is recalcitrant and fails to resolve with conservative treatment, then further differential diagnosis should be conducted. Other common musculoskeletal disorders such as FAI, osteitis pubis, obturator neuropathy, hip or pelvic fracture, lumbar injury, inguinal hernia, and athletic pubalgia should be excluded.120–123,158,159 Although they are less common, proximal adductor longus ruptures can occur. Several published case reports have described the recognition and management (e.g., surgical and nonsurgical) of adductor longus trauma in equestrian,160 soccer,161–163 rugby,164 and football athletes.165,166 The clinician needs to consider this injury during the differential diagnosis because it can be mistaken for another pathologic condition such as inguinal hernia.167
If a nonmusculoskeletal cause is suspected, then the clinician should consider other conditions such as genitourinary (e.g., prostatitis or urinary tract infection), neurologic (e.g., genitofemoral nerve entrapment), gastrointestinal (e.g., Crohn disease), and vascular (e.g., abdominal aortic aneurysm).168 Chapter 2 provides a more comprehensive discussion of the differential diagnosis process.
Related posts:
Hip Osteoarthrosis
Influence of Lumbosacral Disorders on the Differential Diagnosis of Hip Pain
The Female Hip and Pelvis
Femoral Acetabular Impingement and Labral Tears
Musculoskeletal Sources of Abdominal and Groin Pain: Athletic Pubalgia, Hernias, and Abdominal Strains
The Pediatric and Adolescent Hip
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