Sciatic Nerve

General Considerations

Being the largest nerve in the body, the sciatic nerve usually consists of L4–S3 contributions.

After its intrapelvic course in the vicinity of the sacrum, the bladder, the rectum, and the iliac vessels, it leaves the pelvis in the incisura ischiadica major between the piriformis muscle and the gemellus superior muscle passing the infrapiriform foramen.

Different courses above/within/beneath piriformis muscle have been described. ¹

Despite appearing as one nerve, the sciatic is already divided in its peroneal and tibial aspect with respective root supply at an infrapiriform level.

The peroneal portion of the nerve is located laterally, whereas the tibial portion remains medially. In varying manifestations, a dividing groove between these two portions can already be seen at an infrapiriform level.

Its close relationship to the hip joint predisposes the sciatic nerve to traumatic or iatrogenic lesions, the peroneal portion being more frequently affected.

One major drawback of a proximal sciatic nerve lesion is its very limited amenability to imaging and electrophysiological preoperative work-up due to its deep localization.

In patients with previous surgery, metal artefacts, e.g., may impair magnetic resonance imaging (MRI) neurography.

High-resolution neurosonography lacks depth of tissue penetration, impeding detailed nerve depiction.

Therefore, frequently the exact level of compression or lesion remains unclear, necessitating an explorative approach with intraoperative inspection and evaluation. This can be accomplished with minimal surgical morbidity by the endoscopic approach we described. ²

In essence, a small entry port of 3 cm is used via the subgluteal fold to follow the nerve proximally by a retractor-held endoscope along its gluteal course. Simple decompression from scar, adhesions, and venous tethering can easily be accomplished by this route. The same port allows for exploration in the opposite caudal direction along the proximal thigh.

Deep Subgluteal Syndrome/Piriformis Syndrome

There still is controversy concerning the proper diagnosis, assessment, and treatment in piriformis syndrome. ³

Some authors introduced the more adequate term of deep subgluteal syndrome (DSS) encompassing different causes for sciatic nerve entrapment. ⁴

Aside from the “classic” piriformis syndrome caused by a hypertrophic muscle or sharp tendinous muscle border, a large variety of pathologies have been reported—compressive fibrous bands, anatomic variants or acquired changes of surrounding muscles such as obturator internus, quadratus internus, and gemellus muscles or the hamstrings, and more. Inborn or acquired bony alterations of the hip joint/ischial tuberosity or vascular abnormalities such as circumferential or penetrating varices may be the underlying cause.

Clinical symptoms consist of deep gluteal pain and sensory-motor deficits involving tibial, peroneal, and dorsal cutaneous femoral nerve.

External rotation, hip flexion, and simultaneous knee extension may provoke the symptoms. Deep gluteal palpation and pressure overlying the sciatic exit and course at its infrapiriform level in relaxed prone and in a lateral decubitus position with the hip flexed, the knee bent, and the leg rotated inward (“quadripartite position”; stretches sciatic and at the same time lifts the nerve to a more superficial level) may provoke the typical pain. Frequently, patients have problems to sit on the affected half of the buttock and prefer to use an asymmetric sitting position that releases pressure on this side.

In terms of imaging, MRI is the gold standard assessing or excluding space-occupying lesions.

High-resolution neurosonography with detailed depiction of the intraneural anatomy is limited due to restricted tissue penetration.

Some reports on electrophysiology with pathologic H-reflexes in different positions may underline DSS. Electromyogram (EMG) alone might be misleading if only the peroneal part of a lesioned sciatic nerve is affected.

Conservative treatment consists of physiotherapy, anti-inflammatory medication, and local injections of corticoids or botulinum under ultrasound control into the corresponding muscles.

According to the literature, both conservative and surgical treatment seem to be helpful, ^{5,​ 6}

and classically only in conservative therapy refractory cases’ surgery is considered. We think this very general approach should be more nuanced. Fibrovascular compression or the above-mentioned secondary causes can only be relieved surgically (see the next section on Surgical Strategy).

Key to successful treatment will remain exclusion or identification of mechanical encroachment, which at times may be hard to achieve. In cases of high degree of suffering or significant functional loss, (early) surgical exploration is justified.

Surgical Strategy

Different approaches have been described, such as infragluteal, transgluteal, and subgluteal (see ▶ Fig. 14.1a–e). ^{2,​ 7,​ 8}

Position is usually prone; anatomical landmarks and the course of the nerve are highlighted (midline, subgluteal skin fold, coccyx, posterior superior iliac spine) with a skin marker.

Using a small horizontal incision within the subgluteal skin fold, the nerve can be easily and bluntly detected in the proximal thigh entering the space between the long head of biceps femoris and the semitendinosus muscle.

This access facilitates dissection of the nerve in both distal and proximal direction.

If necessary, an additional gluteal incision can be made, allowing for transgluteal exposure and decompression of the nerve.

Endoscopy via a subgluteal port enables dissection of the nerve along its gliding tissue and easy identification of the dorsal cutaneous branch. Even in big-framed patients, visualization of compressive tissue and thus targeted surgery up to the infrapiriform foramen level are possible. If the piriform muscle is the origin of symptoms, it can be partially or completely dissected and incised without subsequent gait impairment. ⁶

This seems to account for gemelli muscles as well. In case of a sudden stop and resistance of endoscopic advancement that cannot be resolved and neurolyzed via this route, it is simple and fast to add a transgluteal focused route in a second step during the same surgery. For this, we use an oblique incision at the buttock overlying the anticipated course of the sciatic nerve.

In case of substantial trauma, these two ports could potentially still be connected to a flap resembling the more classic large question mark–shaped skin incision (classic approach according to Henry). This will provide a more extensile overview to the whole region

at the price of massive gluteal muscle disinsertion. Access-related morbidity and muscle trauma, therefore, is a major drawback of this large approach, and even in sciatic nerve reconstruction or tumor surgery at gluteal level, we do not see the need for this approach anymore.

We prevent cutting the gluteal muscles by atraumatic blunt dissection in a more perpendicular trajectory directly overlying the nerve, which already has been identified via the subgluteal port. Muscle dissection is in line with the fiber orientation of the gluteus maximus after sharp incision of the gluteal fascia. Care must be taken to avoid the plane of the gluteal nerve branches and vessels. Intermediate use of a nerve stimulator to detect branches is most helpful.

When treating big or very athletic patients, a fixed frame-retractor system with long blunt blades is useful.

Proximal intrapelvic compression syndromes within the pelvis are rare. Cases of intrapelvic sciatic nerve compression syndromes have been reported, such as sciatic endometriosis (“catamenial syndrome”), ganglion cysts, varices, or postoperative scarring.

Treatment includes hormonal or anti-inflammatory medication.

In case of surgery, transabdominal or minimal-invasive methods can be used. ⁹

14.1.2 Peroneal Nerve

General Considerations

Anatomy

After emanating from the sciatic, the peroneal nerve descends adjacent to the medial border of the biceps femoris muscle.

It then turns laterally toward the fibular head lying superficially. Its proximity to the bones and knee as well as to the tibiofibular joint favors its vulnerability.

The nerve enters the space between the two heads of the long peroneus muscle at the fibular head.

This is the actual anatomic predefined notch.

At this level, the nerve divides into three branches (from medial to lateral): the tibiofibular joint branch, the deep branch, and the superficial branch.

The deep branch innervates anterior tibial muscle and the toe extensors including the hallux.

It supplies the interdigital space between the hallux and the second toe autonomously.

The superficial branch supplies the foot everting long and short peroneus muscles and the lateral lower leg as well as the instep.

Clinical Aspects

The compression neuropathy of the peroneal nerve at the fibular head is the most common neuropathy in the lower extremity. ¹⁰ Sudden nonpainful functional loss is the leading clinical symptom.

However, there seem to be no reliable data on incidence. ¹¹

Unfamiliar physical activity, sustained work in a kneeling position (“harvester’s palsy”), sitting with legs crossed, uncommon postures, and long periods of immobilization with casts stress the peroneal nerve at its notch. By fortifying an already (latently) existing compressive site, an edematous nerve reaction will be induced that leads to further rise in pressure and more edema in a vicious circle.

Furthermore, systemic illness such as diabetes and polyneuropathy predisposes peroneal neuropathy. If a patient presents with pain in an otherwise atraumatic lesion, tumor or an intraneural ganglion cyst needs to be ruled out.

Intraneural ganglia play an important role in the compression syndromes of the peroneal nerve.

There are different theories on the origin of extra-/intraneural or combined ganglia (degenerative/synovial/tumorous).

In recent years, the “unifying articular (synovial) origin of intraneural ganglia” was established. ¹²

In brief, it postulates that connection of tibiofibular joint synovia to articular nerve branches enables entry of synovial fluid into the nerve’s internal structure and thus paves the way for fluid extension within the intraneural space. The progressive filling with synovial fluid and gel leads to formation and rise of intraneural pressure, and as such to an “internal compression syndrome.”

Clinical symptoms may vary from complete/incomplete, whole/partial nerve, etc., and include foot/toe drop, weakness of foot eversion, sensory impairments, and pain.

Thorough physical examination usually gives clear hints to determine the lesion level (pattern of neurological deficit, Hoffmann–Tinel sign, pain, palpable mass).

Note that the posterior tibial muscle (foot inversion) is a tibial nerve–innervated muscle.

This is of clinical importance discerning pure peroneal from combined peroneal-tibial, sciatic, or L5 lesion.

Imaging usually encompasses MR neurography and high-resolution neurosonography depicting caliber changes of the nerve at the compression site or space-occupying lesions such as intra/extraneural ganglia, varices, popliteal aneurysms, and sesamoid bones (“fabella”). Nerve ultrasound gives excellent resolution of lower extremity nerves up to a level of 1 mm, and is easy to apply. It enables quick differentiation of cyst from classic compression or tumor.

Electrophysiology further enhances nerve lesion assessment and gives clues as to the nerve’s functional state by using EMG and conduction studies (complete vs. incomplete lesion, absence of voluntary muscle potentials).

Polyneuropathies and diabetes seem to promote compression; nonetheless, these patients benefit from surgery. ¹³

Surgical Strategy

Surgical strategy is dictated by the underlying pathology. Timing of surgery depends on the severity of symptoms, as the recovery potential of the peroneal nerve is limited.

With severe symptoms and definitely with complete foot drop, we favor prompt surgery.

At the junction of incomplete traumatic nerve lesions and compressive elements (anatomic notch, constricted scar), external compression can prevent regeneration of otherwise intact internal nerve structure (Sunderland lesions I to III, Millesi A and B).

Decompression can enable or at least facilitate proper recovery in these cases.

This is why we are quite generous when it comes to indicating simple decompression at the fibular head notch. The benefit can be enormous, the risk is minimal, and the surgery is simple.

The patient is positioned prone, allowing for decompression of the nerve in both cranial and caudal direction if necessary.

Some authors prefer lateral or supine position with flexed and slightly internally rotated leg.

A semilunar incision is placed on the fibular head anterior to the nerve, avoiding a direct scar on the nerve.

Already at a fascial level, the nerve can be detected digitally in its course medial and posterior to the fibular head. The fascia is then incised and opened up.

Usually, the nerve is surrounded by a gliding fatty tissue that should be maintained and not manipulated or coagulated as it protects and provides the nerve with vessels enabling passive motion during leg movement.

Following the nerve distally, the superficial fascia of the long peroneal muscle inserting at the fibular head is verified, incised, and kept apart.

One should ensure not to open the superficial layer only but also the deeper lamina.

Then, the trifurcation of the nerve can be worked out once again respecting the surrounding gliding tissue.

Electrostimulation is used to identify and test nerve response of the single branches.

For verification of proper decompression, dissectors can be useful.

After wound closure, we prefer compression dressing instead of wound drains.

Mobilization of the patient can start immediately avoiding novel adherences due to scarring.

Intraneural ganglia require a different approach and setting (see ▶ Fig. 14.2a–f).

Frequently, onset of sensorimotor impairments is quick and substantial.

Timing is crucial and early surgery should be scheduled, as only few patients experience a spontaneous and sufficient recovery.

We prefer prone position and a microsurgical setup including microscope, electrostimulation, intraoperative electrophysiology, and neurosonography. Skin incision is determined by the lesion’s extension.

Exposition should comprise the whole lesion including a healthy nerve segment proximal and distal to the lesion.

By doing that, the healthy nerve sections can be inspected and more importantly tracked into/within the cystic part.

The goal of surgery is to decompress the nerve by epineurotomy and cyst fenestration. At the same time, a recurrence is prevented by disconnecting the “feeding” articular branch (“close the faucet”). This is accomplished by radical ligation and transection of the feeding branch as close to the tibiofibular joint as possible. We prefer to excise a larger segment for histopathology in order to enlarge the distance between joint and nerve.

Disconnection is regarded as the most effective measure to prevent cyst recurrence; as multiple articular branches can occur, these also should be ruled out to minimize this risk.

As the cystic wall cannot be dissected from the epineurium, an attempt to make a “radical resection” of the cyst will definitively lead to fascicular damage and thus is contraindicated. The “cyst treatment” is limited to a microsurgical fenestration of the cyst wall at a fascicle free site where it reaches the epineural surface.

In some patients, there is one big communicating intraneural, i.e., intraepineurial, cyst, compressing, dislocating, and thinning out the fascicles. These cases can be treated easily with one larger fenestration.

However, multiple and multilobular cysts can occur. They complicate surgery in so far as more fenestrations are needed and frequently not all cysts can be opened. The recurrence rate is higher in such cases. Intraoperative ultrasound can help to detect deep lying cyst chambers.

We try to avoid electrocauterization within the nerve and prefer mild focused compression using cottonoids to stop bleeding.

In patients with underlying bony deformations in the form of exostosis, fragments, or additional bones (fabella), the surgical task consists of tissue-sparing bone removal, decompression, and creation of a new and smooth nerve bed using autologous fat pads to enable supple passive motion of the nerve during leg movements.

Rarely intraneural varices are the underlying pathology of peroneal nerve deficit. They demand careful microsurgical interfascicular dissection and disconnection of the vessel after epineurotomy.

Results

For simple entrapment neuropathy, there are only a few systematic outcome studies. In addition, they refer to small patient numbers. They report favorable surgical outcome and low complication rates. ^{14,​ 15} This accounts particularly for patients with mild symptoms. ¹⁶

Pain and motor weakness seem to benefit better than sensory function. ¹⁷

Results of surgery for intraneural ganglia differ from simple decompression.

It has been reported that surgery improves pain in the majority of patients.

Improvement of sensorimotor function is dependent on the severity and duration of symptoms prior to surgery, and the extent of lesion. It occurs in 50 to 64% of cases. ¹⁸

A significant problem is recurrent cyst formation, which is reported in up to 24% of the patients. ¹⁹ Disconnection of the feeding articular branch is the accepted measure to prevent recurrent ganglia. ²⁰

The peroneal nerve has low regenerative capacity in general. ²¹

Therefore, in patients with only fair or insufficient recovery, secondary procedures such as transfer of the tendon of posterior tibial muscle have a definite role to improve gait and should be considered in failed nerve regeneration. There is a need to counsel patients in that regard and offer this type of treatment.

Anterior Tarsal Tunnel

This rare entrapment syndrome affects the terminal branch of deep peroneal nerve at the cruciform ligament or underneath the extensor hallucis brevis tendon.

Both the medial (providing the first interdigital space) and the lateral (providing the dorsum) branch can be affected, provoking different symptoms.

Diabetic patients seem to be susceptible.

Association with lumbosacral radiculopathy and foot deformities has been described. ²²

Local and activity-related pain and paraesthesia are the main symptoms.

Conservative treatment consists of anti-inflammatory medication, infiltration with local anesthetics or corticoids, and shoe orthoses.

When symptoms persist, the nerve can be surgically decompressed.

The longitudinal or transverse skin incision follows the dorsal pedis artery as the most important anatomic landmark. After that, the cruciform ligament and the extensor tendon are dissected. Then, the nerve is identified and decompressed by transecting the cruciform ligament. Rarely, part of the tendon needs to be notched. Surgery can greatly be eased if performed in a bloodless field. Pain relief can be achieved in up to 80%. ²³

Entrapment of the Superficial Peroneal Nerve

Isolated entrapment of the superficial peroneal nerve distal to the fibular head is postulated to occur, at the site where the nerve perforates the deep fascia of the leg. ²⁴

MRI and/or neurosonography help to detect compressive pathologies.

Electrophysiology may display lowered conduction velocities or pathologic EMG of the peroneal muscles.

Skin incision is placed about 5 cm lateral to the lateral tibial border.

Then, the fascia is opened and the nerve decompressed. Reports describe pain relief after surgery, with body mass index being a negative predictor for successful surgical treatment. ²⁵

Sural Nerve

Primary sural nerve entrapment is extremely rare. Compression can occur throughout the whole course of the nerve, with pain and sensory impairments being the clinical features. Due to its rather long course, the nerve can be damaged secondarily after fractures and their treatment. Conduction studies reveal pathologic sural nerve values. Imaging using MRI and neurosonography may reveal bony or vascular anomalies or secondary scarring. In case of failed conservative treatment, the nerve can easily be accessed between the lateral ankle and the Achilles tendon, and decompressed. ²⁶ Patients undergoing diagnostic sural nerve biopsy harbor the risk of painful neuroma formation. As mostly only a few centimeters are harvested for histopathological exam, the proximal neuroma often is located superficially and distal to the fascia. Symptoms such as pain and dysesthesia occur in up to 19% of the patients on contact but also when moving. ²⁷ Conservative treatment consists of medication, serial infiltrations under ultrasound guidance using local anesthetics and/or corticoids. ²⁸ If conservative treatment fails, neuroma resection can be performed. However, a new neuroma will form anyway. Superficial neuromas are much more prone to ectopic nerve activity and painful transformation. Surgery therefore aims at high-level nerve resection to bury the stump deep within the muscular compartment. This implies to extend the resection above mid lower leg.

14.1.3 Tibial Nerve

Anatomy

In contrast to the anatomic course of the peroneal nerve, the tibial nerve proceeds in a straight line along with tibial artery to the lower leg before it changes direction toward the dorsal aspect of the inner ankle to branch into a medial and a lateral plantar nerve that supply the sole of the foot and its intrinsic muscles.

Usually, L5–S2 account for tibial nerve function providing all foot and toe flexors including posterior tibial muscle (foot inversion) and sensation to the sole of the foot and heel (calcaneal branch). The tibial nerve passes the soleal sling at the knee level (two to three fingers’ breadth below the flexor crease) to enter the tarsal tunnel distally behind the medial malleolus.

The calcaneal branch usually forks off the main branch before or within the tarsal tunnel.

The tibial nerve then divides into the sensorimotor medial and lateral plantar nerve before or after entering the flexor retinaculum. There are different anatomically given bottlenecks, with the most important one being within the tarsal tunnel at the ankle.

Proximal Soleal Sling

A fascia connecting the tibial and fibular head of the soleus muscle can compress the tibial nerve. Aside from idiopathic causes, posttraumatic and diabetic forms have been described. Clinical presentation is calf pain and mostly sensory problems in addition to a Hoffmann–Tinel sign. Weakness can afflict flexor hallucis longus muscle. MRI may help to confirm soleal sling syndrome by identification of nerve swelling and hyperintensity at this location. ²⁹ As this entrapment syndrome is very rare, symptomatic patients may have undergone tarsal tunnel surgery prior to its diagnosis.

Surgery consists of a skin incision at the medial calf and dissection of the gastrocnemius fascia. After identification of the space between the gastrocnemius and the most proximal aspect of the soleus muscle, the sling can be divided. ³⁰

Posterior Tarsal Tunnel Syndrome

A proximal tarsal tunnel syndrome (TTS) can be differentiated from the distal one. In nearly 80% of the cases, an underlying pathology such as perineural ganglia, lipoma, and nerve sheath tumors account for TTS.

Clinically, the proximal TTS also affects the calcaneal branch and therefore includes sensory deficits at the heel. This is in contrast to the distal TTS. Toe flexion and/or toe spreading may be impaired. The surface of the sole can be flattened. A Hoffmann–Tinel sign can be elicited along the nerve’s course within the tarsal tunnel. ³¹

Imaging should include MR neurography and high-resolution neurosonography.

Electrophysiologically, lowered conduction velocities of the lateral and medial plantar nerves in combination with altered EMG of toe flexor may empower the diagnosis.

In primary TTS, conservative management with anti-inflammatory medication, physiotherapy, and splinting is of first choice.

Patients with persisting or worsening symptoms may undergo decompressive surgery.

The same accounts for secondary space-occupying lesions provoking TTS.

A semilunar skin incision is placed along the course of the nerve dorsal the medial malleolus.

Dissection of the complete retinaculum flexorum should be performed assuring the decompression not only of the main trunk but also of the medial and lateral plantar nerve. This long incision, however, bears a relatively high risk of impaired wound healing (skin tension, vascular insufficiency, tissue edema, venous insufficiency). Therefore, we prefer one or two short horizontal skin incisions—the first at the proximal and the second at the distal end of the tunnel. The skin bridge can be lifted with a Langenbeck retractor, or alternatively a retractor-held endoscope can be used from a proximal to distal direction. Sparing of the calcaneal branch is of utmost importance.

Surgery can be performed openly or with endoscopic assistance. ³²

Especially in patients with diabetes or venous insufficiency, preservation of veins and arteries is mandatory to prevent impaired wound healing.

We usually advise the patients to intermittently elevate the leg and ambulate on elbow crutches for the first 1 to 2 weeks of mobilization, avoiding full weight bearing on the affected foot.

Results may vary significantly: patients with secondary causes seem to benefit more frequently from the procedure contrasting with those with idiopathic origin. ^{33,​ 34}

Distal Tibial Nerve Compression Syndromes

For the sake of completeness, rare distal entrapments of the medial plantar nerve (“jogger’s foot”) as well as of the lateral plantar nerve (“Baxter’s neuropathy”) are mentioned in the literature. ³⁵

Morton’s Neuroma

Even more distal and certainly more frequent is the entrapment of the terminal branches of the medial and lateral plantar nerve. It affects mainly the nerves between the second and third or third and fourth metatarsal bones. Chronic irritation of the nerve and adjacent bursa intermetatarsophalangea may provoke a painful pseudoneuroma and chronic bursitis. Women are affected four times more often, and multiple Morton’s neuromas are frequent. Association with foot deformities have been reported. ³⁶ Arthritis and other degenerative osseous conditions should be excluded.

Patients often prefer to walk barefoot as narrow shoes may provoke the symptoms.

Clinically, aside from pain and sensory deficits, the characteristic Mulder’s sign is the main feature. It is performed by compressing the arch of the foot in a mediolateral direction and simultaneously applying pointed pressure on the sole between the affected metatarsal bones.

MRI imaging confirms the diagnosis. High-resolution ultrasound is also capable of detecting the mass. ³⁷

In addition to medication, physiotherapy, and splinting, diagnostic therapeutic blocks are indicated. Infiltration can easily be performed with or without ultrasound guidance from a less painful dorsal interdigital approach. Serial infiltration with local anesthetic and corticoids aims at reducing pain and inflammation. However, we think its potential to lead to long-lasting relief in severe Morton’s neuralgia is limited. Surgical excision of the neuroma, in contrast, has a strikingly high success rate.

For surgery, a dorsal and a plantar approach have been described. ³⁸ We have clear preference for the dorsal interdigital “web-space” approach as it circumvents a very painful plantar incision that limits early weight bearing and has high potential for wound infection. Most authors use the dorsal approach and either resect the pseudoneuroma or decompress it. ³⁵ The pseudoneuroma is located directly between the eminences of the metatarsal heads underneath the transverse metatarsal ligamentum (TML).

A 3-cm longitudinal incision is placed from in-between the bases of the affected toes to proximal. Once the metatarsalgia have been identified, they are pushed apart by a small retractor placed on the bone to open the space. The visible TML builds the rooftop of the pseudoneuroma. It is either incised to approach the pseudoneuroma directly from above or left intact to reach from a more anterior trajectory. The conglomerate of pseudoneuroma, bursa, and thickened sensory digital nerve endings in the pseudoneuroma are dissected out and excised. Surgery is greatly eased in a bloodless field and can be accomplished under local anesthesia.

Results are very satisfying even in the long term. ^{36,​ 38,​ 39,​ 40}

14.1.4 Lateral Femoral Cutaneous Nerve (Meralgia Paraesthetica)

The incidence of meralgia paraesthetica (MP) is estimated at 4 to 10 per 10,000. Mean age of occurrence is 30 to 40 years, and correlation with pregnancy and carpal tunnel syndrome has been reported. ⁴¹ A total of 7 to 10% of the patients display bilateral manifestation. ⁴² There seems to be an association with positioning in surgery in prone position, weight change, tight clothing, etc. ⁴³ Being a pure sensory nerve, patients with MP suffer from paresthesias or dysesthesias in the anterolateral thigh depending on posture. Frequently, there is a burning and tingling component on the pain. Classic teaching states retroflexion (“inverse Lasègue”) as pain inflicting posture. In our observation, we find both retroflexion and hip flexion or sitting to provoke pain. In clear cases, there is a punctum maximum (PM) of the pain in the vicinity of the anterior iliac spine, where finger tapping can elicit the typical painful sensations spreading to the anterolateral thigh. The PM should be in accordance with the lateral femoral cutaneous nerve (LFCN) course and is the supposed point of compression.

Electrophysiology may show lowered conduction velocity of LFCN; imaging with high-resolution neurosonography can reveal the nerve and its compressive site.

In addition, MRI may help to exclude compressive pathologies in the nerve’s vicinity.

Anatomically, the nerve arises from L1–L2 and then takes its course beneath the iliac fascia in the retroperitoneum toward the superior anterior iliac spine (SAIS). ⁴⁴

At this point, the nerve bends nearly 90 degrees, entering the thigh usually below the inguinal ligament and lateral to the sartorius muscle border covered by the thigh fascia (85% of the cases). ⁴⁵

There are several variants of the nerves’ course, from intrapelvic to infrainguinal. The LFCN can run underneath, through, or above the ligament. It can also perforate the sartorius muscle. At times, it will run above the iliac spine, and can have a bony roof or its own bony iliac canal. ⁴⁶

Differential diagnoses such as general neuropathy, spinal problems, pathologies of the lumbar plexus, or intrapelvic causes have to be excluded.

In roughly 25% of patients, symptoms will resolve spontaneously especially if associated with pregnancy.

Aside from weight reduction, change of clothing habits and infiltrations using local anesthetics or corticoids can be applied with a high success rate. ⁴⁷ In patients with pain refractory to conservative treatment or intractable pain, surgery is indicated.

There are two surgical techniques available: one is a simple decompression at the inguinal ligament level, the other one is an intra-abdominal transection of the nerve. None has proven significant superiority. ^{48,​ 49}

We prefer decompression as a first surgical step, leaving transection for cases of failed decompression and massive residual pain. After supine positioning, a 4-cm skin incision is placed transversely from SAIS in a medial direction. This allows for supra- and infrainguinal dissection. The subcutaneous tissue is bluntly separated freeing the fascia and enabling identification of the inguinal ligament, the lateral sartorius muscle border, and the fascia lata.

Once the fascia is opened, the LFC nerve usually can be found in a triangle between the SAIS laterally, the inguinal ligament above, and the sartorius muscle medially. The nerve is then followed proximally to its point of compression toward the inguinal ligament.

Now step-by-step decompression of the nerve is carried out by nicking the inguinal ligament, sartorius muscle or other compressive structures. Sometimes the nerve is covered by an own fascia layer on its way from the abdominal space into the thigh, which than should also be incised.

When accessing the nerve via a retroperitoneal route, an incision is placed above and parallel to the inguinal ligament centering the anterior superior iliac spine. Then, the aponeurosis of the external oblique muscles is split.

The fibers of the internal oblique and transversus abdominis muscles are dissected to allow identification of the nerve underneath the iliac fascia heading toward the SAIS. ⁵⁰

At this point, decompression can be performed. Authors postulate a better feasibility of nerve detection ⁵¹ by this more invasive approach. In case the nerve is transected intra-abdominally, the stump should remain without any other compression deep in the abdominal space (e.g., iliac fascia).

In conclusion, the majority of patients can be treated conservatively, and will only have transient symptoms. In refractory cases, surgery is an option. We prefer simple decompression at the inguinal level as the first surgical treatment option. In severe debilitating cases with prior recurrent surgery, we see intrapelvic transection as an option. For this, we can also enter from below the ligament. The nerve can be followed along its intrapelvic course by using a retractor or a retractor-held endoscope.

However, there still is ongoing debate whether the nerve should be approached from a supra- or infrainguinal access.

Moreover, there is disagreement whether decompression or neurotomy is the most appropriate primary surgical treatment.

There are no reliable data assessing large patient collectives favoring one or the other method. ^{47,​ 49}

14.1.5 Ilioinguinal Nerve/Iliohypogastric Nerve/Genitofemoral Nerve

These nerves are provided by T12–L3.

Clinically, the supplied area may vary significantly, overlapping also with the pudendal nerve, complicating a clear diagnosis.

MRI and ultrasound may exclude space-occupying masses.

However, true entrapment syndromes of these nerves are rarities.

Most of the neuropathies arise after iatrogenic manipulation. ⁵²

When reoperating, it can be very difficult to find the nerves within in the scar due to their small diameter.

In analogy to Morton’s neuroma or meralgia, a deep nerve resection can be taken into account.

14.1.6 Femoral Nerve

The femoral nerve is built by L1–L4 contributions. It follows the psoas muscle dorsally and laterally and clings to the femoral vessels entering the thigh underneath the inguinal ligament. At this point, there are variants in the branching pattern.

Although the space beneath the inguinal ligament is narrow, primary compression neuropathies of the femoral nerve are uncommon.

When it comes to traumatic or iatrogenic lesion due to surgery, positioning, or compressive hematomas—either inguinal or retroperitoneal—the nerve is highly susceptible to secondary compression ⁵³ (e.g., by scar).

Depending on the level of impairment, not only knee extension but also hip flexion due to weakness of quadriceps and iliopsoas muscle occurs.

Sensory areas comprise median femoral cutaneous and saphenous nerve.

MRI and ultrasound rule out secondary causes.

Electrophysiological assessment reveals depth of nerve damage.

Treatment depends on the underlying pathology necessitating either trans/retroperitoneal or inguinal approach for nerve decompression.

If compression in the vicinity of the inguinal ligament is suspected, an incision parallel to it allows exploring the nerve’s intra- and extrapelvic portion.

Usually, the nerve lies lateral to the femoral vein and artery.

By either palpation or ultrasound, the vessels can easily be depicted and marked on the skin.

After incision, the subcutaneous fat is mobilized and the fascia identified. Incision of the fascia gives view on both vessels and the nerve.

There is considerable variation of branching pattern and level.

Thus, one has to be particular careful not to harm the rather small-sized muscle and sensory nerve divisions and other nerves such as the femoral branch of the genitofemoral nerve.

The inguinal ligament can now be partially incised for proper decompression.

As the skin in the groin region is very flexible, the same skin incision suffices for a suprainguinal, i.e., retroperitoneal, inspection and decompression of the femoral nerve.

Otherwise, it can easily be extended into a semilunar incision along the ventral iliac bone.

After mobilizing the fat, the aponeurosis of the external oblique muscle, internal oblique muscle, and rectus abdominis muscle can be split bluntly if needed.

Once the peritoneum is identified, it can be retracted by self-holding systems giving view to the iliopsoas muscle.

Usually, the femoral nerve can be found at its medial border within the muscle’s fascia.

Psoas hematomas represent a cause of femoral nerve impairment: in those cases, fascial opening and evacuation of the hematoma significantly improve the situation.

The nerve can be easily followed caudally to the inguinal ligament.

As already detailed for the LFCN, the femoral nerve can also be visualized from its extra- to intrapelvic course by lifting the inguinal ligament. An endoscope with 30 degrees optics enables following its course from an infrainguinal approach without the need to go transmuscular via the abdominal wall (see ▶ Fig. 14.4).

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