Fig. 19.1
Cross sectional anatomy of the leg at mid calf level
Fig. 19.2
Cross sectional anatomy of the thigh
Fig. 19.3
Anatomy of the peroneal nerve
Innervation
For our purposes within the text, especially with our emphasis on nerve compression and neurotization, a different way to conceptualize the anatomy is by visualizing the leg from a purely nervous perspective. This begins superiorly with the lumbar and sacral plexi, a collection of nerve roots that form the source of the nerves to the leg. The lumbar plexus is anterior to the transverse processes of the lumbar vertebrae and is formed from L1–L4 as well as contributions from T12. The most superior branches are the iliohypogastric (T12–L1) and ilioinguinal (L1) nerves, which innervate the transversus abdominis and internal oblique muscles before continuing as sensory nerves innervating the skin of the gluteal region, hypogastrium, and the anterior scrotum or labia. The next is the genitofemoral (L1–2) nerve, which after innervating the cremaster muscle continues on to the femoral and genital rami, supplying sensation to the skin of the anteromedial thigh as well as the scrotum or mons pubis. Next is the lateral femoral cutaneous (L2–3) nerve, a purely sensory nerve that supplies the lateral thigh. The motor innervation of the next two subsequent divisions, the obturator (L2–4) and femoral (L2–4), has been described above. Both of these nerves have sensory terminations in the medial and anterior thigh, respectively. This portion of the femoral nerve is known as the anterior femoral cutaneous (L2–3) nerve. A separate, more inferior portion of the femoral nerve continues inferiorly as the saphenous (L3–4) nerve, which supplies sensation to the medial aspect of the leg.
The sacral plexus is formed from the spinal roots S1–S4. The anterior rami of these nerve roots combine with contributions from L4 and L5 to form the lumbosacral trunk. The first branch is the superior gluteal nerve (L4–S1), which innervates the gluteus minimus, gluteus medius, and tensor fascia latae. This exits the pelvis above the piriformis muscle, while the inferior gluteal nerve (L5–S2) exits below the piriformis and innervates the gluteus maximus alone.
The major offshoot of the lumbosacral trunk is the sciatic nerve, which spans contributions from L4–S3. It is a major motor and sensory nerve. The tibial portion of the nerve innervates all the muscles of the posterior compartment of the thigh, the posterior compartment of the leg, and the sole of the foot (see above for specific muscles innervated). It terminates as a sensory nerve innervating primarily the sole of the foot, as well as the posterolateral and medial surfaces. The nerves innervating the sole of the foot are known as the medial and lateral plantar nerves.
The common fibular or peroneal portion innervates the short head of the biceps femoris, all muscles in the anterior and lateral compartments of the leg, and the extensor digitorum brevis. This branch also terminates as a sensory nerve innervating the anterolateral surface of the leg and dorsal aspect of the foot. Specifically, the nerve innervating the lateral aspect of the leg is known as the sural nerve. The first webspace is innervated by the deep peroneal nerve while the rest of the dorsal foot is innervated by the superficial peroneal nerve.
The posterior femoral cutaneous nerve (S1–3) is the next major branch of the lumbosacral trunk, also passing inferiorly to the piriformis muscle. This nerve, however, is exclusively sensory, innervating the posterior surface of the thigh and leg as well as the perineum. These sensory branches are called the perineal branches and inferior cluneal nerves. The last major branch is the pudendal nerve (S2–4), which has both motor and sensory functions. It innervates the muscles of the perineum, the external urethral and anal sphincters, as well as the levator ani muscle. It also provides sensation to the penis, clitoris, and most of the perineum. Additional direct branches from the plexus innervate the piriformis (S1–2), obturator internus (L5–S1), and quadratus femoris (L4–S1) muscles.
Compression Syndromes
Pudendal Neuralgia
For nearly every major nerve of the lower extremity, there is a corresponding compression syndrome. We will begin superiorly and continue our description inferiorly. The first compression syndrome we will discuss is pudendal nerve compression. Pelvic pain is an extremely complex and heterogenous group of diagnoses. These patients often present emotionally distraught, are ashamed of their problem, and are with little hope of improvement. However, in patients who fit specific criteria, nerve compression syndromes may be the cause of the pelvic pain. In these patients, intervention can provide some hope of relief for this extremely disabling and embarrassing problem.
The pudendal nerve is derived from sacral roots S2–4, though it is primarily derived from S3 in anatomical studies [1]. It is a mixed nerve, containing motor, sensory, and autonomic fibers [2]. After originating from these sacral roots, the pudendal nerve enters the gluteal region through the infra-piriform canal. At this level, it exits between the sacrospinal ligament ventrally and the sacrotuberous ligament dorsally [1]. The nerve then enters the perineal region through the lesser sciatic foramen and then continues into Alcock’s canal [1]. The site of compression is often at the site where the nerve passes between the sarcospinal and sacrotuberous ligaments. Another possible location of entrapment is within the fascia of the obturator externus, through which the nerve passes to enter Alcock’s canal [1].
During this terminal section, the pudendal nerve divides into three branches: the inferior anal nerve, the perineal nerve, and the dorsal nerve of the penis or clitoris [3]. In some patients, the inferior anal nerve may arise more proximally from the pudendal plexus itself [1]. The symptoms of pudendal neuralgia correspond directly to the function of these three branches. These symptoms may include unilateral or bilateral pain in the female vulva, vagina, or clitoris or, in the male, the scrotum, testes, or penis [3]. Patients may describe the pain as burning, torsion, or heaviness or the sensation of a foreign body in the rectum or vagina [1]. In severely affected patients, urgency or incontinence of urine or stool may also be part of the presentation [4].
Many cases are idiopathic. However, there are some known inciting factors. The compression from cycling, especially in competitive or long-range cyclist, has been shown to cause pudendal neuralgia in some patients [5]. Diabetes is also another known risk factor. Certainly, regional surgery – whether urologic, gynecologic, or anorectal – may also create or exacerbate an existing problem [1].
There is no absolute agreement about the exact diagnostic criteria for pudendal neuralgia. However, a group of urologic surgeons, neurologists, and pain specialists in Nantes, France, who have published extensively on this disorder have proposed a five-part set of diagnostic criteria, now known as the “Nantes Criteria.” This includes the following: (1) there is pain in the anatomic territory of the pudendal nerve; (2) pain is worsened by sitting; (3) the patient is not woken at night by the pain; (4) there is no objective sensory loss on clinical examination; and (5) the patient has a positive response to an anesthetic pudendal nerve block [6]. Some of these criteria bear more discussion. Patient will not only complain of difficulty sitting, they can often be observed to be uncomfortable in a sitting position during the interview and clinical exam. Length of time sitting has been used as criteria in some studies to demonstrate postoperative improvement in nerve function. In some patients, sitting on a toilet relieves the discomfort due to a lack of compression on the nerve [6].
In patients who present with sensory loss in the distribution of the superficial perineal nerve, it is mandatory to rule out the presence of a sacral nerve root lesion, including the cauda equina nerve roots or a sacral plexus lesion [6]. In our protocol, patients undergo a CT-guided injection of a steroid-anesthetic combination. These injections are not only diagnostic but potentially therapeutic. The only patients considered for surgery are those who have a temporary but no sustained benefit from these injections. A small percentage of patients improve from this injection alone. In a study by Mamlouk et al., 2 of 31 patients improved with CT-guided injection alone. 14 patients had improvement in symptoms with nerve block, and all 14 patients had improvement postoperatively [7]. On rectal exam, the patients have exquisite tenderness at the region of the ischial spine [1].
There is both surgical and nonsurgical treatment for pudendal neuralgia. The nonsurgical treatment is generalized treatment for neuropathic pain. Therapies include topical lidocaine gel, amitriptyline, and tramadol [2]. However, all of these therapies are nonspecific and have side effects. In patients who meet the criteria described above, especially having temporary relief with the anesthetic block, we recommend surgical release of the nerve. This is performed with the patient in a prone position. We use a nerve stimulator as an adjunct to determine the identity of the nerve as well to verify its function at every point during the procedure. We also do not perform bilateral nerve releases simultaneously out of concern for possible temporary or in rare cases permanent nerve dysfunction after extensive release. The nerve is primarily trapped in two locations: in between the sacrospinous and sacrotuberous ligaments, in Alcock’s canal, and/or the fascia of the obturator internus muscle [8].
We confirm the site of the patient’s Tinel sign preoperatively. We then make a diagonal incision over the medial third of the buttock, extending from superior-lateral to inferior-medial. This is typically over the site of the Tinel. The dissection proceeds down through the soft tissue to reach the level of the nerve. The nerve is most easily identified directly lateral to the anus. We then perform an extensive release and neurolysis of the nerve, confirming its freedom from as far proximally and distally as can be observed through this posterior approach.
During release of this passage in symptomatic patients, we have directly observed the nerve to be often scarred and with abnormal clinical morphology. In some patients with venous stasis disease or dilation of the veins, this venous engorgement itself may be the cause of the compression syndrome. A randomized controlled trial by Robert et al. demonstrates the benefit of the release. 32 patients who had perineal pain and a positive response to a pudendal nerve block at the ischial spine and Alcock’s canal were randomized to either surgery (n = 16) or control (n = 16) groups. At 12 months, 71.4% of the surgery group reported improvement in their pain vs. 13.3% of the control group (p = 0.0025) [8].
Piriformis Syndrome
Piriformis syndrome (PS) is defined by sciatica caused by the direct compression of the sciatic nerve by the piriformis muscle as it exits the pelvis. PS is often misdiagnosed as disc disease and therefore may be diagnosed late. PS is often idiopathic but may be associated with gluteal trauma and posttraumatic scarring [9]. It has been associated specifically with pregnancy, competitive cycling, and certain medications [10–12]. Anything that expands muscle or compresses the sciatic nerve at that level – including lipomas, hematomas, and inflammation of the muscle – can contribute to the development of PS [13–15].
The patient will present with complaints of pain running down the leg, particularly in the gluteal region and posterior leg, exacerbated with sitting or prolonged periods of standing [9, 16, 17]. This may be positional and may radiate to the groin. In patients with long-standing or severe disease, associated foot drop has been reported [18]. Unlike disc disease, there is no associated back pain [17]. On exam, the patient will have pain with leg flexion, adduction, and internal rotation. They will also have a tender sciatic notch and piriformis muscle [9]. The Freiberg sign is specifically associated with this diagnosis. The patient’s hip is placed in extension and internal rotation, and the patient is asked to externally rotate the hip against resistance. Positive findings include pain at the piriformis and reproduction of sciatica symptoms. An additional clinical maneuver is the Pace sign in which the patient is asked to resist abduction and external rotation of the hip while in the seated position, increasing stress on the piriformis muscle [9]. PS is a diagnosis of exclusion, and patients must be ruled out for other causes of sciatica including lumbar radicular compression, inflammatory or mechanical sacroiliac problems, or inflammatory, infectious, or tumor-related pelvic disease [17]. Preoperative imaging includes radiographs of the hip and pelvis, EMG of the sciatic nerve, MRI of the lumbar spine and pelvis, and MR neurography.
Conservative therapy with medication, such as muscle relaxants and physiotherapy may aid a considerable number of patients [9, 17]. In a recent study, conservative therapy significantly ameliorated symptoms in 51.2% of 250 patients who presented with PS [17]. In patients who do not respond to conservative management after a period of 6–12 weeks, pain management specialists may also attempt therapy with either anesthetic or a combination of anesthetic and corticosteroid. In a prospective, randomized controlled trial comparing these two therapies, there was no significant difference in outcome, indicating that the syndrome is mostly muscular in origin [16]. Ultrasound-guided injection improves accuracy of locating the piriformis muscle [19]. Nonsurgical therapy with botulinum toxin can also be attempted in order to decrease the size and thickness of the muscle and then its compression of the nerve. In a case control study, MRI was used to evaluate 12 patients with PS after botox injection vs. eight controls with PS who were not injected. The patients who had been injected demonstrated a significant decrease in the thickness and volume of the muscle as well as an increase in fatty infiltration [20].
In patients with recalcitrant disease, we recommend surgical release. We typically perform this release through a short incision with partial resection (tenotomy) of the piriformis and superior gemellus muscles. The nerve is freed from the scar tissue surrounding it and an extensive neurolysis is performed. Many patients present with both piriformis syndrome and pudendal neuralgia concurrently. Simultaneous releases can easily be performed.
Femoral and Obturator Nerve Compression
As with other compression neuropathies, femoral and obturator neuralgia can present with vague symptoms of pain, weakness, and numbness. However, specific diagnostic considerations can allow for appropriate differentiation. Femoral neuralgia presents with numbness of the anterior thigh and weakness of knee extension. Patients may complain of a subjective feeling of knee instability [21]. The two most common sites of femoral nerve injury are in the retroperitoneal space or under the inguinal ligament [21]. This may occur during urologic or gynecologic surgery, especially when using a large retractor called a Bookwalter [22]. The nerve can also be injured during anterior approaches to hip surgery and even from prolonged lithotomy positioning [21].
In obturator neuralgia, numbness extends down the medial thigh. On exam, the patient will have weakness of hip adduction. Obturator pathology may be associated with an obturator hernia. This can be identified by pain of the medial thigh on internal rotation of the hip, known as a Howship-Romberg sign. Obturator compression may be caused by pelvic fractures, especially those involving the sacroiliac joint, and prolonged labor as well as many of the same causes of femoral compression [21]. It may be related to inferior pubalgia or entrapment within the adductor canal of the medial thigh.
Electrodiagnostic and nerve conduction studies of the involved nerve, as well as the contralateral normal side, are recommended [21]. For example, if the femoral nerve has axonal loss less than 50% of the normal, contralateral nerve, these patients would be expected to have return of functioning within 1 year. However, if axonal loss is greater than 50%, half of these patients showed no improvement [23]. No nerve conduction studies can be performed of the obturator nerve, though EMG studies may have some utility if the diagnosis is uncertain [21].
The treatment for either obturator or femoral nerve compression is initially conservative, using methods such as physical therapy and steroid injections. In select patients who do not improve with conservative management, surgical treatment may be indicated. A neurolysis or nerve release may be combined with a local nerve transfer. For example, if the femoral nerve is not functioning normally, we perform a transfer from one of the branches of the obturator nerve to the quadriceps to the femoral nerve in addition to a neurolysis.
Peroneal Nerve Compression
The peroneal nerve can be compressed at the fibular head, clinically presenting as foot drop. Idiopathic cases are common, but typically there is a recent or remote history of surgery or trauma. Foot drop may also be the first presenting symptom of central nerve disorders, including L4/L5 spinal disc disease and neurologic syndromes such as Charcot-Marie-Tooth disease, which should be ruled out before embarking on surgical treatment. Potential donor muscles, e.g., tibialis posterior and peroneus longus, should be examined for strength during initial evaluation. If the donor muscles are weak, then a central lesion should be considered. Electromyography (EMG) and nerve conduction studies (NCS) can also be helpful in localizing the lesion. Long-standing compression may result in an irreversible denervation of the tibialis anterior muscle. This must be taken into account when planning a treatment strategy [24].
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