- Lumbosacral plexus: network of nerves formed by the ventral rami of the lumbar and sacral spinal cord.
- Lumbosacral plexopathy (LSP): an injury to the nerves in the lumbar or sacral plexus.
- Lumbosacral-radiculoplexus neuropathy (LRPN): injury involving the nerve roots, plexus, and nerves
- Sciatic neuropathy: any injury to the sciatic nerve.
There are multiple causes of LSP which can be categorized into structural versus non-structural causes which include the following:1,2
- Structural Causes
- Tumor or Mass
- Malignant invasion: colon, cervix, ovary, urinary bladder, prostate gland
- Metastasis: breast, lung, lymphoma
- Benign tumor: neurofibroma, perineurioma,
- Motor vehicle accident
- Sports Injury
- Postoperative/Stretch Injuries
- Obstetric related 3,4
- Direct compression by fetus
- Stretch injuries
- Forceps application although not frequently encountered
- Vascular Lesions
- Tumor or Mass
- Non-Structural Causes
- Local organs: gastrointestinal tract, urinary tract, spine
- Generalized infection, diffuse infiltrative lymphocytosis syndrome (DILS)
- Inflammatory/micro vasculitis
- Diabetic lumbosacral radiculoplexus neuropathy
- Non-diabetic lumbosacral radiculoplexus neuropathy
- Postsurgical inflammatory neuropathy
- Radiation – Induced
Etiology of sciatic neuropathy is largely similar to that of LSP with a few distinct clinical differences. Sciatic nerve injuries can occur anywhere along its course as it exits the pelvis through the sciatic foramen and runs posteriorly down the thigh. Origin of sciatic neuropathy can be categorized based on location of injury which are summarized below.5,6
- Hip/Gluteal Region
- Total Hip Arthroplasty (most common cause)
- Hip dislocation (especially posterior) or fracture
- Positioning/ External compression (lithotomy, prolonged sitting, or coma)
- Gluteal/Piriformis injury or entrapment
- Gluteal contusion/ compartment syndrome
- Piriformis syndrome
- Injections (upper outer quadrant)
- Obstetric related (vaginal delivery)
- Thigh Region
- Femur fracture
- Baker’s cyst (at popliteal fossa)
- External Compression (thigh tourniquet)
- Internal Compression (hematoma, edema)
- Either Hip or Thigh Region
- Direct nerve injury/ infarction
- Vasculitis (mononeuritis multiplex)
- Bypass surgery
- Iliac artery arteriosclerosis
- Delayed radiation effects
- Penetrating injury (gunshot or knife wounds)
- Mass lesions/Tumors
- Arteriovenous malformations (aneurysm, persistent sciatic arteries)
- Tumors (lymphoma, neurofibroma, schwannoma, metastasis)
- Myositis ossificans
- Direct nerve injury/ infarction
Epidemiology including risk factors and primary prevention
Lumbosacral plexopathies are far less common than brachial plexopathies. The prevalence of lumbosacral plexopathies is not well documented for most etiologies. Traumatic lumbosacral plexopathies occur far less frequently than traumatic brachial plexopathies because of the lumbosacral plexus’ location deep in the retroperitoneum, protected by the pelvic brim.1 Among the non-structural causes, complications of diabetes are the most common. Diabetic lumbosacral radiculoplexopathies, classically known as diabetic amyotrophy, occurs in approximately 0.8% of all patients with diabetes.7
Sciatic neuropathy is one of the most common lower extremity mononeuropathies, second to peroneal (fibular) neuropathy. Most sciatic neuropathies occur at the hip region for which the most common presentation is following hip or femur fracture or total hip arthroplasty.8 In sciatic nerve injury, the peroneal (fibular) division is preferentially affected compared to the tibial division.6
Risk factors for LSP or sciatic neuropathy vary based on etiology, they include, but are not limited to the following:
- Family or personal history of pelvic cancers, Hodgkin Lymphoma, or autoimmune diseases
- Personal history of pelvic or thigh radiation, autoimmune disease or diabetes mellitus type 2
- History of pelvic trauma which can occur during high force trauma, birth delivery especially prolonged labor, abdominopelvic surgery, or pelvic girdle or lower extremity fractures
- Increased bleeding risk, as seen in anticoagulation use, hemophilia, iliac artery aneurysms
- Prolonged immobilization as in coma, intoxication, or complicated hospital course
Primary prevention is based on early recognition, prevention of prolonged positioning (hospitalization, surgery), early intervention (e.g., post trauma/abdominopelvic surgery), and close monitoring of disease progression (e.g., cancer metastasis, diabetes, autoimmune disease).
The lumbosacral plexus contains around 200,000 axons that give rise to six sensory nerves to the thigh and leg and six major sensorimotor nerves innervating approximately 43 muscles of the leg4. It consists of two separate parts: the lumbar plexus and the sacral plexus lying above and below the pelvic rim, respectively, which are connected by the lumbosacral trunk. The lumbar part of the plexus lies embedded between and in the paraspinal quadratus lumborum and psoas muscles, and the sacral plexus lies within the pelvis. The lumbar plexus is formed from the T12, L1 through L4 nerve roots, and the sacral plexus is formed from the L4 to S4 nerve roots. The lumbosacral plexus can be further divided into anterior and posterior divisions. The anterior division provides innervation to muscles involved in hip adduction while the posterior division primarily innervates the muscles involved in hip flexion and extension as well as movement of the lower leg.
The regional anatomy of the lumbar plexus and sacral plexus contributes to the various pathophysiologies. A local lesion may affect each separately, but a diffuse process usually causes more generalized involvement. If the pathological involvement involves the nerve roots, nerves, and plexus, these conditions are not pure lumbosacral plexopathies, but rather referred to as lumbosacral radiculoplexus neuropathies (LRPN).
The sciatic nerve originates from the L4-S3 nerve roots, with nerve fibers arising from the lumbosacral trunk and sacral plexus, forming the sciatic nerve as it exists the pelvis through greater sciatic foramen. The sciatic nerve is composed of two nerve divisions referred to as the common peroneal (lateral) and tibial (medial) division which distally divide into the common peroneal and tibial nerves. The muscles innervated by the sciatic nerve of the posterior thigh are mostly by the tibial division which the exception of the short head of the biceps femoris, which is innervated by the common peroneal division. This exception has important electrodiagnostic implications for distinguishing common peroneal neuropathy from a sciatic neuropathy or other proximal lesion.
Please see Table 1 for detailed functional innervation of the lumbosacral plexus.
Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)
As listed above, lumbosacral plexopathies and sciatic neuropathies arise from various disease processes: neoplasm, infection, trauma, radiation treatment of pelvic or thigh neoplasm, hematoma and other vascular lesions in the retroperitoneal, pelvic, or thigh areas, mechanical or stretch injury (especially after hip surgery), ischemia, inflammation, infiltration (amyloid), and idiopathic causes. The clinical course depends on the etiology which are discussed below.
Neoplasm has been reported to be the most common cause of nontraumatic LSP.9 The clinical presentation often includes the subacute onset of pain followed by motor and/or sensory loss in a distribution dependent on which area of the plexus is affected.10 Neoplasm in the upper lumbosacral plexus causes pain in the costovertebral area radiating to the upper thigh, and a lower lumbosacral plexus lesion causes pain in the iliac crest, buttocks, and the posterior aspect of the thighs.11 The major differential diagnoses of neoplastic LSP include local pelvic bone infection, avascular necrosis of the hip, and radiation-induced plexopathy.12
The following are the predominate types of tumor/mass causing LSP:
- Direct malignant invasion: due to its location, the lumbosacral plexus is vulnerable to direct invasion from pelvic organs, namely the colon, cervix, ovaries, and urinary bladder12
- Metastases: direct infiltration or retroperitoneal lymph node enlargement can lead to compression of the lumbosacral plexus, either from remote solid organs (e.g., lung, breast) or hematologic malignancy (e.g., lymphoma). Metastatic lesions involving the posterior femur can result in compression or infiltration of the sciatic nerve.
- Intra-neural lymphomatosis: lymphoma cells can directly invade peripheral nerves/plexus – the nerves themselves can act as a safe haven for the lymphoma cells as the chemotherapeutic agents may not be able to cross the blood nerve barrier.
- Perineural spread of prostate cancer: a rare cause of LSP resulting from tumor cells spread up the small sacral nerve root fibers innervating the prostate gland and then grow down the nerves into the lumbosacral plexus within the perineural lining of the nerve
- Primary nerve sheath tumors affecting the lumbosacral plexus, such as neurofibromas, can be seen but are uncommon.
- Intraneural perineurioma is a benign hypertrophic tumor that presents insidiously in young people and presents a focal motor neuropathy. It worsens slowly with time however does not require resection.1
Both local and systemic infection has been found to cause LSP. Local infection is more common and includes infection/abscesses in the psoas and gluteal musculature, retroperitoneal space, as well as infection in nearby organs such as the gastrointestinal or urinary tract, or lumbar spine. Systemically, varicella zoster virus, mycobacterium tuberculosis (Pott’s disease), HIV, and hepatitis C have all caused LSP.13 HIV patients can have diffuse infiltrative lymphocytosis syndrome (DILS) – a painful, paralytic lower limb LSP with large T-cell infiltrates on nerve biopsy that mimic lymphoma.14 Clinically, pain/neurological symptoms are similar to neoplasm, with symptoms such as fever, malaise, point tenderness, weight loss, and night sweats also being common. Treatment includes drainage of abscess, appropriate antimicrobial medication, and in the case of DILS, corticosteroids and antiretroviral therapy.
Damage to the sciatic and lumbosacral plexus has been observed in patients with severe COVID-19 infection with prolonged hospital stay. Although the mechanism for nerve injury resulting from COVID-19 infection is unclear, its pattern appears to have similar clinical patterns to vasculitic and inflammatory neuropathies rather than infectious.15
Trauma, Operative Complications, and Labor/Delivery Related Injuries
The trauma that causes a LSP is usually severe, involves very high velocity and energy at the time of impact, and is often associated with pelvic fractures (along with many other significant injuries). This is due to the anatomy: the lumbosacral plexus lies within the retroperitoneal space (a minimally mobile space) and is otherwise protected and encased within the bony environment of the pelvic brim.1 Etiologies include high-velocity car accident, gunshot wound, and traumatic dislocation of the hip – which can cause LSP predominantly involving its lower portion, particularly at the major branches of the sciatic nerve (most commonly peroneal, followed by tibial), and is seen in up to 20% of cases.16 Traumatic lumbosacral plexopathies typically cause paresis in the distribution of the common fibular nerve, followed by the gluteal, tibial, and obturator nerves. Symptoms may also arise from associated injuries to local pelvic organs, such as urinary bladder dysfunction, intestinal perforation, or vascular injury.17
Intrapartum or postpartum LSP has rarely been seen. Acute foot drop is the usual presentation believed to be caused by compression of the lumbosacral trunk of the plexus preferentially effecting the peroneal division of the sciatic nerve from the fetal head against the pelvic brim. This is most often seen in women of short stature giving birth to large newborns.17
Postoperative lumbosacral plexopathies can occur following abdominopelvic and gynecologic surgeries.18 There has also been case reports of LSP associated with spine surgery, associated with posterior lumbar interbody fusion with retractor use.19 Etiologies of postoperative LSP are felt to be due to scar tissue formation, development of post-operative hematomas, prolonged positioning, or retraction of tissues.1
Similarly, sciatic neuropathies can occur from trauma such as motor vehicle accidents or falls resulting in hip fracture or dislocation (primarily posterior). The most common cause of sciatic neuropathy is neurologic complications following total hip arthroplasty, suspected to be due to nerve stretch during surgery, direct injury from instrumentation, or compression from prolonged positioning.8 Penetrating trauma or combat-related injuries from gunshot wounds or lacerations can result in sciatic nerve injury in the hip or thigh region.20
Radiation treatment of primary or metastatic pelvic neoplasms can cause permanent damage to the lumbosacral plexus and the corresponding peripheral nerves. Radiation causes endothelial damage, which promotes inflammatory cell migration and then initiates a state of chronic inflammation.21 A phase of active fibrosis occurs next, followed by an irreversible state of microvascular injury and ischemic damage. These phases can take months to years to occur, and the extent of damage depends on the dose and intensity of the radiation. Those who receive a larger total dose of radiation, a larger dose per fraction of radiation, have a larger nerve exposure per radiation area, receive concomitant chemotherapy, and those with underlying peripheral neuropathy, are at the highest risk for radiation-induced injury.
Symptoms of radiation induced lumbosacral plexopathies are insidious, often occurring years to decades after radiation, with an asymmetric, progressive muscle weakness and atrophy pattern. Involvement of pelvic organs, such as the urinary bladder or rectum, as well as vertebral body compression fractures, can also be seen due to radiation-induced changes in these areas. Neither pain nor sensory abnormalities are common findings in radiation-induced plexopathies, and if they do occur, these symptoms are often milder and occur later in the course. Pain may be related to surrounding soft tissue radiation-induced fibrosis causing extrinsic compression of the nerves.
Delayed radiation effects rarely result in an isolated sciatic nerve injury and more likely to cause damage to the lumbosacral plexus with sciatic nerve involvement.8
Hematomas and other Vascular Lesions in the Retroperitoneal, Pelvic, or Thigh Region
Vascular lesions, such as a retroperitoneal hematoma (whether traumatic or non-traumatic) or an iliac artery aneurysm, can cause structural damage to the lumbosacral plexus.10,22 Retroperitoneal hematomas can be secondary to trauma or non-traumatic bleeding episodes seen in patients with an increased bleeding risk (e.g., hemophilia, anticoagulant use, hematologic malignancy). Compression of the psoas muscle, ischemic secondary to intravascular abdominal procedures, or increased pressure from a hematoma causing compartment syndrome, can all damage the lumbosacral plexus. The symptoms associated with hematoma compression lumbosacral plexopathies are acute, unilateral painful back or flank with radiation of symptoms along with weakness in the ipsilateral involved lower limb.1 Symptoms often resolve after evacuation of the hematoma if ischemic changes have yet to occur.
The sciatic nerve can also be damaged from vascular lesions and hematomas of the gluteal or thigh region by direct compression. Examples include hematomas resulting from gluteal injections, arterial aneurysms, or arteriovenous malformations near the piriformis muscle.2
Inflammatory, Vasculitis, and Immune-mediated causes
Lumbosacral plexopathies caused by inflammatory/microvasculitic changes are seen in diabetic lumbosacral radiculoplexus neuropathy (LRPN), nondiabetic LRPN , postsurgical inflammatory neuropathy, sarcoidosis, and in some cases, intrapartum LSP.1 This category of lumbosacral plexopathies often present with an acute to subacute onset of spontaneous, asymmetric (whether bilateral or unilateral), pain with lower extremity weakness, sensory loss and/or paresthesia.
Diabetic LRPN occurs most frequently in patients with a mild form of Type 2 Diabetes Mellitus after weight loss, initiating an exercise regimen or tightening glycemic control.23 Symptoms include acute-subacute onset of severe, focal, neuropathic pain, most frequently in the thigh or leg, followed by ipsilateral spreading of the pain and progressive weakness and sensory loss; contralateral symptoms can occur as well. Symptoms, especially pain, worse at first that generally improves without treatment; however, weakness can persist. Classic diabetic distal sensorimotor neuropathies, on the other hand, are secondary to abnormal glucose metabolism, present distally, do not improve over time and pain is not as frequently a presenting factor. Nondiabetic LRPN presents similarly to diabetic LRPN, however the patients do not have diabetes mellitus.1 Severe pain is again the predominating symptom. Weight loss is also common in this population.
While most cases of postsurgical lumbosacral plexopathies are secondary to direct trauma to the plexus, some cases are found to have an inflammatory etiology and are categorized as postsurgical inflammatory neuropathies.23,24 These neuropathies can present as focal (involving only one nerve), multifocal or generalized, with pain again seen as the major symptom.1 Continued progression of these symptoms post-operatively, distinguishes it from a typical traumatic postoperative LSP in which direct nerve trauma leads to immediate symptoms of pain and weakness that should dissipate with time. Postsurgical inflammatory neuropathies can be confirmed via nerve biopsy showing inflammation or microvascular changes.
Sarcoidosis can present as a painful, asymmetric, proximal LSP or polyradiculopathy.1 Weakness and sensory loss may also be present. Patients with sarcoidosis who are found to have CSF pleocytosis, a short time from onset to treatment, and those found to have a higher grade of disability on initial evaluation, are more likely to respond to treatment and neurologically recover when compared to others.
Mononeuritis multiplex is a vasculitic neuropathy that can result in sciatic nerve injury by mechanism of nerve infarction. It refers to damage to two or more isolated nerves and presents in the setting of systemic disorders with pain and asymmetrical weakness and sensory changes.2
Essentials of Assessment
A thorough history and physical exam are key to diagnosis and determining the underlying cause of a LSP and sciatic neuropathy. Determining the onset, presenting symptom(s), and accurate progression of symptoms can help with developing a differential diagnosis. Many cases of plexopathies often have an acute to subacute onset with progression over days to weeks, however radiation induced lumbosacral plexopathies can occur years after radiation exposure. Sciatic neuropathies are typically slow, progressive, and painless but can have acute or subacute onset with pain after direct injury from trauma.
The location and severity of the pain is critical in evaluating a patient with suspected LSP or sciatic neuropathy. Lumbosacral plexopathies caused by neoplasms often present with back, hip or buttocks pain, while other causes often present with lower extremity pain.1 Additional important questions to ask include sensory involvement, weakness, and history of trauma. If a patient has a history of trauma, understanding the mechanism of trauma as well as the expected degree of deficits associated with the trauma is important to consider. For example, a patient with a femur fracture may have lower extremity weakness and pain as expected, however flank pain could be associated with an underlying retroperitoneal hematoma which could inevitably affect the LSP. Laterality is also an important qualifier as plexopathies are often unilateral, however, bilateral asymmetric involvement can be seen in massive traumas, autoimmune diseases, diabetic LRPN and radiation-induced plexopathies. History should also include questions regarding recent infections, surgeries, birth/deliveries, or joint problems.
A thorough investigation into a patient’s past medical history and family history is also important. A family or personal history of hemophilia, bleeding disorders, cancers, radiation therapy, autoimmune disorders, or diabetes mellitus is important to note. A thorough review of systems should also be conducted. Autoimmune diseases can present with systemic symptoms such as weight loss and fever, along with lumbosacral plexus involvement. Weight loss can also be an early sign in diabetic and nondiabetic LRPN, as well as autonomic symptoms such as erectile dysfunction, blood pressure changes and sweating.25
Observation of ungowned lower extremities may reveal bruises secondary to trauma, skin changes seen post-radiation or in autoimmune diseases, and/or decreased muscle bulk in a peripheral nerve distribution pattern. Muscle fasciculations may also be seen.
Palpation of involved regions compared to non-involved regions can help determine the severity of pain and demonstrate any signs of increased compartment pressure, fractures, or large sensory losses. A thorough musculoskeletal and neurological exam is key to diagnosis, and it is vital to rule out upper extremity involvement as well. Understanding joint range of motions, both passive and active, in the involved versus uninvolved sides is important. Understanding the pattern of changes noted during manual muscle strength testing in combination with areas of sensory loss can help localize the involved peripheral nerves. However, it may be difficult to distinguish a multilevel radiculopathy from a plexopathy or more distal mononeuropathy based on physical exam alone. If bilateral plexopathy has occurred, it may be difficult to distinguish it from cauda equina syndrome; however, bowel and bladder function should be normal with a plexopathy (unless the inferior sacral plexus is involved). Comparing strength, assessing for increased muscle tone or spasticity is necessary. Decreased muscle tone with absent or diminished lower extremity strength on the affected side are usually seen in lumbosacral plexus or sciatic injury (lower motor neuron signs). If the lumbar plexus is involved, the patellar reflex is usually diminished, whereas if the sacral portion of the plexus is involved (as in the sciatic nerve), the hamstrings and Achilles reflexes can be diminished.
Special tests, such as provocative hip maneuvers, should also be performed. Gait analysis, balance tests and checking for clonus and Babinski sign should also be considered.
Functional history focuses on the lower extremity, gait, transfers, and dressing.
LSP shares similar clinical characteristics to diseases or injuries resulting in lower motor neuron pattern dysfunction. Differential diagnosis of LSP may include lumbosacral radiculopathy, cauda equina or conus medullaris compression, mononeuropathies (femoral, sciatic, common peroneal nerve palsy), hereditary sensori-motor polyneuropathies (Charcot-Marie-Tooth disease), or spinal stenosis.1 The diagnosis of LSP can be challenging given the clinical overlap between these conditions. Isolated injury to the conus medullaris may present with upper motor neuron features on clinical examination (hyperreflexia and spasticity), distinguishing this condition from LSP.
Laboratory studies are ordered based on suspected etiology. Obtain blood glucose and glycosylated hemoglobin levels if diabetic nerve disease is suspected; sedimentation rate and white blood count if abscess is suspected; or prothrombin time and platelets if hematoma is suspected.
Pursue infectious workup depending on clinical picture: with skin lesions consider Herpes Simplex and Varicella-Zoster serology, and with history of an insect bite consider screening for tick-borne disorders such as Borrelia burgdorferi.
For inflammatory LSP (e.g. diabetic LRPN, non-diabetic LRPN, and postsurgical inflammatory neuropathy), serum inflammatory markers (ESR, CRP) are typically non-diagnostic, whereas CSF studies demonstrate elevated protein with a normal white cell count. In LSP from sarcoidosis, both protein and cell count can be elevated in the CSF. In LSP from lymphoma, cytology may confirm the malignancy.
Neuroimaging studies of the lumbosacral plexus are invaluable tools in the workup and diagnosis of a LSP. Prior to the advent of magnetic resonance imaging (MRI), computed tomography (CT) was the most effective radiological method to examine the lumbosacral plexus. However, the superior anatomic resolution of MRI increases its diagnostic accuracy and boosts interventionalists’ planning and has demonstrated high sensitivity in identifying early changes in the lumbosacral plexus.26 MRI of the lumbar spine and the pelvis are excellent tools in identifying space occupying lesions (e.g., cancer, hematoma, abscess) that may be compressing the plexus, verifying EMG/NCS findings, evaluating the extent of disease in pelvic tumors, clarifying a confusing clinical presentation, and providing localization for image guided delivery of pain medication or surgical interventions.27 Higher field strength MRIs (e.g. 3 Teslas vs. 1.5 Teslas) are preferable for its greater signal to noise ratio.28 Full evaluation of the lumbosacral plexus should include both T1-weighted images and a fluid sensitive fat suppressed sequence (i.e. STIR, “short tau inversion recovery”).29
Intravenous gadolinium can be used as a contrast agent to indicate areas of breakdown of the blood-nerve barrier, i.e. tumor-related plexopathies, inflammatory conditions, and posttraumatic neuromas.29 In diabetic LRPN, non-diabetic LRPN, or postsurgical inflammatory neuropathy causing LSP, an MRI of the lumbosacral plexus may show abnormal images with increased T2 signal in STIR of the involved plexus or a normal result.28 MRI of the lumbosacral plexus is also of value in distinguishing neoplastic from radiation-induced LSP.
Imaging of the lumbosacral plexus in the acute post-traumatic setting could be challenging due to hemorrhage and soft-tissue edema that may obscure the plexus. Ideally, dedicated imaging of the plexus should be delayed for 1 month to allow for resolution of hemorrhage and edema.30 CT myelography of the lumbar spine is another imaging modality that can be considered in the setting of traumatic LSP. Myelography provides high-resolution imaging of the thecal sac and is ideal in assessing for pre-ganglionic nerve root injury, however, it is limited in assessing the lumbosacral plexus. Therefore, MRI remains the imaging of choice in evaluating injury to the lumbosacral plexus.30
Despite the superiority of the MRI, CT may be more readily available and remains the optimal choice in patients where MRI is contraindicated.
Supplemental assessment tools
Electrophysiologic studies can be useful for accurate localization of the neurological injury and to characterize the process and are seen as an extension of the physical exam.31
The electrophysiological definition of a LSP is involvement of muscles from at least two lumbosacral root levels from at least two peripheral nerves in a pure lumbosacral plexopathy.1 Typically, a nerve conduction study will yield decreased amplitudes of compound action potentials and sensory nerve action potentials asymmetrically.1 Conduction velocities are usually normal as myelin is preserved. A prolonged late response (F wave) may also be seen. Needle EMG can demonstrate fibrillation potentials as well as neurogenic motor unit potentials in involved muscles. Testing the lumbosacral paraspinal muscles is important. Fibrillation potentials in the paraspinal muscles can be seen in both LRPN and lumbar radiculopathies, however they are absent in a pure LSP Needle EMG can be useful in detecting specific patterns to help aid in diagnosis. Muscle testing of multiple muscles innervated from L2 to S1 with differing peripheral nerves is important for distinguishing patterns. Bilateral testing can be done if systemic nerve involvement is being considered in the differential. After 3 weeks of onset of symptoms, positive sharp waves and fibrillations are expected to be seen in involved innervated muscles. In chronic injuries, evidence of terminal reorganization seen as increased polyphasicity, duration and amplitude of motor units along with a neuropathic recruitment pattern, can be seen. In the case of root avulsion, the plexus is severely damaged, and no motor recruitment will be seen.7 In radiation induced plexopathies, myokymic discharges can be seen on EMG, but their absence does not rule out the possibility of a radiation-induced injury. In diabetic LRPN, a concurrent distal diabetic neuropathy may be seen on EMG as well, however the asymmetric proximal changes and plexus involvement help to distinguish the two.
Electrodiagnostic evaluation of suspected sciatic neuropathy includes evaluation of sural and superficial peroneal sensory nerve action potentials (SNAP) to confirm post-ganglionic injury and provide information on the degree of involvement of tibial versus peroneal divisions. Standard electrodiagnostic evaluation of sciatic neuropathy also includes testing ipsilateral common peroneal and tibial motor nerve conductions. Findings of sciatic neuropathy most commonly demonstrate reduced peroneal compound motor action potential (CMAP) amplitudes and often normal to reduced tibial CMAP amplitude.
Needle EMG of carefully selected muscles will help differentiate sciatic nerve injury from LSP injury or more distal common peroneal injury. Needle examination should include peroneal-innervated muscles above (short head biceps femoris) and below the knee (tibialis anterior or extensor hallucis longus); tibial-innervated muscles (medial gastrocnemius or posterior tibialis); proximal non-sciatic innervated muscles (gluteus maximus, gluteus medius or tensor fascia lata); non-sciatic, non-L5-S1 muscle (thigh adductor); and paraspinal muscles. In general, EMG abnormalities in sciatic neuropathy are more commonly seen in peroneal-innervated muscles than tibial-innervated muscles.8
A nerve biopsy can be useful in diagnosing inflammatory/microvasculitic causes such as diabetic and nondiabetic LRPN. Evidence of ischemic injury and perivascular inflammation would be seen.
Please see Table 2 for the diagnostic workup for lumbosacral plexopathy.
EMG = electromyography; SSA = Sjogren syndrome A; SSB = Sjogren syndrome B; HIV = human immunodeficiency virus; CSF = cerebrospinal fluid; MRI = magnetic resonance imaging; CT = computed tomography.
Early predictions of outcomes
There are no large studies predicting outcomes in lumbosacral plexopathies or sciatic neuropathies. The best predictors are based on the etiology of injury. Neoplastic injury from tumor compression or infiltration depends on the type of malignancy and the available oncological treatment options. Radiation plexopathy tends to have a poor prognosis with expected progression of symptoms with time.32
Traumatic plexopathies in general result from significant force and result in severe injuries. Despite the general perception that traumatic plexopathies have poor outcomes, a case series involving 72 patients with traumatic lumbosacral plexopathies demonstrated that 70% of cases recovered spontaneously, most within 18 months.33 Presence of root avulsions noted on imaging is indicative of a poor outcome.
In Diabetic LRPN, significant improvement in symptoms is expected with time, on average lasting up to 18 months; however, some deficits may remain.1 Compared to typical diabetic mellitus type II patients, patient with DLRNs often have less long-term complications of hyperglycemia.34 In general, diabetic lumbosacral radiculoplexus neuropathy, lumbosacral radiculoplexus neuropathy, and postsurgical inflammatory neuropathy have a better prognosis.1
Various case reports of compressive plexopathies from hematomas also generally report good outcomes, often to the point of near or complete resolution of symptoms.35
Needle electromyography may assist with making the prognosis in these cases because recruitment of many different motor units during muscle activation is a good prognostic sign that terminal reorganization will result in meaningful strength recovery. Evidence of avulsion is a very poor prognostic sign for any functional recovery.
Rehabilitation Management and Treatments
Current management and treatment guidelines
Specific management of LSP depends on the underlying etiology and has been alluded to in previous sections. Despite the diverse spectrum of the root cause pathology, the greatest morbidity from LSP remain pain and functional impairment.1 Thus, pain management and physical therapy remain critical elements of to the treatment of such pathology. Furthermore, due to the limited evidence available to guide the rehabilitation of patients with lumbosacral plexus injury, practitioners rely on using core rehabilitation principles as they relate to lower motor neuron nerve disease.
Pain management can include ice/heat modalities; electrical stimulation; stretching; oral or topical medications (e.g., NSAIDs; neuropathic agents such as gabapentin, pregabalin, duloxetine, tricyclic antidepressants; opioids, topical lidocaine, capsaicin, compounding formulations), acupuncture, therapeutic injections such as nerve blocks, and in some cases spinal cord stimulators or intrathecal therapies.
Physical therapy is used to strengthen partially affected muscles, address muscular imbalances, maintain flexibility, and improve balance and gait. Assistive devices and braces as indicated for the location and severity of weakness. Ankle-foot orthoses (AFOs) can be used in lumbar plexus injuries to limit dorsiflexion of the foot and, therefore, promote knee extension in the setting of quadriceps weakness. AFOs are generally essential in sacral plexopathies because of the predominance of foot drop.
For neoplasms, management includes systemic or local treatments consisting of chemotherapy, surgery, immunotherapy, and/or radiation. Ultimately treatments depend on several factors including the pathology and stage of the underlying malignancy, patient’s functional status, and overall goal of treatment (palliative versus disease control). Observation is recommended for management of benign tumors such as perineurioma.
Surgery is the preferred treatment for root avulsions and sharp lacerations, and surgical consultation is indicated as soon as this diagnosis is made.35 Microbial infections require appropriate antibiotics, and abscesses require drainage.
Diabetic and non-diabetic LRPN, and postsurgical inflammatory neuropathy may be treated with immunotherapies (immunoglobulins, plasma exchange) or IV steroids to stop inflammatory etiology/damage.36 Studies investigating the use of oral steroids for treatment of this condition are limited to a few small case series and the findings remain inconclusive.37,38 It is important to consider the risks of using steroids in the diabetic population due to concerns of disrupting glycemic control. In general, there is a lack of clear evidence regarding use of immunotherapies or steroids (IV or PO) due to conflicting outcomes. Diabetic amyotrophy is self-limiting in most cases, but with variable degrees of recovery and residual impairment.
Patient & family education
The lumbosacral plexus anatomy is unfamiliar to most patients; therefore, education regarding the cause of symptoms needs to be appropriate to the patient’s medical knowledge. The prognosis is variable depending on the cause of the nerve dysfunction; therefore, education needs to be individually tailored for each patient.
Cutting Edge/ Emerging and Unique Concepts and Practice
A small study demonstrated the potential role of selective dorsal rhizotomy in the management of intractable pain from neoplastic LSP. A small case series of 6 patients with terminal pelvic cancer demonstrated improved pain scores and decreased narcotic use following treatment with selective dorsal rhizotomy.39 To date, there is a paucity of studies to support the findings of this small case series. Larger scale studies are needed in order to validate it’s use in standard practice. Therefore, this interventional method is typically reserved for palliative purposes.
Neuromuscular ultrasound (NMUS) is a diagnostic tool that can provide real-time information on the anatomic and physiologic integrity of a peripheral nerve. The utility of NMUS in conjunction with imaging and electrodiagnostic studies has shown to be useful in evaluating peripheral nerve injuries. A study by Bilgici et al. demonstrated the benefit of real-time NMUS for qualitative evaluation of sciatic nerve injury.40
Gaps in the Evidence-Based Knowledge
Some research regarding the treatment of diabetic lumbosacral radioculoplexus neuropathies suggests the use of immunomodulatory therapies such as plasma exchange, IV immunoglobulin or steroids, however no large study has been conducted and only mild benefit has been noted in research.1
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- Preston DC, Shapiro BE. Lumbosacral Plexopathy. In: Electromyography and Neuromuscular Disorders. W.B. Saunders; 2013:501-517. doi:10.1016/b978-1-4557-2672-1.00032-5
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Original Version of the Topic
Karen Barr, MD. Lumbosacral plexopathy and sciatic neuropathy: differential diagnosis and treatment. 9/20/14
Previous Revision(s) of the Topic
Christian Custodio, MD, William Douglas, DO, Kristian von Rickenbach, MD. Lumbosacral plexopathy and sciatic neuropathy: differential diagnosis and treatment. 9/6/2018
Christian Custodio, MD
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Chanel I Davidoff, DO
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