Lesions of the ligamentum teres have been increasingly recognized as a source of pain. Byrd reported them as the third most common diagnosis in athletes undergoing hip arthroscopy [9]. A complete lesion is usually associated with traumatic dislocation but may be also seen in high-impact athletes [10, 11].

Clinical diagnosis can be difficult. Symptoms are nonspecific during clinical evaluation, characterized by a reduced or painful range of motion, a painful straight leg raise test, and locking of the joint [12]. O’Donnell et al. [13] have proposed a diagnostic test for ligamentum teres tears with a sensitivity and specificity of 90 % and 85 %, respectively. The clinician passively flexes the hip fully and then extends 30°, leaving the hip at about 70° flexion (knee is flexed 90°); the hip is then abducted fully and then adducted 30°, typically leaving it at about 30° abduction; the leg is then passively internally and externally rotated to available end range of motion; the test is positive when there is reproduction of pain either upon internal or external rotation [14].

Imaging rarely identifies ligamentum teres injuries and a preoperative diagnosis varies from 1 to 5 % [15]. MRI and MRA (magnetic resonance arthrography) appear to be accurate diagnostic tools [16, 17], while arthroscopy remains the gold standard in identifying these lesions.

In case of failure of conservative treatment such as physiotherapy, arthroscopic debridement [18] is indicated in patients with pain caused by partial-thickness lesions, while reconstruction with autografts [19], allografts, or synthetic grafts may be indicated in patients with full-thickness lesions that cause instability or in which debridement was not effective in reducing symptoms [11].

Pigmented villonodular synovitis (PVNS) is a rare proliferative disorder of the synovium. Eventhough PVNS is a benign disease, it may be aggressive in certain cases. PVNS may also occur in a localized or more diffused form.

Patients typically present with mild to severe pain and impaired joint function. Recurrent hemarthrosis is typical. The concurrent presence of FAI can mistakenly lead to a diagnosis of a secondary synovial reaction instead of PVNS. Diagnosis is suspected through MRI and confirmed by histology.

Treatment is often surgical, either via open or arthroscopic synovectomy, or, in more severe cases, a total hip arthroplasty (THA) is indicated once significant degenerative changes are present. Treatment with radiation and intra-articular injections of radioisotope are indicated in incomplete synovectomy or recurrences. Treatment of hip PVNS presents a high rate of failure. Hip arthroscopy has been shown to be effective but with a recurrence rate of 12 % and a conversion rate to THA ranging from 8 to 46 %. A high rate (31 %) of aseptic loosening in THA after PVNS has been also reported. An open transtrochanteric approach has been recently suggested with some success [20–24].

The term bone marrow edema syndrome (BMES) refers to several different clinical conditions. They are usually self-limiting (may take up to 24 months) and they are best seen on MRI [25].

Different clinical entities have been reported, such as transient osteoporosis of the hip (TOH), transient marrow edema, regional migratory osteoporosis (RMO), and reflex sympathetic dystrophy (RSD) also known as complex regional pain syndrome (CRPS) [25, 26].

The main differential diagnosis is avascular necrosis of the femoral head (AVN), and it is still controversial, whether BMES represents a distinct self-limiting disease or merely reflects a subtype of AVN [25].

Etiology remains unclear in most patients, but appears to be multifactorial and related to increased intraosseous pressure with increased bone turnover, a diminished perfusion, and subsequent hypoxia producing pain [27].

TOH mainly affects male patients who are 30–50 years old and women in the third trimester of pregnancy, without history of trauma. The main symptoms are severe hip pain with weight bearing and functional disability. Radiographs may show diffuse osteoporosis in the hip after several weeks from the onset of hip pain. In addition, MRI shows bone marrow edema in the femoral head, sometimes involving the femoral neck. MRI is also useful in differentiating between BME, FAI, and greater trochanteric pain syndrome (GTPS) that may present as localized bone marrow edema but with different edema patterns [28].

A bone scan may differentiate BME from AVN at its initial stage where a “cold in hot” image is seen. A “cold” zone of decreased tracer uptake (the necrotic zone) is surrounded by a half-moon-shaped area of increased uptake (crescent) [29].

Regional migratory osteoporosis presents a similar clinical course but is characterized by a polyarticular involvement.

RSD, also called algodystrophy, complex regional pain syndrome (CRPS), or Sudeck’s dystrophy, is characterized by a history of trauma and presents three phases: acute, dystrophy, and atrophy. Symptoms are dull and burning pain with a rapid onset and subsequently skin atrophy, sensorimotor alteration, and joint contractures. Osteoporosis is early visible radiographically [29].

The recommended treatment is often nonsurgical, with protected weight bearing and analgesics. Once diagnosed, to shorten the duration of symptoms, hyperbaric oxygen therapy, bisphosphonates, and, more recently, prostaglandin inhibitors have been used with encouraging results. In a controlled randomized study, hyperbaric oxygen therapy showed a significant resolution of bone marrow edema in 55.0 % of the patients compared to 28 % in the control group [30, 31]. In a series of 186 patients treated with prostaglandin inhibitors, there was a significant decrease in bone marrow edema on MRI and an increase in the mean Harris Hip Score from 52 points to 79 at latest follow-up [32].

Avascular necrosis or osteonecrosis (AVN or ON) of the femoral head is caused by inadequate blood supply [33, 34] and can be idiopathic or secondary to different predisposing factors such as trauma, alcoholism, use of steroids, barotraumas, and hematological or coagulation diseases [35, 36]. Different classification systems have been developed with the aim to provide guidelines for treatment. Ficat and Arlet published the first classification system based on radiographic changes [37]. Subsequently the ARCO classification system was introduced [38]. Steinberg et al. introduced an MRI classification subdivided in six stages [39].

The suspicion of osteonecrosis should be always high in case of a deep groin pain with a history of trauma (femoral neck fracture or fracture dislocation) or other predisposing factors. Standardized radiography is the first step to evaluate the presence of the pathognomonic “crescent sign” (sign of early femoral head collapse due to necrotic subchondral bone). It is not rare to find FAI signs that may divert attention from the real cause of the pain. MRI is the gold standard to confirm the diagnosis with a high sensitivity and specificity [40]. The use of bone scan is debated and mainly used to aid with determining the definitive diagnosis [41].

The treatment of AVN is still controversial and depends on the stage and the location of the pathology following the different classification systems.

Nonsurgical treatment alternatives such as shock wave therapy (still debated [42]), intravenous iloprost, bisphosphonates, pulsed electromagnetic fields, hyperbaric oxygen [41, 43, 44], enoxaparin [45], and, more recently, injection of stem cells and platelet-rich plasma have been reported in the literature [46].

Intravenous use of iloprost, a prostacyclin derivate with vasoactive action, appears to give good results in some studies, both if used alone and in combination with core decompression [43, 44].

Surgical salvage procedures, in the early stages of AVN, include core decompression, rotational osteotomies, and vascularized bone grafting [47, 48]. Stem cell therapy in adjunction of core decompression is growing; in a review by Houdek et al., MRI showed a decrease in the zone of marrow edema from 32 % to more than 75 % in patients treated with core decompression and stem cells [49].

In more advanced stages, total hip replacement is the only alternative treatment to achieve pain relief and improved function [50].

Greater trochanteric pain syndrome (GTPS) is a term used to describe chronic pain localized at the lateral aspect of the hip [51]. This pain syndrome, once described as “trochanteric bursitis” (TB), is also known as the “great mimicker” because its clinical features overlap with several other conditions including myofascial pain, degenerative joint disease, and some spinal pathologies [52]. Typical presentation is pain and tenderness over the greater trochanter region. GTPS is very common, reported to affect between 10 and 25 % of the general population. The most affected population is middle aged (ages 40–60 years) with a high female predominance (4:1) [53].

The pathogenesis is still unclear. It could be related anatomical factors such as a wide pelvis, stresses on the iliotibial band, hormonal effects on bursal irritation, or alteration in physical activities [54, 55]. Gluteus minimus and medius tendinopathy is also one of the primary causes of greater trochanteric pain [56, 57].

A history of lateral hip pain and pain on palpation of the lateral hip are the most common clinical findings of GTPS. Other symptoms are pain during weight bearing and lying on the affected side during nighttime [58]. On examination, patients complain of pain during direct compression of the peritrochanteric area, often reproducible with a FABER test (flexion, abduction, and external rotation). The Ober test is useful to assess iliotibial band (ITB) tightness [58–61]. Kaltenborn et al. [62] have described the hip lag sign as useful to identify gluteal musculo-tendinous lesions.

Plain radiographs are useful to exclude other concurrent pathologies (osteoarthritis, FAI, coxa profunda, avulsion fractures). Calcification adjacent to the greater trochanter may be seen in up to 40 % of patients presenting with GTPS. Insertional tendinopathic calcification rather than bursal calcification is usually present [54]. Several studies have demonstrated the association between a low femoral neck-shaft angle or an increased acetabular anteversion and GTPS [63, 64]. Small-field MRI is very useful to assess tendon insertions and surroundings [54].

Greater trochanteric bursitis should initially be managed nonoperatively with rest, stretching, physical therapy, and weight loss (when indicated). Other treatment options are extracorporeal shock wave therapy and steroid injections [54, 60, 65–68].

About one-third of the patients suffer chronic pain. In these patients there may be an indication for surgical intervention [69–72]. Currently, there are different endoscopic techniques for local decompression (ITB release), bursectomy, and suture of torn gluteal tendons. Unfortunately there are only few studies and no long-term follow-up for these treatments. Good results have been shown in endoscopic gluteus medius repair at minimum 2-year follow-up in more than 90 % of 15 patients. Interestingly, 100 % of those patients had concomitant intra-articular pathologies (labral tears and cartilage damages). A recent study [72] on endoscopic treatment of GTPS in 23 patients demonstrated significant improvement in pain and functional score at 12-month follow-up [43, 59, 61, 73–76].

Snapping hip, or coxa saltans, is a condition that involves an audible or palpable snap during movement of the hip, with or without pain. It was first described at the beginning of the last century [77, 78]. The iliotibial band was usually considered the only cause until Nunziata and Blumenfeld suggested the psoas tendon, slipping over the iliopectineal eminence, as another source [79].

An important contribution was by Allen and Cope [80] who described three different etiologies of the snapping hip: intra-articular, internal, or external. They also introduced the use of coxa saltans as a general term [79, 80].

In the general population, the incidence of asymptomatic snapping hip is 5–10 % with a female predominance. In most cases the condition is associated with sporting activities, such as soccer/football, weight lifting and dance (up to 90 and 80 % of these bilaterally), and running [77, 78].

Radiographs are usually negative and useful only to rule out other diseases or to identify predisposing factors such as coxa vara, prominence of the greater trochanter, and reduced bi-iliac width for the external or hip dysplasia for the internal. MRI usually may reveal a cause of an intra-articular snap. Dynamic ultrasound can identify the snapping tendon and may give additional information, such as the presence of inflammation, tendinopathy, or bursitis [77, 79].

Initial treatment includes rest, ice, anti-inflammatory medications, and activity modification avoiding triggering the snap. Physical therapy, stretching of the involved structures, and a reduced training usually lead to good results. Many symptomatic snapping hips, between 36 and 67 %, resolve without surgery [77, 79, 81].

External snapping hip is caused by the thickening of the posterior aspect of the iliotibial band (ITB) or anterior aspect of the gluteus maximus close to its insertion. The greater trochanter bursa may become inflamed because of the recurrent snapping and causes pain [77].

Patients with external snapping hip often report a sensation of subluxation or dislocation of the hip (pseudosubluxation).

The goal of surgery, when needed, is the releasing or lengthening of the ITB [77]. A Z-plasty of the ITB transects, transposes and reattaches the ITB with resolution of symptoms in most patients. A reported complication is a Trendelenburg gait that in an athlete or dancer takes on added importance [82]. Usually an endoscopic ITB diamond-shaped release at the level of the greater trochanter is successful [83]. A new interesting technique, the endoscopic gluteus maximus tendon release, has recently been introduced [84].

In the internal snapping hip, the iliopsoas tendon snaps over a bony prominence, usually the iliopectineal eminence or the anterior femoral head. The snap usually occurs when extending the flexed hip or with moving the hip from external to internal rotation or moving the hip from abduction to adduction. Running and standing up from a seated position are difficult for patients with this condition [77, 79].

The aim of surgery is to release the iliopsoas tendon. Today the preferred approaches to perform a tenotomy are endoscopic, at the lesser trochanter, or arthroscopic, at the joint level. A high rate of associated labral tears have been reported [81, 85–89]. Particular attention should be paid to bifid or trifid psoas tendons that may result in an unsuccessful procedure [90, 91]. It was reported that arthroscopic surgery had better results than open techniques with fewer complications and less pain. Open fractional lengthening could lead to an increased postoperative pain than open transection at the lesser trochanter, but it is more efficacious. These results must be read considering the deficiency of high-quality literature evidence or direct comparison [81].

Intra-articular snapping hip has a variety of causes, including synovial chondromatosis, loose bodies, labral tears, (osteochondral) fracture fragments, and recurrent subluxation [77, 79, 80]. Intra-articular lesions may create a snap, click or pop, but, usually, it is the sensation of catching, locking, or sharp stabbing pain that is first reported by the patient [77, 79, 92]. The injection of anesthetic into the iliopsoas bursa (internal snapping hip) or the hip joint (intra-articular pathology) helps in diagnosis and in identifying the involved structure [77, 79].

Ischiofemoral impingement (IFI) is an uncommon cause of hip pain caused by an abnormal contact between the ischium and the lesser trochanter with compression of the quadratus femoris muscle [93]. It was first described in 1977 by Johnson [94] in patients previously treated with hip replacement or osteotomy of the femur. Only recently it has been diagnosed and described as a stand-alone pathology [95–97]. This disease is more common in women, is bilateral in about a third of cases, and usually occurs later in life compared with femoroacetabular impingement (mean age at presentation 51–53 years) [95, 98].

The typical symptoms are pain localized to the hip, groin or buttock level and sometimes irradiation to the lower extremities, probably caused by irritation of the adjacent sciatic nerve [95, 98]. There is pain upon direct palpation of the ischiofemoral space and when the hip is in extension and adduction. Clinical tests are the long-stride walking test, in which the patient feels pain during extension of the hip (the pain is relieved by walking in short strides or by abduction of the hip during walking), and the ischiofemoral impingement test, which is performed with the patient in contralateral decubitus, extending the affected hip passively in adduction or neutral position [99].

Imaging studies include a standing anteroposterior view of the pelvis and a frog-leg projection [96, 99] where a reduction of the ischiofemoral distance can be seen (normal 23 ± 8 mm, pathological 13 ± 5 mm) [95]. Moreover, there are a variety of possible associated malformations, such as coxa breva, coxa valga, or others that lead to medialization of the femoral head in the acetabulum [99]. MRI can be valuable to detect diffuse edema of the quadratus femoris muscle [95, 98].

Treatment includes guided steroid infiltrations. In some patients surgical decompression of the quadratus femoris with resection, either by endoscopy or by open surgery, of the lesser trochanter may be indicated, but there is still low-quality evidence about the success of this procedure [93, 99, 100].

Osteitis pubis is a painful, noninfectious, inflammatory process involving the pubic bone, the symphysis, and the surrounding structures, such as cartilage, muscles, tendons, and ligaments [101, 102].

The true incidence and prevalence of osteitis pubis are unknown. The condition was first described as a complication of suprapubic surgery in 1924 [103] and then in a fencer athlete in 1932 [104]. Usually, osteitis pubis is a self-limiting inflammatory condition secondary to trauma, pelvic surgery, childbirth, pelvic functional instability, or overuse (particularly in athletes). It also has the potential to turn into a chronic pain problem in the pelvic region [105–107].

FAI appears to represent a major predisposing factor for this condition. Reduced hip rotation associated with FAI may result in increased stress to the rest of the pelvis generating an osteitis pubis as loads are applied to adjacent joints [108]. In a study on 125 American collegiate football players (239 hips), there was a high prevalence of osteitis pubis in FAI symptomatic hips [109]. The only independent factor, for hip or groin pain in these athletes, was an increased alpha angle [108].

A gradual onset of pain in the pubic region is the main symptom. The pubic symphysis or the superior pubic ramus may be painful upon palpation. The pain typically radiates to the inner thigh (adductor musculature), to the groin, or upward to the abdomen. The perineal region and scrotum may also be involved. Running, hip flexion or adduction against resistance and abdominal eccentric exercises usually aggravate the pain. Later in the disease a reduction in the internal and external rotation of the hip joint, muscular weakness, and sacroiliac joint dysfunction are reported. In severe cases, pain limits walking capability promoting an antalgic or waddling gait. Pain can be also be evoked when getting up from a sitting position [110–112].

Standard anteroposterior radiographs usually show widening of the symphysis and sclerosis, rarefaction, cystic changes, or marginal erosions in the subchondral bone of the symphysis. In acute cases, or in mild form, radiographs may also be normal in some cases. Instability can be evaluated with “flamingo view” radiographs. However, the correlation with symptoms is always necessary, because similar radiographic findings may be seen also in asymptomatic persons [111].

Bone scan may show an increased uptake at the symphysis, but this is a late sign, and may take months to appear.

CT scan may show marginal stamp erosions of the parasymphyseal pubis bone, insertional bony spur or periarticular microcalcifications.

MRI has a superior role in visualization of soft-tissue abnormalities (e.g., microtears of the adductor tendons) and changes within the bone marrow (e.g., bone edema) and is useful for differential diagnosis of osteitis pubis, bursitis and stress fractures [111, 112].

Because osteitis pubis is normally self-limiting, initial treatment is nonoperative. In highly competitive athletes, activity modification is recommended. Many different therapeutic modalities and rehabilitation protocols have been successfully used [113]. Corticosteroid injections may be beneficial.

Surgical treatment includes open curettage of the symphysis pubis with or without subsequent fusion of the joint, wedge resection, posterior wall mesh repair and a variety of procedures to reinforce or repair the abdominal and pelvic floor musculature, with or without adductor tendon release with an average return to sports of 6 months [111, 112].

Recently an arthroscopic technique has been described to debride the symphysis and, eventually, to divide and reattach the degenerated origin of adductor tendon. With this technique the stability of the symphysis pubis is maintained and time to return to sports is supposed to be shorter. More recent reports document that five competitive nonprofessional soccer players were able to return to full-activity sports in an average period of 14.4 weeks after the arthroscopic surgery with satisfactory results [114–116].

Sports hernia (also called “athletic pubalgia”) is a condition characterized by a strain or a tear of any soft tissue (such as muscle, tendon and ligament) in the lower abdomen or groin area. Unlike a traditional hernia, the sports hernia doesn’t create a defect in the abdominal wall. As a result, there is no visible bulge under the skin and a definitive diagnosis is often difficult. It often occurs where the abdominal muscles/tendons and adductors attach at the pubic bone at the same location.

Groin pain caused by sports hernia can be disabling, and it most often occurs during sports that require sudden changes of direction, intense twisting movements, cutting and/or kicking [117, 118].

Sports hernias typically affect young males who actively participate in sports. Females are affected, but much less commonly than males, comprising just 3–15 % of cases [119]. Sports hernia is a frequent cause of acute and chronic groin pain in athletes [120] and there is a high incidence of symptoms of sports hernia in professional athletes with FAI [121].

The exact cause of sports hernia is not completely known and remains heavily debated. The soft tissues most frequently affected are the oblique muscles in the lower abdomen (especially vulnerable are the tendons of the internal and external oblique muscles). When both oblique and adductor muscles contract at the same time, there is a disequilibrium between the upward and oblique pull of the abdominal muscles on the pubis against the downward and lateral pull of the adductors on the inferior pubis. This imbalance of forces can lead to injuries of the lower central abdominal muscles and the upper common insertion of the adductor muscles [122].

Muschaweck and Berger described sports hernias as a weakness of the transversalis fascia portion of the posterior wall of the inguinal canal [123]. This weakness of the pelvic floor can lead to localized bulging and compression of the genital branch of the genitofemoral nerve. Compression of this nerve appears to be the major reason of pain in these patients [124].

Although the physical examination reveals no detectable inguinal hernia, a tender, dilated superficial inguinal ring and tenderness of the posterior wall of the inguinal canal are often found. The patient typically presents with an insidious onset of activity-related, unilateral, deep groin pain that abates with rest, but returns upon sports activity, especially with twisting movements [125]. The pain may be more severe with resisted hip adduction, but the most specific finding is pain in the inguinal floor with a resisted sit-up. Pain can also be elicited in the “frog position” [126]. Gentle percussion over the pubic symphysis is performed to assess concurrent presence of osteitis pubis. Next, the patient is asked to adduct the thighs against resistance. Alternatively, the athlete can suspend the ipsilateral straight leg in external rotation, against resistance, and then perform the abdominal crunch and test the medial inguinal floor for tenderness.

Experienced clinicians will identify this condition only from history and physical examination [127]. Even if the role of imaging studies is unclear [125], plain radiographs, bone scans, ultrasound, computed tomography scans and, especially, magnetic resonance imaging (MRI) may be necessary to rule out related or associated pathology [127]. Shortt et al. have imaged over 350 patients. In their experience, patients with a clinical sports hernia almost always exhibit abnormalities on MRI. The two dominant patterns of injury include the lateral rectus abdominis/adductor aponeurotic injury just adjacent to the external inguinal ring and the midline rectus abdominis/adductor aponeurotic plate injury [127, 128].

The available literature favors early surgical management [129, 130] for those athletes who are unable to return to sports at their desired level after a trial of nonsurgical treatment for 6–8 weeks [118, 131–136].

Nonsurgical treatment consists primarily of rest and cryotherapy. Two weeks after the injury, the physical therapy exercises can improve strength and flexibility in the abdominal and inner thigh muscles. The nonsteroidal anti-inflammatory therapy can be useful to reduce swelling and pain [118].

Surgery is indicated as either a traditional open procedure or as an endoscopic procedure. Some surgeons perform also an inguinal neurectomy to relieve pain or an adductor tenotomy to release tension and increase range of motion [124, 135].

Continued groin pain after surgery may be caused by an underlying concurrent FAI; Economopoulos et al. have demonstrated a high prevalence of radiographic FAI signs in patients with athletic pubalgia that should be always closely evaluated [137].

Most studies have reported that 90–100 % of patients returned to full activity in 6 months [122].

Piriformis muscle syndrome (PMS) is an entrapment neuropathy caused by sciatic nerve compression in the infrapiriformis canal [138, 139]. Some researchers account PMS for up to 5 % of all cases of low back, buttock and leg pain [140]. Other anatomical anomalies have been reported to explain its etiology [141]. Similar sciatic compression-type pathology has also been referred to the obturator internus, evocating the obturator internus syndrome (OIS) [142].

Yeoman in 1928 first reported that sciatica may be caused by sacroiliac periarthritis and piriformis muscle entrapment [143]. Freiberg and Vinke in 1934 stated that sacroiliac joint inflammation may primarily cause reaction of the piriformis muscle and its fascia that may secondarily irritate the overlying lumbosacral plexus [144]. Based on cadaveric dissections, Beaton and Anson 1938 hypothesized that a piriformis muscle spasm could be responsible for the irritation of the sciatic nerve [145]. Robinson in 1947 has introduced the term “piriformis syndrome” [146].

The classic features of piriformis syndrome include “sciatica-like pain,” aggravated by sitting, buttock pain, external tenderness over the greater sciatic notch and augmentation of the pain with maneuvers that increase piriformis tension [147]. Other clinical features may be pain with straight leg raise test, a positive Pace test (pain with resisted hip abduction in a seated position) [148], and a positive Freiberg test (pain upon forceful internal rotation of the extended hip) [144].

The piriformis entrapment is often diagnosed via exclusion. The diagnosis is often difficult to establish. There are no laboratory or radiographic methods for diagnosing the syndrome. An MRI may in some cases show variations in anatomy, muscle hypertrophy, as well as abnormal signal of the sciatic nerve [149].

EMG may provide findings for sciatic nerve compression at the level of the piriformis muscle [142]. A “piriformis syndrome” may be confirmed through a positive response to the injection of a local anesthesia [150].

Traditional treatment is nonsurgical with physical therapy, stretching, extracorporeal shock wave therapy (ESWT) and steroid or analgesic injections [151, 152]. Open tenotomy has been reported [153]. Recently, botulinum toxin [154, 155] and arthroscopic release have been used with promising results in selected cases [156, 157].

Meralgia paresthetica is a clinical condition characterized by paresthesia and burning pain over the anterolateral thigh, due to entrapment of the lateral femoral cutaneous nerve (LFCN) [158].

It was first described by Martin Bernhardt in 1878, but the term meralgia paresthetica (MP) was coined by Vladimir Roth, a Russian neurologist, in 1895 who noticed this condition in a horseman who wore tight belts [159].

It most commonly occurs in 30–40-year-old men with an incidence of 1–4.3 per 10,000 patients in the general population [160, 161].

Other than idiopathic, causes of meralgia paresthetica are mechanical factors as obesity, pregnancy, and other factors that increase abdominal pressure, such as strenuous exercise, sports and tight belts. Lower limb-length discrepancy has also been associated with this neuropathy and also different metabolic factors, as diabetes mellitus, alcoholism, lead poisoning and hypothyroidism [160, 162]. Iatrogenic causes are due to surgical procedures, such as ilioinguinal approach for acetabular fracture fixation, iliac crest bone graft, anterior approach for total hip replacements, laparoscopy for cholecystectomy or inguinal hernia, coronary artery bypass grafting, aortic valve surgery and gastric reduction [160].

The lateral femoral cutaneous nerve originates from different combinations of lumbar nerves (L1–L3); its course is extremely variable. Passing from the pelvis to the thigh, the nerve crosses a tunnel between the ileopubic tract and the inguinal ligament, where it enlarges its diameter developing, in some cases, the meralgia paresthetica [160, 163, 164].

Patients usually present with paresthesia, dysesthesia, numbness, pain, burning, buzzing, muscle aches and coldness on the lateral or anterolateral thigh. Prolonged standing or long walking exacerbates symptoms. Pain relief is usually obtained with sitting [160].

Clinical tests are represented by the pelvic compression (described by Nouraei et al. [165]) executed with the patient lying on the contralateral side; a manual compression is applied downward to the pelvis for 45 seconds to achieve inguinal ligament relaxation. The maneuver is positive if there is a relief of the symptoms. Another test described by Butler is the neurodynamic testing executed with the patient lying on the contralateral side with the knee flexed; with one hand the pelvis is stabilized and with other hand the affected leg is sustained, and then the knee is flexed and adduction is performed obtaining the tension of the inguinal ligament. The test is positive if the neurological symptoms are evoked [158].

Differential diagnosis includes lumbar stenosis, disc herniation, nerve root radiculopathy, iliac crest metastasis and anterior superior iliac spine avulsion fracture. Ahmed has speculated about a possible association between meralgia paresthetica and FAI: the anatomical variability of LFCN could be compressed by abnormal hip structures typical of FAI [160, 166].

Neurophysiological studies can help to confirm the diagnosis, especially somatosensory evoked potential and sensory nerve conduction, even if they have some limitations and a sensitivity and specificity of 81.3 % and 65.2 %, respectively. In recent times, magnetic resonance neurography (MRN) has been introduced and appears to produce better results with an accuracy >90 % [158, 167]. Nerve block with local anesthetics is a good diagnostic test [162].

Nonsurgical treatment includes nonsteroidal anti-inflammatory drugs and to avoid compression to the area and physical therapy as the first step.

In case of continuous pain, ultrasound-guided nerve block with a combination of corticosteroids and lidocaine appears to give good results in some patients [168, 169]. Usually the course of this condition is benign and in most cases the resolution is within 4–6 months of nonsurgical treatment.

Pulse radiofrequency ablation of the nerve is infrequently used [158].

Surgical treatment is indicated only in refractory cases. The most common procedures are neurolysis and resection of the lateral cutaneous femoral nerve. Best results are obtained with nerve resection, but patients must accept a permanent change of thigh skin sensation. Some cases of recurrence have been described with neurolysis [158, 160, 165].

Obturator neuropathy is an uncommon mononeuropathy that usually occurs acutely after a well-defined event (surgery or trauma). The pain related to obturator neuropathy can be difficult to distinguish from the pain due to the recent surgical procedure or trauma [170, 171].

Injury to the obturator nerve is rare because the nerve is located deep and protected in the pelvis and medial thigh [172]. The injury can result from entrapping, sectioning, stretching, or crushing the nerve. Other common injury mechanisms are electrocoagulation, ligation, or neuroma formation [172]. Reports have described obturator nerve injury during total hip replacement (poor acetabular screw placement or cement extrusion) and after abdominal procedures or major pelvic surgery [171, 173–181].

The most prominent symptom of obturator neuropathy is pain radiating from the groin into the medial upper aspect of the thigh. Dysesthesia (less frequent) and weakness of the muscles supplied by the obturator nerve can occur in some cases [170, 171, 173].

Ultrasonography, MRI, and plain radiographs can be useful for a complete diagnosis and a proper differential diagnosis. The most accurate diagnostic investigation to confirm obturator neuropathy is needle electromyography (EMG) [170, 171].

Acute obturator neuropathy tends to have good prognosis after nonsurgical treatment [171] that should be initiated as soon as possible to prevent motor deficits or permanent hypotrophy of the muscle group innervated by the nerve [174]. Rest, NSAIDs, and modification of the activities may offer relief too [170, 171]. Surgery, which includes nerve decompression or repair with grafting or end-to-end anastomosis, should be considered in those patients with pain and weakness resistant to nonsurgical treatment and documented EMG changes or response to nerve block [170, 172, 182].