The sciatic nerve is formed by the L4–S3 ventral rami in the sacral plexus. Nerve fibers of the fibular and tibial components maintain a pattern of fiber separation in these branches and in the sciatic nerve. The sciatic nerve physically splits in tibial and fibular divisions at highly variable locations from the pelvis to the popliteal fossa, although this split is more frequent at the distal thigh [24]. Often, the split is oblique and may not be seen in a uniplanar MRI view [25]. Most sciatic neural fibers are destined to motor and sensory innervation distal to the knee. However, important branches arise from the nerve in the deep gluteal space and thigh. A summary of the sciatic nerve branches in the thigh is depicted in Fig. 6 according to Seidel et al. [26] and Sunderland and Hughes [25].

Neural tissue and nonneural tissue compose the sciatic nerve. The ratio neural/nonneural tissue changes from 2/1 at the level of piriformis muscle to 1/1 at the midfemur, i.e., there is an increase in the nonneural tissue contribution as the sciatic nerve courses distally [27] (Fig. 7). The composition of the sciatic nerve also varies during the aging process, with increase in connective tissue and decrease of myelinated nerve fibers [28].

The nerve fibers of the sciatic nerve do not course between the tibial and fibular divisions [17]. However, fibers are often changing from one fascicle to another within each division [25]. Sunderland reported 6 mm as the maximum length of nerve trunk with a constant fascicular pattern, although an individual fascicle can maintain the same neural fibers for greater distances [25]. In general, most fascicles contain fibers for the majority, if not all, of the peripheral branches. Nevertheless, there is a tendency of grouping fibers for different muscles with similar function, for example, the fibers for the hamstring muscles are located anterior-medially in the proximal portion of the sciatic nerve. A progressive arrangement is found until the appearance of fascicles with nervous fibers exclusively destined to specific branches [25].

The sciatic nerve has a segmental arterial supply by branches of the IGA, MCFA, and perforating arteries of the thigh (usually the first and second) [29–31] (Fig. 8). The venous drainage of the sciatic nerve is performed through the perforators to the femoral profunda system in the thigh and to the popliteal vein at the knee [32] (Fig. 9). Nonfunctioning sciatic veins have been related to sciatic nerve symptoms [9].

The sacral plexus is anatomically close to the internal iliac vessels, their branches, and tributaries. The superior gluteal vessels run either between the lumbosacral trunk (L4–L5 ventral rami) and first sacral ventral ramus or between the first and second sacral rami, whereas the inferior gluteal vessels lie between either the first and second or second and third sacral rami (Fig. 10) [17, 33]. The ovaries are close to the sacral plexus, although on the left side the sigmoid is usually between the ovary and sacral plexus. The intimate anatomic relation between the iliac vessels, ovaries, and sacral plexus is an important consideration in sciatica caused by sacral plexus vascular compression and endometriosis [34].

The sciatic nerve is the terminal branch of the sacral plexus and courses anterior to the piriformis muscle in the pelvis. Variation in the relationship between the sciatic nerve and the piriformis muscle is present in 16–17 % of the subjects and can be a cause of sciatic nerve entrapment [35, 36]. After leaving the piriformis muscle, the sciatic nerve runs posteriorly to the obturator/gemelli complex and quadratus femoris muscle, located at an average of 1.2 ± 0.2 cm from the most lateral aspect of the ischial tuberosity and maintaining an intimate relationship with the hamstring origin [18] (Fig. 4). The sciatic nerve then enters the thigh posteriorly to the adductor magnus muscle and crosses anteriorly the long head of the biceps femoris. Next, the nerve runs between the semimembranosus and biceps before accessing the popliteal fossa.

Under normal conditions, the sciatic nerve is able to stretch and glide in order to accommodate moderate strain or compression associated with joint movement. During a straight leg raise with knee extension, the sciatic nerve experiences a proximal excursion of 28.0 mm [37] at 70–80° of hip flexion. Strain of the sciatic nerve increases 6.6 % relative to the extended hip [37]. Fleming et al. measured the sciatic nerve strain throughout ten hip arthroplasty procedures [38]. The strain increased on average 26 % during hip flexion with the knee in extension. This amount of strain is significant and may cause nerve dysfunction. An animal study reported the nerve conduction was completely blocked after stretching of 12 % of the nerve length for 1 h [39]. At 6 % strain, the authors found a decrease of 70 % in amplitude of the action potential after 1 h [39]. The changes in femoral bone morphology may influence sciatic nerve kinematics during hip mobilization [2]. Therefore, it is always important to assess osseous parameters, including femoral and acetabular version (Figs. 11 and 12). Hip flexion, adduction, and internal rotation increases the distance between the greater trochanter and posterior superior iliac spine and the distance between the greater trochanter and ischial tuberosity. This hip position stretches the piriformis muscle and causes a narrowing of the space between the inferior border of the piriformis, the superior gemellus, and the sacrotuberous ligament [40].

The piriformis muscle and tendon are the most common source of extrapelvic sciatic nerve impingement. Yeoman first described the possibility of sciatic nerve entrapment by the piriformis muscle in 1928 [41]. The introduction of the term “piriformis syndrome” has been credited to Robinson, in 1947 [42]. The diagnostic resources have improved over the past decades, and a number of structures have been associated with sciatic nerve entrapment within the deep gluteal space: the piriformis muscle [2, 3, 11, 12, 43–49], fibrous bands containing blood vessels [2, 3, 43] (Fig. 13), gluteal muscles [1], gemelli-obturator internus complex [6, 7], hamstring muscles [4, 5], ischial tuberosity [8, 50], and space-occupying lesions [11, 12]. Additionally, vascular abnormalities [10, 47], prolonged surgery in the seated position [51], acetabular reconstruction surgery [52], and total hip replacement [53] have been reported to cause compression of the sciatic nerve. Considering the variation of anatomical structures causing the entrapment, the term “deep gluteal syndrome” [1] seems to be a more accurate description of this nondiscogenic sciatica.

The piriformis muscle is the most common source of sciatic nerve entrapment [2, 3, 11, 12, 43–49]. The risk of nerve compressive symptoms is increased by the existence of variation in the relationship between the piriformis muscle and the sciatic nerve. Six categories of piriformis-sciatic nerve variations have been identified [35] (Fig. 14). The prevalence of anomalies was 16.9 % in a meta-analysis of cadaveric studies [36] and 16.2 % in a review of published surgical case series [36] (Table 2). It is important to mention that the anomaly itself may not be the etiology of the Deep Gluteal Syndrome symptoms. Martin et al. [2] reported on 35 patients endoscopically treated for deep gluteal syndrome. Eighteen patients involved the piriformis muscle as etiology, including the sciatic nerve passing through the piriformis muscle or a portion of piriformis muscle/tendon passing through or anterior to the sciatic nerve [2]. A thick piriformis tendon hidden under the piriformis belly has been indentified as a cause of sciatic nerve compression (Fig. 15). Hypertrophy of the piriformis muscle has also been associated with sciatic nerve compression [12, 46, 47, 54]. However, of 14 patients with posttraumatic piriformis syndrome, Benson and Schutzer found that only two had larger piriformis muscles on the symptomatic side and seven appeared smaller than the unaffected side [44].

Atypical fibrovascular scar bands and hypertrophy of the greater trochanteric bursae have been reported in many cases of sciatic nerve entrapment [2, 3] (Fig. 13). In 27 of the 35 patients previously described by Martin et al. the greater trochanteric bursa was found to be excessively thickened, and large fibrovascular scar bands were present in many patients [2]. The fibrovascular bands extended from the posterior border of the greater trochanter to the gluteus maximus on to the sciatic nerve and then proximally to the greater sciatic notch [2]. The obturator internus/gemelli complex is commonly overlooked in association with sciatica-like pain [6, 7, 15]. As the sciatic nerve passes under the belly of the piriformis and over the superior gemelli/obturator internus, a scissor effect between the two muscles can be the source of entrapment. In one case, Martin et al. found the obturator internus penetrating the sciatic nerve.

The sciatic nerve courses close to the hamstrings origin at the most lateral aspect of the ischial tuberosity (Fig. 4). Avulsions of the hamstring tendons or congenital fibrotic bands can affect the sciatic nerve causing symptoms of entrapment [4, 5, 55–57]. Other sources of sciatic nerve entrapment within the deep gluteal space include malunion of the ischium or healed avulsions, greater trochanter ischium impingement (Fig. 16), tumor, sciatic nerve venous varicosities [9] (Fig. 17), and gluteus maximus (from a prior iliotibial band release). Intra-articular hip disorders may also be involved with sciatic nerve symptoms. Patients submitted to surgical treatment of femoroacetabular impingement often recover hip mobility or can move the hip without having intra-articular pain. Considering that neural structures are sensitive to strain [39], increased mobility can lead to strains greater than normal in the sciatic nerve, triggering the sciatic nerve entrapment symptoms in patients with variations in the piriformis-sciatic nerve relationship. This factor may be even more important in patients with capsular laxity and abnormal bone morphologies, such as increased femoral version, retroversion, or greater trochanteric dysmorphism.

The fibers of the sciatic nerve can be also entrapped in the lumbar spine, pelvis, extrapelvic, and thigh. A discussion regarding intrapelvic etiologies of sciatic nerve entrapment will be provided in the differential diagnoses section. The table 3 summarizes the etiologies of sciatic nerve entrapment reported within the literature.