Lumbosacral plexus

• Lumbosacral plexus: anterior rami of L1-S3 roots.

  • All major lower extremity nerves arise from it.

  • Anatomically divided into upper lumbar plexus and a lower lumbosacral plexus.

• Lumbar plexus is formed by contributions from T12 to L4.

  • Lies retroperitoneally behind the psoas muscle.

  • Gives rise to 3 major and 3 minor nerves. 

    • The 3 minor nerves are the iliohypogastric, ilioinguinal, and genitofemoral. 

      • The first two arise from a common trunk originating from L1 with some contributions from T12. 

      • The genitofemoral nerve arises from L1 and L2. 

    • The 3 major nerves are the femoral, obturator, and lateral femoral cutaneous. 

  • The lateral femoral cutaneous nerve originates from L2 and L3. 

    • Pure sensory nerve

  • The femoral nerve originates from the posterior divisions of L2, L3, and L4.

    • Innervates iliopsoas, pectineus, sartorius, and quadriceps muscles

    • Sensation to medial calf via saphenous nerve, and anterior-medial thigh via the medial and intermediate cutaneous nerves of the thigh.  

  • The obturator nerve originates from the anterior divisions of L2, L3, and L4 and divides into an anterior and a posterior division. 

    • The anterior division gives innervation to the adductor brevis, adductor longus, and gracilis muscles. 

    • The posterior division gives innervation to the obturator externus and a portion of the adductor magnus (which is also innervated by the sciatic nerve). 

    • Cutaneous sensation to a small area of skin on the medial aspect of thigh.

• The lower lumbosacral trunk is a structure that originates from L5 and S3 roots, with an additional component from L4 root. It then joins the sacral plexus to form the sciatic nerve (L4-S3), which is not only the largest nerve of the lumbosacral plexus, but the largest nerve in the body. 

  • The anterior divisions of L4 through S3 contribute to form the tibial division of the sciatic nerve. 

  • The posterior divisions from L4 through S2 contribute to the common peroneal division of the sciatic nerve. 

• The superior gluteal nerve originates from L4, L5, and S1 and innervates the gluteus medius, gluteus minimus, and tensor fascia latae. 

  • These muscles contribute to thigh abduction, with the tensor fascia latae acting as the main abductor when the hip is flexed, and the gluteus medius and minimus acting as the main abductors when the hip is extended. 

  • There are no cutaneous sensory fibers.

  • Superior Gluteal Nerve Injury.

• The inferior gluteal nerve originates from L5, S1, and S2 and innervates the gluteus maximus, which is an extensor of the hip joint. 

• The posterior cutaneous nerve of the thigh originates from S1, S2, and S3 and gives sensory cutaneous innervation to the lower buttock and posterior thigh. 

  • It courses adjacent to the sciatic nerve and given its proximity almost gets affected in traumatic injuries to the sciatic nerve.

• The pudendal nerve originates from S2, S3, and S4 and provides sensory innervation to the perineal region and perianal region through the inferior rectal nerve, perineal nerve, and dorsal nerve of the penis or clitoris.+

• The DRG may be intraspinal within the lumbosacral spine.  In some cases, this results in mechanical nerve root compression distal rather than proximal to DRG, producing a potentially confusing pattern of EDX findings.  

Distribution of Lumbosacral pelxus.

• The upper portion of the plexus supplies major motor functions to the lower and anterior abdominal muscles, hip flexion and adduction, and knee extension.  Sensory perception in the groin; anterior, medial, and lateral thigh; and the medial part of the leg down to the ipsilateral ankle is also supplied by the upper lumbosacral plexus.

• The lower portion of the plexus supplies major motor function to hip abduction and hip extension, knee flexion, all movement at the ankle joint, and the urinary and anal sphincters.  The lower lumbosacral plexus provides sensory supply to the lower extremity below the knee (except for the medial part of the lower leg) including the posterior thigh, buttocks, and perineal region.

Etiologies of lumbosacral plexopathy

Tumor or mass

• Malignant invasion: colon, cervix, ovary, urinary bladder, prostate gland

  • Direct malignant invasion from adjacent organs.

  • Metastatic deposits from remote solid organs, such as breast or lung cancer

  • Direct infiltration as seen in hematologic malignancy, such as lymphoma (intraneural lymphomatosis)

  • Compression from retroperitoneal lymph node enlargement.

• Metastasis: breast, lung, lymphoma

• Benign tumor: neurofibroma, perineurioma

• Amyloidosis: amyloidoma

Infection

• Local organs: gastrointestinal tract, urinary tract, spine

• Generalized infection: HIV, diffuse infiltrative lymphocytosis syndrome (DILS)

• Psoas abscess or other retroperitoneal abscess.

Trauma

• Motor-vehicle accident

  • Usually high-velocity and energy impacts causes LS plexus injury and associated pelvic trauma. 

• Sports injury

• Postoperative

  • Hip surgery

Radiation

Hematoma

Vascular lesions

Inflammatory/microvasculitis

• Diabetic lumbosacral radiculoplexus neuropathy

• Lumbosacral radiculoplexus neuropathy

• Postsurgical inflammatory neuropathy

• Sarcoidosis

Diagnostic Workup for Lumbosacral Plexopathy

• EMG/NCS 

• Blood tests:

  • CBC, CMP, HbA1c, ESR, RA, ANA, ENA, ANCA, lyme titer, ACE, HIV, SPEP with IFE, paraneoplastic panel

• CSF studies: routine cell count, protein, glucose, viral studies (CMV), cytology, ACE, lyme 

• MRI of lumbosacral plexus

• MRI of lumbosacral spine

• Positron emission tomography (PET)/CT (for neoplasm)

• Nerve biopsy

Femoral nerve and mononeuropathy

The femoral nerve is a large nerve that originates from the posterior divisions (rami) of L2, L3, and L4 nerve roots, traveling through the psoas major and iliacus muscles both of which it innervates.  It runs within the groove between the iliacus and psoas muscles and then passes under the inguinal canal and enters the thigh into the femoral triangle and lies lateral to the femoral artery.  It then divides into anterior and posterior divisions. The anterior division gives rise to the medial femoral cutaneous, and intermediate femoral cutaneous nerves of the thigh providing sensation to the anteromedial aspect of the thigh.  It also gives muscular branches to sartorius muscle.  The posterior division innervates the pectineus and the quadriceps femoris (rectus femoris, vastus lateralis, vastus medialis, and vastus intermedius muscles and continues along the medial border of calf as the saphenous nerve to provide sensation to the medial aspect of the leg. The lateral thigh is not supplied by the femoral nerve but is innervated by the lateral femoral cutaneous nerve, which is derived directly from the lumbar plexus, with fibers originating from the L2-L3 nerve root.  

The cutaneous branches of femoral nerves (medial, intermediate and saphenous nerves) carry sensory information from the anteromedial thigh, medial leg, medial malleolus, and arch of the foot. 

The patellar reflex is carried through the femoral nerve.  Femoral nerve injury will manifest as weakness in hip flexion and knee extension, loss of the patellar reflex and sensory findings in the anteromedial thigh and medial leg. 

The femoral nerve can be injured in the retroperitoneal or intrapelvic space, or at the inguinal ligament. Clinically, the distinction between injury at these sites can be made by detection of weakness on hip flexion that will represent psoas muscle weakness and electrophysiologically by the presence of fibrillations in the iliopsoas muscle. Both these muscles are innervated above the level of inguinal ligament, and their involvement suggests an intrapelvic injury rather than an inguinal injury.  At the inguinal region, the femoral nerve can be damaged by inguinal masses or hematomas, during hip surgery or perineal surgeries, especially associated with prolonged lithotomy position, and pseudoaneurysm formation following cardiac cath. via the femoral artery in the groin. 

It is important to distinguish femoral nerve injury from L2-L3-L4 radiculopathy and lumbar plexopathy. The presence of impairment of other nerves will suggest these possible diagnoses. For example, adductor weakness suggests involvement of the obturator nerve, which can occur in L2-L3-L4 radiculopathy or a lumbar plexopathy. Also, the presence of weakness in the distal lower extremity muscles will imply injury to other nerves, excluding a selective femoral nerve injury. 

Mid-lumbar radiculopathy (L2, L3) due to disc herniation of the mid lumbar nerve roots may present with anterior hip, thigh, and knee pain. The pain distribution is similar to pain arising from an orthopedic source such as hip osteoarthritis. Passive hip range of motion, active hip flexion, and getting into and out of an automobile represent common signs or symptoms of orthopedic causes of hip pain. A Trendelenburg gait pattern can result from either an orthopedic source of hip pain or from severe lower lumbar radiculopathy with weak hip abductor muscles (L5 innervation). Passive flexion of the knee with the patient prone (Ely’s test or femoral nerve stretch test) is a provocative maneuver for eliciting mid-lumbar radicular pain.

Femoral Neuropathy Etiologies:

• Retroperitoneal or iliacus hematoma

• Lithotomy positioning

• Hip arthroplasty or dislocation

• Iliac artery occlusion

• Femoral arterial procedures

• Femoral artery aneurysms or pseudoaneurysms

• Neoplastic

• Penetrating groin trauma

• Pelvic surgery

• Idiopathic

• Mechanical pressure clamp on the femoral artery

• Weakness of thigh flexion (iliopsoas - localizing prox. to inguinal lig), and knee extension, loss of patellar reflex.  Ankle reflex should be normal. 

• Buckling of knee (quadriceps weakness), difficulty lifting up the thigh, and dragging the leg (iliopsoas weakness).

• Numbness and tingling in medial and anterior thigh and medial calf and just distal to the medial malleolus. 

• Sensation is spared over the lateral thigh (territory of lateral femoral cutaneous nerve) and the very proximal medial thigh (obturator nerve cutaneous territory). Abnormalities in these areas implies a lesion of the lumbar plexus or roots. 

• Wasting and weakness of quadriceps in severe cases. 

• Test by having the patient arise from floor from a kneeling position (test for subtle weakness, as the quads are strong muscles)

• DDx: L2-L4 radiculopathy (L2-L4 radiculopathy, however, may include weakness of thigh adduction which is an obturator nerve function).

• EMG of quadriceps, iliopsoas, paraspinal muscles, adductor muscles

• Physiotherapy

Obturator nerve and neuropathy

The obturator nerve is generated within the psoas muscle by motor axons derived from the anterior division (rami) of the L2 through L4 nerve roots.  It courses through the pelvis and then innervates the obturator externus muscle while traversing the obturator canal to enter the medial aspect of the thigh.  It divides into a posterior division and an anterior division.  The sensation to the upper portion of the medial aspect of the thigh is through the sensory terminal branch of the anterior division.  The anterior division innervates pectineus, adductor longus, adductor brevis, and gracilis muscles.  The posterior division innervates adductor magnus and adductor brevis. 

Endometriosis in the Lumbar Plexus Mimicking a Nerve Sheath Tumor - PMC (nih.gov) 

Sciatic nerve and neuropathy

The sciatic nerve of the largest nerve derived from the lumbosacral plexus.  The other nerves that arise from the sacral plexus and pass through the sciatic notch are the gluteal nerves, the posterior cutaneous nerve of the thigh, and the pudendal.   The nerve fibers of the sciatic nerve originate from the ventral rami of spinal nerves L4-S3.  The lumbar contributions pass to the lumbosacral trunk to join the S1 ventral ramus.  This trunk and the ventral rami of the spinal nerves then pass laterally and downward along the inner wall of the pelvis, fusing to form the sciatic nerve that leaves the pelvis through the greater sciatic foramen (sciatic notch).  The sciatic nerve usually passes below the piriformis muscle with the whole nerve, or more commonly, one of the trunks, may pass over or through the muscle.

The sciatic nerve is made up of 2 distinct nerve trunks: Medial and lateral.  These normally share a common sheath from the pelvic cavity to the popliteal fossa, but they may be separate from all or part of this course.  The lateral trunk, which forms the common peroneal nerve, arises from the posterior divisions of the ventral rami of spinal nerves L4-S2.  The medial trunk, which forms the tibial nerve, originates from the anterior divisions of the ventral rami L4-S3.

In the buttock, the sciatic nerve courses downward between the ischial tuberosity and the greater trochanter, lying close to the posterior capsule of the hip joint and covered by the gluteus maximus muscle.  The nerve then continues distally deep in the thigh.  The trunks separate at variable levels, usually just proximal to the popliteal fossa.

The sciatic nerve in her aids the hamstring group of muscles.  The lateral trunk of the nerve supplies only one of these, the short head of the biceps femoris; all the other hamstring muscles are supplied by branches from the medial trunk which also partially innervates the adductor magnus muscle.  No cutaneous sensory branches arise from the sciatic nerve trunks.

The superior gluteal nerve (L4, L5, S1) exits the sciatic notch above the piriformis muscle and supplies the gluteus medius and minimus and tensor fascia lata muscles.  The inferior gluteal nerve (L5, S1, S2) passes out of the sciatic notch below the piriformis muscle and supplies the gluteus maximus muscle.  The posterior cutaneous nerve of the thigh (S1-S3) descends at first deep to the gluteus maximus and then superficially down the back of the thigh.  It supplies the skin of the lower buttock and posterior thigh.  It also gives rise to perineal branches (the cluneal or clunical nerves) that innervate the upper medial thigh and, together with branches from the pudendal nerve, the skin of the perineum and scrotum or labia.  

The pudendal nerve (S2-S4) is the principal nerve of the perineum.  It passes through the lower part of the sciatic notch and then runs deep to the sacrospinous ligament into the perineal area.  In its passage adjacent to the levator ani muscle, the nerve and accompanying artery traverse a fascial plane termed the pudendal or Alcock canal.  The first branch of the pudendal nerve is the inferior rectal (hemorrhoidal) nerve that innervates the external anal sphincter and contains sensory fibers from the lower anal canal and perianal skin.  The next branch, the perineal nerve, supplies the muscles of the perineum, erectile tissue of the penis, the external urethral sphincter, and the skin of the perineum, scrotum or labia.  The final nerve of the pudendal nerve is the dorsal nerve of the penis or clitoris. 

Causes of Sciatic Neuropathy:

Proximal neuropathies: 

• • Trauma: Pelvic and hip joint fractures, missile wounds, hip arthroplasty and other hip operation

  • External compression: Perioperative, prolonged pressure ("toilet seat" neuropathy").

  • Compression from mass lesions: Endometriosis, nerve tumor, hematoma, lipoma, aneurysm, fibrosis, myositis ossificans

  • Injection injury

  • Piriformis syndromes

  • Infarction due to vasculitis or vascular surgical procedures of the lower extremity

  • Spontaneous ischemic neuropathy of the sciatic nerve due to arterial occlusion 

  • Intraoperative thigh tourniquet

  • Infiltration by lymphoma

  • Persistent sciatic artery

  • Revision hip surgery can result in the possibility of methlymethacrylate cement (heat: exothermic reaction when setting), and spurs which can then slowly erode into the nerve.

  • Almost all cases of "sciatica" are due to lumbosacral radiculopathy

  • Involvement of the genicular branches in cystic adventitial disease of the popliteal artery as a possible marker of unfavourable early clinical outcome: a case report | Journal of Medical Case Reports | Full Text (biomedcentral.com) 

  • Cystic adventitial disease of the popliteal artery presenting with features of entrapment syndrome - PMC (nih.gov) 

  • Adventitial cystic disease of the popliteal artery - PMC (nih.gov) 

  • Popliteal Adventitial Cystic Disease (Maham Rahimi, MD and Travis Vowels, MD) (youtube.com) 

Neuropathies in thigh:

• Trauma: missile wounds, lacerations, fracture of femur, hematoma.

• External compression: Fibrous band, myositis ossificans, popliteal aneurysm

• Nerve tumor 

Piriformis syndrome:  

It is caused by compression of the sciatic nerve by the piriformis muscle as it passes through the sciatic notch.  

• • • It results in buttock and posterior thigh pain, tenderness in the region of sciatic notch and buttock, and pain reproduction by maneuvers that stretch the sciatic nerve. 

    • "Very thin patients who sit on their butts all day, are prone to get it."

    • Symptoms are aggravated on sitting than standing

    • A controversial nerve entrapment/compression syndrome. 

    • Maneuvers:

      • The FAIR (flexion, adduction, and internal rotation position), where simultaneous downward pressure of the flexed knee and passive superolateral movement of the shin, with both acetabula oriented vertically, maximize adduction and internal rotation at the flexed thigh.  The angle between the ground and flexed leg should be 20° to 35°.

      • Freiberg maneuver: patient laying supine, forcefully internally rotate the leg.

      • Pace maneuver: patient is seated position, abduction of hip against resistance.

      • Beatty maneuver: patient lying on side, abducts hip.

    • Aneurysm of inferior gluteal artery

  • Vasculitic lesions

  • Neurolymphamatosis, infiltration by lymphoma

  • Nerve sheath tumor, schwannoma, myxomatous intramuscular tumors of gluteus maximus. 

  • Intraoperative high tourniquet

  • Gluteal varicosities, persistent sciatic arteries

  • Endometrial implants leading to "catamenial sciatica."

  • "Toilet-seat" neuropathy which is actually a compressive sciatic neuropathy from a hematoma in the posterior thigh and gluteal compartment syndromes, due to prolonged sitting on the toilet seat. 

  • IABP placement in PAD patient is reported to result in sciatic neuropathy in post-cardiac surgery patients in cardiogenic shock.

  • Sciatic nerve branches into the tibial and common peroneal nerves.

    • Peroneal fibers in the sciatic nerve innervate the short head of the biceps femoris.  It is the only muscle innervated by the peroneal nerve above the fibular neck.

  • Sciatic nerve: L4-S3 roots.  

    • Muscles supplied: internal hamstrings (semimembranosus, semitendinosus, long head of biceps femoris, short head of biceps femoris), and lateral division of adductor magnus.  All these muscles, except short-head of biceps femoris (supplied by peroneal division) is supplied by the tibial division of the sciatic nerve. 

      • Short head of biceps femoris is affected by sciatic neuropathy (posterior division - fibular fibers) but is spared in common fibular neuropathy, and involvement of both superficial and deep fibular nerves. 

    • Peroneal division of sciatic nerve runs lateral to the tibial division of sciatic nerve.  The two divisions physically separate in the mid-thigh into their respective nerves.

• Clinical features:

  • Weakness of knee flexion (hamstring weakness) and loss of ankle and toe movement in all directions.  

  • Abduction and extension of the thigh at the hip should be spared.  There is no weakness of glutei.

  • Sensation is lost over the webspace of great toe (deep peroneal), dorsum and sole of foot, lateral calf, and lateral knee. Sensation to the posterior thigh, lateral thigh, anterior thigh, medial calf is spared.  

  • Ankle reflex is depressed or absent.

  • Peroneal functions of the sciatic nerve are typically involved disproportionately to their tibial components.  Misdiagnosis of a common peroneal neuropathy can be readily made by those unaware of this phenomenon. 

• EDX: 

• NCS are abnormal.  Low amplitudes sural and superficial peroneal SNAPs.  Low amplitude peroneal, and tibial CMAPs.  Check peroneal to AT in addition to peroneal to EDB for peroneal neuropathy at fibular neck. F-waves are usually prolonged on the affected side. H-reflex may be diminished or absent on symptomatic side. 

• Sample peroneal (deep and superficial) innervated muscles: TA, EHL, PL

• Sample tibial innervated muscles: MG, TP, and FDL

• Abnormalities in both peroneal and tibial innervated muscles rules out an isolated lesion of peroneal nerve. 

• Sample SHB which is the only muscle innervated by the peroneal division of sciatic nerve.  If abnormal, an isolated lesion of peroneal nerve at fibular neck is ruled out and implies a more proximal lesion is present.

• Sample LHB, GMax, and GMed or TFL.  If these muscles are abnormal, then an isolated lesion of the sciatic nerve is ruled-out and the lesion may be more proximal (lumbosacral plexus or L5-S1). 

• Sample the L5-S1 paraspinal muscles to check if it is a root lesion. 

• Also check non-sciatic innervated L5-S1 muscles to rule out a lumbosacral plexus lesion (VL, VM, iliacus, AL).

• DDx of sciatic neuropathy:

  • Lumbosacral plexopathy, L5 radiculopathy, common peroneal neuropathy, ischemic stroke lesions in the foot area of the motor cortex.

Sacral plexopathy

Common presentation is foot drop and pelvic pain. Cancer and cancer related causes is the common etiology, trauma (GSW) radiation injury, crush injuries, idiopathic, iatrogenic (lumbar laminectomy, aortic surgery), maternal injuries.

EDX criteria: 

1. More than 50% reduction of the sural and superficial peroneal SNAP on the affected side.

2. Denervation of the muscles innervated by sacral plexus.

   • TA, MG, TP, FDL, EDB, AH, VM, GMax, GMedius/TFL, sacral paraspinals

3. Absence of denervation in sacral paraspinal muscles. 

Tibial nerve

It gives rise to the medial sural cutaneous nerve and innervates the popliteus, plantaris, soleus, and gastrocnemius muscles.

Foot drop (fibular nerve palsy)

• It is the most common mononeuropathy of the lower extremity.

• L4-S1 nerve root. 

• The common fibular nerve fascicles within the sciatic nerve, lie separately and lateral to the tibial nerve.   Within the sciatic nerve, the fibers that eventually form the common peroneal nerve run separately from those that distally become the tibial nerve.  In the posterior thigh, the peroneal fibers within the sciatic nerve innervate the short head of the biceps femoris, the only peroneal-derived muscle above the level of the fibular neck.  More distally, the sciatic nerve bifurcates above the popliteal fossa into the common peroneal and tibial nerves.  The common peroneal nerve first gives rise to the lateral cutaneous nerve of the knee, which supplies sensation to the lateral knee before winding around the fibular neck and passing through the fibular tunnel between the peroneus longus muscle and the fibula.  At the fibular neck, the internal fascicular anatomy is such that the fibers destined for the deep peroneal nerve lie more medial (adjacent to the fibula), whereas the fibers destined for the superficial peroneal nerve are more lateral.  The common peroneal nerve then divides into superficial and deep branches, in addition to an articular branch to the proximal tibiofibular joint.  The deep peroneal nerve innervates the peroneus tertius and the dorsiflexors of the ankle and toes, including the tibialis anterior (TA), extensor digitorum longus, extensor hallucis longus (EHL), and extensor digitorum brevis (EDB).  It continues on to supply sensation to the web space between the first and second toes.  The superficial peroneal nerve innervates the ankle evertors (peroneus longus and peroneus brevis) and then supplies sensation to the mid and lower lateral calf.  Just proximal to the ankle, it divides into the medial and intermediate dorsal cutaneous nerves of the foot, supplying sensation to the dorsum of the foot and to the dorsal medial three or four toes up to the level of the interphalangeal joints.  In 15%–20% of patients, an accessory peroneal nerve leaves the main superficial peroneal nerve and runs posterior to the lateral malleolus to ultimately supply the lateral EDB muscle.  This is an important normal variant often encountered during routine nerve conduction studies.

• Deep peroneal nerve is often affected in common peroneal neuropathies.  

  • Foot drop with weakness of foot dorsiflexion (deep peroneal n. palsy)

  • It innervates AT, EHL, EDL, EDB, and peroneus tertius muscles, and has a terminal sensory branch.

  • Sensory loss over the dorsolateral aspect of foot and shin.

  • It also innervates the skin between the 1st and 2nd toes (dorsal digital cutaneous branch) and patients will feel numbness in the webspace of these toes (deep peroneal n. palsy).

• Superficial peroneal nerve is responsible for foot eversion.

  • It innervates peroneus (fibularis) longus and brevis muscles and just proximal to the ankle, it divides into the medial and intermediate dorsal cutaneous nerves of the foot, supplying sensation to the dorsum of the foot and to the dorsal medial three or four toes up to the level of the interphalangeal joints.  In 15%–20% of patients, an accessory peroneal nerve leaves the main superficial peroneal nerve and runs posterior to the lateral malleolus to ultimately supply the lateral EDB muscle.  This is an important normal variant often encountered during routine nerve conduction studies.

  • Sensory loss over the mid and lower lateral calf and dorsum of foot.

• Clinical features:

  • In most cases, both the deep and superficial peroneal nerves are affected.  Involvement of the deep peroneal nerve leads to weakness of toe and ankle dorsiflexion, resulting in a foot and toe drop.  Dysfunction of the superficial peroneal nerve results in weakness of foot eversion.  Clinically, weakness of these muscles results in a stereotyped set of symptoms.  Patients note a slapping quality of their foot as it hits the ground while they are walking. Weakness of eversion leads to a tendency to trip, especially on uneven sidewalks or curbs, and an increased risk of sprained ankles.  When observed while walking, patients have a so-called steppage gait whereby they bring their knee up higher than usual so that the dropped foot clears the floor.  Sensory disturbance develops over the mid and lower lateral calf and the dorsum of the foot.  Local pain and a Tinel’s sign may be present over the lateral fibular neck.

  • In isolated peroneal neuropathy at the fibular neck, the function of the sciatic, tibial, and sural nerves remains normal.  Most important, ankle inversion is spared as it is mediated by the tibialis posterior (L5, tibial-sciatic innervated nerve).  The remainder of the muscles innervated by the tibial and sciatic nerves are normal (ankle and toe plantar flexion, knee flexion).  Hip abduction, internal rotation, and extension also are normal, innervated by the superior and inferior gluteal nerves, which come directly off the lumbosacral plexus.  Sensation is normal over the lateral foot (sural territory), sole of the foot (medial and lateral plantar territory), and medial calf and foot (saphenous territory).  Sensation over the lateral knee is preserved because that area is innervated by the lateral cutaneous nerve of the knee, which arises from the common peroneal nerve above the fibular neck.  Finally, all reflexes, including the ankle reflex, remain normal in an isolated peroneal neuropathy.

  • Intraneural ganglion cysts may account for up to 18% of peroneal neuropathies. Clinical features more suggestive of a ganglion cyst include a body mass index of greater than 30, knee pain, neuropathic pain, fluctuating deficit with weight bearing, and a palpable mass at the fibular head. There is no significant difference in the electrodiagnostic abnormalities, although there is a lower incidence of conduction block in the setting of an intraneural cyst.  Fibrillation potentials tend to be more prominent in deep peroneal-innervated muscles in both cases.  Advanced imaging with either ultrasound or magnetic resonance imaging are diagnostic, and surgical intervention is indicated.

• On the clinical examination, any of the following abnormalities in a patient with a foot drop should suggest a lesion more proximal to the peroneal nerve at the fibular neck:

  • Weakness of ankle inversion (tibialis posterior—innervated by the tibial nerve)

  • Preferential weakness of the EHL (L5–S1) out of proportion to the TA (L4–L5) when the two are compared.  In a peroneal neuropathy, these two muscles usually are equally affected; in an L5 radiculopathy, the EHL usually is weaker than the TA because of its predominant L5 innervation.

  • Sensory loss over the lateral knee (distribution of the lateral cutaneous nerve of the knee).

  • Sensory loss over the sole of the foot, lateral foot, or medial calf (distribution of the plantar, sural, or saphenous nerves, respectively).

  • Any weakness of hip abduction, internal rotation, or extension (gluteus medius, tensor fascia latae, gluteus maximus—innervated by the superior and inferior gluteal nerves).  Because these muscles are quite strong, they must be tested at mechanical disadvantage to demonstrate subtle weakness.  

  • Any asymmetry of the ankle reflex.

• Foot drop Etiology:  

Unilateral foot drop:  Foot drop may result from any insult at the level of the deep peroneal nerve, common peroneal nerve, sciatic nerve, lumbosacral (LS) plexus, L5 nerve roots, motor neurons, neuromuscular junction (NMJ), muscles, spinal cord, and brain. 

• • Peroneal neuropathy, often as a result of compression at the neck of the fibula at knee level, where the common peroneal nerve is covered only by skin and subcutaneous tissue. 

  • Trauma: Penetrating injury, fractures (fibular, acetabular), stretch (forcible ankle inversion), revision THA, trochanteric fractures, TKA (rare), knee joint disruption (ACL, PCL, lateral collateral ligament tears).

  • Compression or entrapment at fibular neck:  Habitual leg crossing, squatting crossed leg, Vajrasana yoga position, casts, tight stockings, immobilization after anesthesia, sedation, or intoxication, lithotomy position with prolonged knee flexion during childbirth.

  • Lower lumbosacral plexopathies

  • L5 radiculopathies

  • Mass lesions: tumors, nerve sheat tumors, perineuroma, intraneural ganglion cyst, Baker’s cyst, perineural cysts, hematoma, osteoma, lipomas

  • Habitual leg crossing

  • Weight loss : Systemic diseases including malignancy, following bariatric surgery (slimmer’s palsy)

  • Occupational: Gardening, farm work (squatting, kneeling) – strawberry picker’s palsy

  • Vascular: Acute occlusion of femoral or popliteal arteries

  • Leprosy

  • Painful asymmetrical foot drop is typically seen in vasculitis (mononeuritis multiplex).

  • MMN

  • DADS-M (anti-MAG)

  • Inherited neuropathies: CMT, HNPP

  • Central causes: Parasagittal tumors

  • Myopathic causes of foot drop:  Painless asymmetrical foot drop with preserved ankle reflexes is typically seen in amyotrophic lateral sclerosis (ALS), myasthenia gravis (MG), and distal myopathies. 

    • Foot drop may be the first presenting feature of ALS.

    • Myopathies: Post-partum myopathies, Hypothyroidism

    • Distal myopathies: Nonaka, Laing, Udd, and Markesbery-Griggs

    • Facioscapulohumeral muscular dystrophy (FSHD) may present with foot drop. 

    • Preservation or hypertrophy of the extensor digitorum brevis (EDB) muscle distinguishes myopathic from neurogenic foot drop. 

    • MG (bilateral foot drop – rare manifestation) 

Bilateral foot drop:

• Myopathies

• Distal myopathies

• Scapuloperoneal muscular dystrophy

• Facioscapulohumeral muscular dystrophy

• Myotonic dystrophy

• Neuropathies

• Multifocal motor neuropathy with conduction block

• Chronic inflammatory demyelinating polyneuropathy

• Bilateral peroneal neuropathies

• Bilateral sciatic neuropathies

• Bilateral lumbosacral plexopathies

• Radiculopathies

• Bilateral L5 radiculopathies

• Conus medullaris lesion

• Anterior horn cell disorders

• Amyotrophic lateral sclerosis

• Poliomyelitis and the postpoliomyelitis syndrome

• Cerebral lesions

• Bilateral cortical or subcortical parasagittal lesions

Exam of ankle/foot.

EDX: Focal slowing of nerve conduction across fibular head. Denervation of tibialis anterior and peroneus longus muscles. 

• • In demyelinating lesions, if focal slowing or conduction block is seen across the fibular neck in the peroneal motor study, this can be used to localize the lesion.  Usually, any slowing of more than 10 m/s is considered significant.  Any drop in amplitude or area of more than 20%, especially over a very short segment, suggests focal conduction block.  The amount of conduction block can be approximated by comparing the compound muscle action potential (CMAP) amplitude at the lateral popliteal fossa with that below the fibular head.  In purely demyelinating lesions at the fibular neck, the distal superficial peroneal sensory response remains normal.

  • If axonal loss predominates, peroneal CMAP amplitudes will be reduced at all stimulation sites (ankle, below the fibular head, lateral popliteal fossa). As in other axonal loss lesions, conduction velocities and the distal motor latency may be normal or slightly slowed if the fastest-conducting axons have been lost.  Likewise, the superficial peroneal sensory nerve action potential (SNAP) amplitude will be reduced or absent.  If the pathophysiology is entirely axonal loss, the nerve conduction studies, although they demonstrate a peroneal neuropathy, cannot localize the level of the lesion. The amount of axonal loss can be approximated by comparing the distal CMAP amplitude on the involved side with that on the contralateral asymptomatic side. There may often be evidence of axonal loss and demyelination in the same patient.  The EDB muscle is usually chosen as the peroneal motor study recording site.  However, in patients with a foot drop, the TA's weakness accounts for the clinical deficit.  Hence, recording the TA when performing the peroneal motor study often is more useful than the routine motor study recording the EDB.  Indeed, in some cases of peroneal neuropathy at the fibular neck, a conduction block may be seen when recording the TA but not the EDB.  If recording the EDB does not localize the lesion by demonstrating focal slowing or conduction block, the peroneal motor study should be repeated recording the TA, stimulating below the fibular head and at the lateral popliteal fossa.

  • In addition to the peroneal motor and sensory studies, tibial motor, F response, and sural sensory studies must be performed.  Because lesions of the sciatic nerve and lumbosacral plexus can present in a similar manner to peroneal neuropathy, excluding a more widespread lesion is imperative.  Of course, if any motor or sensory study is borderline, comparing it with the contralateral asymptomatic side often is useful.

  • Most peroneal lesions affect both the superficial and deep branches.  However, it is common that the deep branch is more affected than the superficial. Occasionally, only the deep peroneal branch is involved.  This presumably happens due to selective fascicular vulnerability of the deep fibers that lie closest to the fibula and are more prone to compression.  In such cases, interpretation of the nerve conduction studies can be more difficult.  The sensory response, which is mediated by the superficial branch of the peroneal nerve, will be normal.  If peroneal motor studies show evidence of axonal loss only, without focal slowing or conduction block across the fibular neck, the nerve conduction studies in an isolated deep peroneal neuropathy may appear identical to those seen in a severe L5 radiculopathy associated with axonal loss.

  • Needle EMG:  

    • At least two muscles innervated by the deep peroneal nerve (e.g., tibialis anterior, extensor hallucis longus).

    • At least one muscle innervated by the superficial peroneal nerve (e.g., peroneus longus, peroneus brevis)

    • Tibialis posterior and at least one other tibial muscle (e.g., medial gastrocnemius, soleus, flexor digitorum longus).

    • Short head of the biceps femoris.

    • If any muscle is borderline, compare with the contralateral side.

    • If the short head of the biceps femoris or any tibial-innervated muscle is abnormal or if nerve conduction studies demonstrate a non-localizing peroneal neuropathy or abnormal tibial motor or sural responses, a more extensive needle examination of other sciatic and gluteal-innervated and paraspinal muscles should be performed to identify the level of the lesion.

• DDx:  Common peroneal nerve, deep peroneal nerve, or superficial peroneal nerve compression: lumbosacral plexopathy, L5 radiculopathy, sciatic neuropathy involving peroneal division of nerve. 

  • L5 radiculopathy.  L5 radiculopathy includes weakness of foot dorsiflexion, eversion, and inversion, while in peroneal palsy foot inversion is spared as this function is carried out by the tibialis posterior (innervated by tibial nerve).

• Tx: Foot brace (AFO) remove external source of compression. 

Tarsal tunnel syndrome

The tarsal tunnel is a fibro-osseous tunnel below the medial malleolus with a bony floor and a roof formed by the flexor retinaculum.  In addition to the tibial nerve, the tibial artery, the tibial veins and tendons of the flexor hallucis longus (FHL), flexor digitorum longus, and tibialis posterior pass through the tarsal tunnel.  The distal tibial nerve typically divides into three branches.  One branch, the medial calcaneal sensory nerve, is purely sensory and provides sensation to the heel of the sole.  The other two branches, the medial and lateral plantar nerves, contain both motor and sensory fibers that supply the medial and lateral sole of the foot, respectively.  Typically, the medial plantar nerve supplies the first three and a half toes (including the great toe), whereas the lateral plantar nerve supplies the little toe and the lateral fourth toe.  The first branch of the lateral plantar nerve is the inferior calcaneal nerve (a.k.a., Baxter’s nerve).

The medial plantar nerve innervates: Abductor hallucis, FDB, FHB, lumbrical 1 and 2, and has a cutaneous branch.  The lateral plantar nerve innervates: ADM, FDM, Adductor hallucis, interossei, lumbricals 3 and 4, and has a cutaneous branch.   

• Focal neuropathy due to entrapments of the tibial nerve or its branches in the tarsal tunnel, under the flexor retinaculum. TTS is exceptionally rare.  Lesions of the medial and lateral plantar nerves most often occur as a result of trauma (including sprain and fracture) or occasionally from degenerative bone or connective tissue disorders.  Rare cases of TTS are caused by varicosities or other unusual mass lesions (e.g., lipomas, ganglions, cysts, exostoses, varices).  TTS caused by hypertrophy of the flexor retinaculum from repetitive use (akin to CTS) is unusual.

• It causes burning pain in the ankle and/or foot.  Mostly pain around the malleoli.

• Pain and paresthesias in the sole of foot but not heel

• At the end of the day after standing or walking; pain is worse at night.

• Sensory loss in the sole of the foot. Tinel's sign at tarsal tunnel

• EDX: reduced amplitude in sensory or motor component of medial and plantar nerves with prolonged distal latencies (side to side comparison)

• Ultrasound can be very helpful in cases of suspected tibial neuropathy at the tarsal tunnel, especially in cases of trauma or unusual structural lesions.

• DDx: polyneuropathy, foot deformity, poor circulation, tendonitis and fasciitis, proximal tibial neuropathy, and, especially early on, mild polyneuropathy. S1 radiculopathy or lumbosacral plexopathy may cause sensory loss over the sole, but neither is typically associated with local foot pain.  

• Tx: Surgery if no external cause identified. 

Anterior Tarsal Tunnel  syndrome or Deep Peroneal Neuropathy at the Ankle

Compression of the deep peroneal nerve at the ankle is known as “anterior tarsal tunnel syndrome.”  This is a rare entrapment neuropathy that occurs from compression of the deep peroneal nerve under the inferior extensor retinaculum at the ankle (tight ski boots, dancing boots, ganglion cysts, and bony abnormalities of ankles, pes-cavu).  Patients present with foot pain and paresthesias of the dorsum of the foot between the great and second toes. Atrophy and weakness of the EDB muscle may be present.  Sensation may be decreased in the web space between the great and second toes.  Plantar flexion may result in increased symptoms, which may be relieved by dorsiflexion.  A Tinel’s sign may be elicited by percussing over the anterior ankle.

EDX:  The only abnormality will be denervation and/or reinnervation limited to the EDB.  However, caution must always be used in assessing the EDB. It is not uncommon that “normal” individuals without any symptoms will have reinnervation in the EDB.  In patients with symptoms limited to one side, comparison to the contralateral EDB is recommended.  However, keep in mind that abnormalities in the EDB on needle EMG are much more commonly due to either peripheral neuropathy, peroneal neuropathy at the fibular neck or L5 radiculopathy, rather than anterior tarsal tunnel syndrome.

Meralgia Paresthetica

• Lateral femoral cutaneous nerve (L2, L3) can be entrapped as it passes under the inguinal ligament or fascia lata producing paresthesias and loss of sensation in the lateral thigh. 

• Pain and numbness in the anterior thigh

• Sensory loss in the pocket of the pant distribution

• EDX: Sometimes slowing of sensory response across the inguinal ligament. 

• No motor involvement or reflex changes.

• Obesity, pregnancy, weight loss, heavy equipment belts. Symptoms may be worse after prolonged walking, standing, or sitting. 

• DDx:  

  • It is important to exclude a lumbar plexopathy and especially an L2 radiculopathy. 

  • In this regard, the iliacus, thigh adductors, and less so the quadriceps are important muscles to check on the nEMG exam.

  • There are motor changes or decreased patellar reflex in lumbar plexopathy involving the femoral nerve. 

Morton's metatarsalgia:

• Tight-fitting shoes can compress the digital nerves, especially the 3rd and 4th toes, producing patches of numbness and paresthesias.

Case Vignettes:

A 52-year-old undergoes knee replacement surgery. Afterwards, she has pain on the lateral aspect of her distal leg and dorsiflexion weakness. Which of the following will best help in differentiating between sciatic neuropathy from L5 radiculopathy? 

A. Low amplitude tibial motor nerve conduction study (NCS). 

B. Abnormalities in the short head of the biceps femoris. 

C. Low amplitude peroneal motor NCS. 

D. Low amplitude sural sensory NCS. 

E. Abnormalities in the anterior tibialis on needle electromyography 

Answer:  Anatomic variability must be taken into account when assessing findings on nerve conduction studies (NCSs) and electromyography.  Although the adductor hallucis assessed on tibial motor NCSs and the short head of the biceps femoris are predominately S1-innervated muscles, they can have significant L5 involvement.  The sural sensory NCS is only involved in rare cases of radiculopathy and is therefore the best answer in helping to differentiate between a sciatic neuropathy and L5 radiculopathy. 

https://www.tampapainmd.com/cluneal-neuralgia/

https://orthopedicreviews.openmedicalpublishing.org/article/35505-a-comprehensive-review-of-cluneal-neuralgia-as-a-cause-of-lower-back-pain

Cluneal Neuralgia

Abstract

Lower back pain (LBP) is one of the most common presenting complaints in clinical adult medical patients. While most often diagnosed as “nonspecific mechanical” in etiology, several lesser known, rarer causes of LBP exist, some of which can even cause neuropathic pain. One of these infrequent causes, cluneal neuralgia (CN), is associated most often with damage or entrapment of the cluneal nerves, particularly the superior cluneal nerve (SCN) and/or the middle cluneal nerve (MCN). These nerves supply sensation to the posterior lumbar and buttock area. However, the LBP caused by CN is often difficult to recognize because it can mimic radiculopathy or sacroiliac joint (SIJ) pain or lead to symptoms in the legs. This makes CN significantly important for clinicians and surgeons to include in their differential. A thorough history proves beneficial in the diagnostic workup, as many risk factors for CN have been reported in the literature. If a CN diagnosis is made, several effective conservative measures can alleviate patients’ pain, such as nerve blocks, peripheral nerve stimulation, or high frequency thermal coagulation. Additionally, surgical treatments, such as CN release or endoscopic decompression, have resulted in fantastic patient outcomes. The purpose of the present investigation is to investigate the existing literature about CN as a cause for LBP, consider its epidemiology, discuss its pathophysiology and risk factors, elucidate its clinical presentation and diagnosis, and examine the various treatment modalities that have been reported across the world.

Introduction

Cluneal nerves are sensory nerves that branch from the lumbar and sacral spinal nerves and the posterior femoral cutaneous nerve, dividing into superior, middle, and inferior types that supply sensation to the lower back and buttocks. The superior cluneal nerves originate from the lumbar spinal nerves (L1-L3), the middle cluneal nerves come from the sacral spinal nerves (S1-S3), and the inferior cluneal nerves are branches of the posterior femoral cutaneous nerve.  

Lower back pain (LBP) is a frequently encountered clinical complaint and is nonspecific in most cases. A relatively rare but overlooked cause of LBP is cluneal neuralgia (CN), or neuropathic pain caused by damage to the cluneal nerves. The cluneal nerves function as purely sensory nerves and the superior cluneal nerve (SCN) and middle cluneal nerve (MCN) both provide cutaneous innervation to the buttock and posterior parasacral region. Both nerves may cause acute and chronic LBP, in addition to leg symptoms, in the cases of superior cluneal nerve-entrapment (SCN-E) and middle cluneal nerve (MCN-E). Generally, CN is thought of as a diagnosis of exclusion, but clinicians familiarizing themselves with and recognizing the presence of SCN-E and MCN-E will prove beneficial in diagnosing and treating CN. The present investigation summarizes treatment modalities of CN, which are comprised of various conservative and interventional pain measures and surgical management.

Epidemiology

The incidence and prevalence of CN need stronger evidence and further investigation. However, the literature review suggests that it is a relatively rare etiology of LBP. In patients with LBP, the incidence of SCN-E is somewhere between 1.6%-14%. Another prospective study reported that SCN disorders comprised 12% of all patients presenting with LBP and/or leg symptoms and approximately 50% of SCN disorder patients had leg pain and/or tingling. The average duration of these SCN symptoms was found in that study to be 27.3 months +/- 56.5 months (range 0.1-444 months). Epidemiological data on MCN-E is lacking, but the incidence in LBP patients was found to be 13%. A distinct population that had much more transient cluneal neuralgia was postpartum mothers. The incidence in over 13000 reported obstetric cases was found to be 0.73%.

Pathophysiology/Risk Factors

The pathophysiology of SCN-E and MCN-E involves mechanical irritation when the peripheral nerve is locally compressed. This trauma can result from traction, friction, or repetitive compression, which all result in edema around the nerve and interference with its normal sliding movement. Though histopathologic evidence on CN is lacking, one pathological study on 2 patients s/p SCN-neurectomy revealed thickened perineurium, subperineurial edema, Renaut bodies, and nerve enlargement related to an increase in thinly myelinated fibers, which paralleled findings in other studies as well. This sheds some light on the microanatomical considerations on cluneal neuralgia, but more literature exists on SCN-e and MCN-e on a macroscopic level. In the following paragraphs, we investigate the anatomy of the SCN and its described pathophysiologies, followed by that of the MCN, and conclude with a brief investigation of risk factors and possible associations relating to, and causing, cluneal neuralgia.

The SCN is a purely sensory peripheral nerve, derived from the cutaneous branches of the dorsal rami of T11-L4/L5 which passes through the psoas major and paraspinal muscles and travels posterior to the quadratus lumborum. It is relatively thin, with a mean diameter of 1.1 mm. The SCN has been found to exhibit various branching patterns, and a variable number of branches among the population (more than 3 branches in one-third of subjects).The SCN’s medial branch in particular has been shown to penetrate the gluteal fascia and may become entrapped in the fascia attached to the iliac crest, termed the “osteofibrous tunnel,” (OT) or a bony groove in the iliac crest itself. Other investigations have corroborated that in a variable percentage of cases (16-95%) SCNs pass through the OT, many of which reveal entrapment. A recent study proposed that the SCN’s proximity to a rigid fascial edge over which it runs can subject the nerve to mechanical forces upon flexion of the hip joint and stretching of the gluteus maximus, leading to edema, irritation, inflammatory cell infiltration, scarring, and subsequent entrapment. The superficial thoracolumbar fascia and gluteal fascia attaching to the iliac crest were incriminated as entrapping branches of the SCN in all patients requiring SCN release in this recent study. Although Maigne et al initially reported that the SCNs passing through the OT most commonly arose from L1 & L2 nerve roots (60% and 27%, respectively), another anatomical study on 37 dissections showed that SCN branches passing through the OT originated from L3-L5. Most of these SCNs at risk of entrapment originate from the lower lumbar nerve; this evidence may explain why SCN-E disorder can cause leg symptoms mimicking sciatica.

The MCN provides sensation to the posteromedial area of the buttock and is most often composed of sensory branches of the dorsal rami of S1-S3, but its origin and pathways can vary. In addition, it may anastomose with the SCN in the subcutaneous tissues of the buttock. Overall, the MCN is less likely to be entrapped than the SCN because it travels superficially to the long posterior sacroiliac ligament (LPSL), and is shorter and thinner than the SCN (at an average of 0.8mm), and courses through paraspinal muscles attaching onto the dorsal sacrum. However, being within or under the LPSL is a possible source of entrapment. The proposed etiology of pain is either from mechanical stress in the ligament or nerve compression under the ligament. Anatomically, the LPSL sustains tensile stresses during physiological loading of the SIJ, which helps describe the clinical picture of MCN-E (Dumas). Similarly to SCN-E, MCN-E can also cause leg symptoms. However, the authors advised thorough workup before sending these patients to surgery, as half of their subjects with intractable LBP with MCN-E had concomitant sacroiliac joint pain (SIJ) or contributed by other diseases like SCN-E and radiculopathy. Another important cause of MCN-E that needs more evidence is lumbar disc herniation. This case report suggests that surgery for this cause of LBP could be avoided with the treatment of the MCN-E.

Recent scientific literature has shed light on many possible risk factors associated with cluneal nerve entrapment/injury. Importantly, a recent prospective study of LBP reported more women and older patients included in the SCN disorder group than in the non-SCN disorder group, which included those suffering from LBP. The average age in the SCN disorder group was 64.4 It has been shown that as populations age, the incidence of LBP increases. Thus, it can be inferred that SCN-E and MCN-E prevalence (diagnoses of exclusion) is higher in the older population, although more studies are certainly warranted on this topic. Also, vertebral fractures have been described as predisposing to SCN disorders. Kuniya et al reported that the prevalence of SCN disorders was significantly higher in patients with vertebral fractures (26/96, 27%) than in the remaining patient population (87/738, 12%) without vertebral fractures (p<0.01). The authors proposed a mechanism for this injury: entrapment over the iliac crest by irritation of the SCN at its origin from unstable facet joints and/or stretching of the SCN stemming from spinal kyphosis. Similarly, another study also proposed that SCN-E should be considered after vertebral compression fracture patients presented with LBP (Kim et al 2015).

Though stronger studies are indicated, it seems in the current literature that past surgical history in the posterior sacral and lumbar spine area could predispose patients to LBP caused by SCN-E and MCN-E. Delawi et al reported that the most common complication of autologous bone graft harvest at the iliac crest is postoperative pain in the donor. Similarly, lumbar disc surgery with fusion using the iliac crest resulted in persistent graft site pain and could cause injury to the SCN. The L1-L3 nerves, and consequently the SCN, seem to be the most likely sensory nerves to be encountered during posterior iliac crest harvesting for spinal fusion. However, a newer publication expressed that nerve injury following iliac crest harvest could be considered a risk factor for cluneal neuralgia, although, on the whole, nerve entrapment was a much more common cause. Other surgeries may also lead to SCN injuries, such as spinal fusion procedures, sacroiliac screw placements, decubitus ulcer debridement, or muscle flap surgeries. Any patients with lumbar or pelvic procedures are at risk of SCN-E. Another anatomic study suggested that most SCNs were found to pierce the iliocostalis muscle, which could compress the SCN and lead to LBP, or conversely, a surgical approach to either the iliocostalis muscle or erector spinae mm could injure/compress the SCN, although a further clinical investigation is warranted.

While more investigation needs to be done on the causes of cluneal neuralgia, two more studies regarding pathophysiology are worth mentioning. First, transient cluneal neuralgia can be observed in some postpartum mothers. Physiological and anatomical changes during pregnancy, but also parturition itself or operative delivery can lead to this nerve injury. In the studied obstetric cases, postpartum cluneal nerve injury caused loss of sensation over the buttocks. In another prospective observational study, the overall incidence of early postpartum neurological deficits was found as 2%, with about 13% of those presenting with cluneal nerve injury. Risk factors of injury in these mothers that were statistically significant included a past history of neurological conditions or history of a prior back injury. However, these postpartum deficits were all resolved in a few weeks’ time. Lastly, Ermis et al did a diagnostic prospective study on military personnel that showed the medial branch of the SCN as suffering entrapment in “muscle disorganization” and a taut, thickened peri-iliac band. However, limitations to the study’s clinical application were acknowledged, including that those results were unclear as to whether the “muscle disorganization” they found was related to nerve pathology or if it gave rise to nerve pathology. Also, given the military personnel subject population, the authors acknowledged that truly generalizable results should be seen more often in athletes and other physically trained people, but this is not the case.

The authors feel that other causes of CN should be investigated in future studies, including soft tissue pathology, such as obesity and Parkinson’s disease. The latter particularly has been hypothesized to lead to abnormal muscle tone and posturing, which could theoretically compress the cluneal nerves. However, the current literature indicates that SCN-E and MCN-E are far and away from the most common causes of LBP due to CN

Clinical Presentation/Diagnosis

Cluneal neuralgia, due to superior and middle cluneal nerve (SCN and MCN) entrapment, most often presents in the form of low back pain (LBP). LBP is commonly defined as pain, tension, or stiffness found between the costal margin and inferior gluteal folds. With cluneal nerve entrapment, however, there may be tenderness at the rim of the iliac crest, decreased sensation of the buttocks below the iliac crest, and leg pain usually radiating to the ipsilateral leg. The pain is often exacerbated by moving the lumbar region, movements such as rotating, bending, extending, prolonged sitting, or walking. Leg symptoms are seen in 47-84% of patients, a symptom that mimics lumbar radiculopathy. In a study by Strong and Davila in 1957, twenty-one out of the thirty patients complained of leg pain in various areas.49

Although the features of SCN and MCN entrapment remain to be fully elucidated, the correct identification of symptoms is required in order to prevent misdiagnoses. Cluneal nerve entrapment needs to be suspected when the following criteria are met- LBP is present with iliac crest and buttocks involvement. The pain is exacerbated upon movement; a trigger point, corresponding to the pressure zone of the nerve, is present over the posterior iliac crest. Upon palpitation of the trigger point, there is tenderness, numbness, or radiating pain, which signifies a positive Tinel sign. Finally, there should be relief of symptoms upon nerve block. The SCN and MCN are very thin, so imaging studies such as computed tomography (CT) and magnetic resonance imaging (MRI) studies are not diagnostically helpful.

Multiple studies help to illustrate the criteria that are first met before diagnosing SCN and MCN entrapment. In a 2013 case report, a 48-year-old woman presented with LBP and radiating buttock pain; mid-posterior thigh pain was provoked by palpitation of the MCN trigger points. This pain was relieved by infiltration of a local anesthetic, Lidocaine. In a similar prospective study, the diagnostic criteria consisted of 1) a tender point on the posterior iliac crest where the medial branch of SCN runs and 2) palpitation triggered the complaint of LBP and/or leg symptoms. The LBP and leg symptoms were assessed using a visual analog scale (VAS) score. The VAS score was recorded before the injection (68.6 ± 19.2 mm), fifteen minutes (31.6 ± 27.0 mm), and again one week after (45.2 ± 28.8 mm). Although there was a marked decrease in the VAS score both fifteen minutes and one week after, the biggest decrease was seen fifteen minutes after the injection; however, both demonstrated a significant decrease compared to the mean VAS score before injection (p < 0.05). Another significant finding was more women and older subjects (p < 0.05) were in the suspected SCN disorder group compared to the non-SCN disorder group. Although nerve block injections had to be repeated up to three times, symptom relief was achieved in 85% of SCN disorder patients. Nerve block proved to be an effective treatment modality in this patient population. One study sought to investigate MCN entrapment and ascertain the relationship between the MCN and long posterior sacroiliac ligament (LPSL), using cadavers. The anatomical study identified 64 MCN branches in thirty hemipelves, ten of which penetrated the LPSL. Four of those ten branches had evident constriction under the ligament. Being that this was the first anatomical study performed to elucidate MCN entrapment in cadavers, it is highly likely that this clinical phenomenon is not rare and may be underdiagnosed. A separate anatomical study considered the relationship between the SCN to the posterior iliac crest and thoracolumbar fascia in fifteen cadavers. While the intermediate and lateral branches of the SCN pierced or passed through a fissure in the fascia, the medial branches of the SCN appeared to be trapped between the taut fibers of the thoracolumbar fascia and superior rim of the iliac crest. Anatomical knowledge of the cluneal nerves may help to highlight future decompressive procedures when entrapment is suspected.

Differential Diagnosis

Multiple pathologies must be considered when clinically presented with a patient suffering from low back pain (LBP) and/or leg involvement. There are mechanical causes (97%), nonmechanical spinal conditions (1%), and visceral diseases (2%) which lead to LBP. Some mechanical causes of low back pain include internal disk disruption, facet joint pain, sacroiliac joint pain, sacroiliac ligament pain, torsion injuries, vertebral insufficiency fractures, scoliosis, interspinous tissue injury, lamina impaction, and spondylolysis in a sportsperson. A retrospective study found that the younger the patient, the higher the likelihood that the LBP was discogenic in nature, whereas in older patients, sacroiliac joint pain or an facetogenic cause was more likely. Statistically, 40% of adults suffer from disc-related pain, 30% suffer from facet joint pain, and 20% suffer from sacroiliac joint-related pain. It is clinically important to note that MCN entrapment mimics sacroiliac joint pain: sacroiliac joint pain is also associated with LBP and buttock pain; however, the SIJ score helps to differentiate between SIJ-related pain and pain caused by other factors such as lumbar spinal canal stenosis and lumbar disc herniation. If the SIJ block is ineffective, MCN entrapment should be considered. A retrospective analysis investigated LBP due to SCN entrapment versus lumbar spinal canal stenosis using the Roland Morris Disability Questionnaire (RMDQ).The study found that SNC entrapment heavily affects physical and psychological function; RMDQ scores were significantly higher, and an increased level of disability was seen in the patients with SCN entrapment compared to patients with lumbar spinal canal stenosis. On the other hand, nonmechanical spine conditions such as neoplasia, spondylarthritis, Scheuermann disease (especially Type II), Paget disease, and diffuse idiopathic skeletal hyperostosis, can also cause LBP. LBP can also signify other visceral diseases: prostatitis, endometriosis, pancreatitis, cholecystitis, ulcer, chronic pelvic inflammatory disease, nephrolithiasis, pyelonephritis, and pyelonephritic abscess, to name a few.

In a clinical review on the diagnosis and treatment of LBP, 90% of patients with LBP have “non-specific low back pain,” a diagnosis solely based on the exclusion of other specific pathologies. Some “red flags” which seem to indicate an underlying pathology include an onset of <20 or >55 years of age, non-mechanical pain, thoracic pain, weight loss, feeling unwell, widespread neurological symptoms, a structural spinal deformity, or previous history of carcinoma, steroids, or HIV. The following indicators are more suggestive of a nerve root problem: unilateral leg pain that is greater than the low back pain, pain that radiates to the foot or toes, numbness and paresthesia, localized neurology, and when a straight leg test incites more leg pain. Diagnostic imaging studies should be considered when patients exhibit little to no improvement after 6 weeks of medical management and/or physical therapy. Imaging should also be considered for patients with a suspected underlying condition or patients with severe or progressive neurologic deficits.

Treatment

Cluneal Neuralgia has a wide array of treatment options for those suffering from the condition. The treatments range from a simple nerve block all the way to peripheral nerve stimulation and surgical procedures. After an individual has been diagnosed with CN, the options for treatment are divided into broad categories: conservative management, peripheral nerve stimulation, or surgical intervention.

Conservative Treatment

If an individual chooses conservative management, one of the first and simplest treatments is a nerve block. In a nerve block, a local anesthetic with or without a steroid is injected directly into the area causing the pain. This will desensitize the nerve and the steroid can provide an anti-inflammatory effect, leading to a temporary resolution of pain. This procedure can be diagnostic and therapeutic. It can be used as a diagnostic tool in that if it causes a resolution of pain then the individual is likely to have a form of CN. However, if the procedure does not help resolve the pain, then it is unlikely that the individual has a diagnosis of CN. It is therapeutic in that if the individual has CN then the procedure is likely to help resolve the pain, producing a therapeutic effect. Related to the entrapped middle cluneal nerve usually being found in the Long Posterior Sacroiliac Ligament (LPSL), researchers have found that ultrasound-guided nerve block into the LPSL is able to reliably anesthetize the superior cluneal nerve with a success rate of 90%. This treatment is also beneficial for individuals who are planning to undergo surgery in that it anesthetizes the skin, which can control postoperative pain at the incision site. A downfall of local anesthetic alone is that it is temporary and will wear off over time, causing individuals to have to receive more injections if they continue to choose conservative management.

Another conservative management option is high-frequency thermal coagulation. This treatment uses a needle, placed in the LPSL, that transmits high-frequency radio waves and heat, which are used to degenerate the cluneal nerve, rendering it unable to transmit pain signals. The needle is heated to a temperature of 90°C and is left in place for 90 seconds. This process is done in three different areas along the LPSL. In a recent study, all individuals who received high-frequency thermal coagulation reported pain alleviation with no reports of complications. In addition, thermal coagulation extended the duration of pain relief to 145.7 ± 38.7 days compared to 7.7 ± 6.6 days of pain relief from a simple nerve block. Although the duration of pain relief is significantly extended with high-frequency thermal coagulation, the pain will still eventually return and will require further treatment. Related to this, high-frequency thermal coagulation is an attractive option for individuals wanting to avoid the operating room. On the other hand, it may not be the best long-term option for those wanting to permanently eliminate the pain.

Another conservative management option for cluneal neuralgia is the use of a Capsaicin patch. Capsaicin is a highly selective TRPV1 vanilloid receptor ligand. The TRPV1 vanilloid receptor is largely involved in the transmission of pain signals. By prolonged exposure of these receptors to Capsaicin, they essentially become desensitized to the pain signals. In addition to desensitizing the fibers to pain, the presence of the Capsaicin patch also decreases the density of these fibers in the skin, as well as decreasing the expression of the TRPV1 receptor. Researchers have been able to use Capsaicin patches to significantly reduce pain in 24% of patients making Capsaicin patches a potential first-line treatment for individuals with chronic CN.

Another conservative management option for CN is wireless peripheral nerve stimulation. In this treatment, after a diagnosis of CN is made, a Tuohy needle is advanced into the area of the nerve using ultrasound guidance. Leads are inserted through the needle and the needle is removed, and a receiver is then inserted. This treatment allows for wireless nerve stimulation of the CN, eliminating the need for surgery. Researchers were able to use peripheral nerve stimulation to provide satisfactory pain control to all individuals in the study. Using this technique, researchers were able to lower the pain score from 6.4 before treatment, to 1 after treatment. Although peripheral nerve stimulation, using this technique, has been shown to significantly reduce the pain caused by CN, it is likely to not be used as the initial, non-surgical treatment. It is most useful in individuals whose pain is resistant to other non-surgical medical treatments.

Surgical Treatment

In many instances, individuals who have refractory CN consider a surgical treatment when more conservative measures are unsuccessful. Individuals who undergo surgical procedures are usually those whose non-surgical medical treatment has been ineffective or those who choose to forgo non-surgical treatment and instead elect surgery. Fortunately, there are several highly effective surgical methods that can provide a significant reduction of pain for these individuals. The benefit of surgical procedures is that there is direct visualization of the nerve and its surroundings, making it safer for the patient and limiting the possibility of potentially harmful effects. The potential negative effect of surgical treatment is that anytime there is a surgical procedure, there are risks of general anesthesia, unintentional nerve damage, or damage to surrounding tissue.

First, individuals can undergo an open surgical procedure to release the cluneal nerve from its entrapment. This procedure is done by making a small incision in the gluteal area where the pain is localized. The surgeon then dissects the subcutaneous soft tissue and exposes and identifies the nerve by placing a nerve stimulator in the area. Related to the anatomical path of the nerve, the thoracolumbar fascia is cut along the path of the superior cluneal nerve until there are no kinks in the nerve. This will free the nerve from its entrapment. This technique was found to be highly effective, resulting in all 34 individuals who underwent the procedure reporting symptom improvement, while none of the individuals reported worsening of their symptoms. This procedure is relatively quick and lacks in serious potential complications with the average duration of surgery being 45 minutes. The fallback of this procedure, when compared to other surgical treatments, is that it requires a larger incision site, which potentially exposes the individual to more surgical site trauma.

The second surgical approach is a minimally invasive surgery. In the minimally invasive technique, a trans-gluteal endoscopic approach is performed, in which a surgeon uses a camera and endoscopic instruments, each inserted into a port surrounding the path of the cluneal nerve. The surgeon then uses the camera and instruments to decompress the nerve, similarly to the open approach. This procedure has been shown to provide excellent relief of pain caused by Cluneal neuralgia. At one year, 73% of individuals reported having a good treatment response, while 40% claimed that the procedure provided optimal results. This is increased from 57% and 31% at six months, respectively. A major benefit of the minimally invasive procedure is that individuals are left with two small incision sites, both less than 5 mm, which decreases the chance of incision site complications.72 A downfall of this procedure is that the tissue is not as clearly visualized, which can lead to unintended damage to the nerve or surrounding tissue.

A problem that some surgeons run into during surgery is identifying the cluneal nerve surgery, due to its small size, and confirming that it has been sufficiently decompressed. A unique tool that surgeons can utilize to help solve this problem is intraoperative indocyanine green video angiography. Indocyanine green video angiography provides real-time patency information and flow dynamics of the vessels supplying the cluneal nerve. This allows surgeons to more accurately identify the nerve and confirm that adequate decompression is achieved. This technology has been shown to be effective in identifying not only the cluneal nerve but also other peripheral nerves, leading to a more precise and effective decompressive surgery.

Overall, individuals who undergo surgery for CN report excellent long-term treatment regarding their pain. The reoccurrence rate is 13%.This is likely due to a lack of full decompression of the nerve, an entrapment of other branches of the nerve, or entrapment of a different nerve altogether. This can be avoided by decompressing as many of the cluneal branches as possible during the original surgery. This would prevent the need for another operation, which would expose the individual to the risks associated with doing so. All individuals who experience a reoccurrence experienced it in the first 25 months after surgery, suggesting the need for reevaluation for a minimum of 25 months post-op.74

Conclusion

The cluneal nerves, particularly the SCN and MCN, are cutaneous sensory nerves that innervate the posterior lumbar and buttock region and infrequently cause LBP. A thorough review of SCN and MCN anatomy reveals that CN is most often caused by entrapment from various etiologies, and can lead to varied symptoms.The SCN is most likely to become entrapped or constricted in the OT, while the MCN can be entrapped within or under the LPSL. Risk factors leading to the development of SCN-E or MCN-E most notably include age, sex, vertebral fractures, and past surgical history. CN most commonly presents as LBP, although it can often have leg symptoms or mimic radiculopathy or SIJ pain. The following specific criteria should be met when diagnosing cluneal nerve entrapment: pain exacerbated by movement, trigger point eliciting tenderness, numbness, or radiating pain on palpation, and relief of symptoms with a nerve block. Once cluneal nerve entrapment is diagnosed, it can be managed conservatively, with nerve blocks, high-frequency thermal coagulation, capsaicin patches to “defunctionalize” nociceptor fibers, and wireless peripheral nerve stimulation.These options can help avoid surgical treatment. However, many forms of efficacious surgical treatment possibilities exist, and they provide patients with excellent long-term outcomes. These surgical approaches include cluneal nerve release or minimally invasive endoscopic decompression and can be augmented by indocyanine green video angiography.

In summary, the etiology of LBP should be investigated for possible CN. Spinal surgeons and clinicians evaluating LBP should consider SCN-E and MCN-E before treatment of these patients to prevent misdiagnoses. Subsequently, conservative and surgical options should be evaluated on an individual level and based on symptom severity to best treat patients suffering from LBP related to CN.