Lumbosacral plexopathy and lower extremity neuropathies
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.
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
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.
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
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
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:
More than 50% reduction of the sural and superficial peroneal SNAP on the affected side.
Denervation of the muscles innervated by sacral plexus.
TA, MG, TP, FDL, EDB, AH, VM, GMax, GMedius/TFL, sacral paraspinals
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.
In the thigh the branch of the sciatic nerve that innervates the short-head of biceps femoris muscle comes from the common fibular nerve. The next branch occurs in the popliteal fossa and is the sural communicating branch that joins the medial sural branch from the tibial nerve in the calf and contributes variably fibers to the sural nerve. The lateral cutaneous nerve of the calf innervates the skin to the lateral aspect of the calf. It then winds around the fibular neck and passes 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.
Common peroneal (fibular) nerve is often injured at the fibular head due to its superficial location.
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 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.
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: 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, intraneural ganglion cyst, Baker’s cyst, perineural cysts
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
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
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. Often, there may be evidence of both axonal loss and demyelination in the same patient. The EDB muscle usually is chosen as the recording site for peroneal motor studies. However, in patients with a foot drop, it is weakness of the TA that 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, 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. 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.