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  • 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.
  • Sciatic neuropathy: any injury to the sciatic nerve.


There are multiple causes of LSP including the following1:

  • Tumor or Mass
    • Malignant invasion: colon, cervix, ovary, urinary bladder, prostate gland
    • Metastasis: breast, lung, lymphoma
    • Benign tumor: neurofibroma, perineurioma,
  • Infection
    • Local organs: gastrointestinal tract, urinary tract, spine
    • Generalized infection, diffuse infiltrative lymphocytosis syndrome (DILS)
  • Trauma
    • Motor-vehicle accident
    • Sports Injury
    • Postoperative/Stretch Injuries
    • Childbirth
  • Obstetric related 2,3
    • Direct compression by fetal parts
    • Stretch injuries
    • Forceps application although not frequently encountered
  • Radiation
  • Hematoma
  • Vascular lesions
  • Inflammatory/micro vasculitis
    • Diabetic lumbosacral radiculoplexus neuropathy
    • Lumbosacral radiculoplexus neuropathy
    • Postsurgical inflammatory neuropathy
    • Sarcoidosis

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 brim1. Diabetic lumbosacral radiculoplexopathies occur in approximately 0.8% of all patients with diabetes4.

Risk factors 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 radiation, autoimmune diseases or diabetes mellitus type 2
  • Pelvic trauma which can occur during high force trauma, birth delivery especially prolonged labor, abdominal surgery, or pelvic girdle or lower extremity fractures
  • Increased bleeding risk, as seen in anticoagulation use, hemophilia, Iliac Artery aneurysms
  • Primary prevention is based off of early intervention (e.g. post trauma/abdominal surgery) and close monitoring of disease progression (e.g. cancer metastasis, diabetes, autoimmune diseases)


The lumbosacral plexus consists of two separate parts: the lumbar and the sacral plexus lying above and below the pelvic rim, respectively, which are connected by the so-called 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 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 muscles4.

The local anatomy of each contributes to the various patho-physiologies affecting the lumbar and lumbosacral plexi.  A local lesion may affect each separately, but a diffuse lesion usually causes more generalized involvement.  If the pathological involvement involves the nerve roots, nerves, and plexus, these conditions are not pure lumbosacral plexopathies, but are lumbosacral radiculoplexus neuropathies.

Please see Table 1 for detailed innervation of the lumbosacral plexus.

Table 1: Innervation of the Lumbosacral Plexus

NerveOriginMuscles InnervatedSensory Distribution
Lumbar Plexus L1-L4
Iliohypogastric T12-L1-Transversus abdominus

-Internal oblique

-Anteriomedial abdominal wall

-lateral buttock

Ilioinguinal L1 -Transversus abdominus

-Internal oblique

 -Medical aspect of upper thigh

-Base of penis and anterior scrotum

-Mons pubis and superior labia majora

Genitofemoral L1-L2-Cremaster (males)-Anterior aspect of the upper thigh

-Spermatic cord and posterior scrotum

Inferior labia majora

Femoral L2-L4-Psoas

-Rectus femoris

-Vastus lateralis

-Vastus medialis

-Vastus medialis




 -Anterior and medial aspects of the mid and distal thigh

-Knee joint

Lateral femoral cutaneous L1-L3None-Lateral thigh
Obturator L2-L4-Obturator externus

-Adductor magnus

-Adductor longus

-Adductor brevis


 -Medial aspect of upper thigh
Lumbosacral Trunk L4-L5nonenone
Sacral PlexusL4-S3
Sciatic – Tibial division


 L4-S3-Biceps femoris (long head)



Sciatic – Common Peroneal division


L4-S2-Biceps femoris (short head)-Leg
Superior gluteal L4-S1 -Gluteus medius

-Gluteus minimus

-Tensor fascia latae

Inferior gluteal L5-S2-Gluteus maximusnone
Pudendal S2-S4-External anal sphincter

-External urinary sphincter

-External genitalia
Posterior femoral cutaneous S1-S3None-Inferior and medial buttock

-Hip joint


-Popliteal fossa

Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)

As listed above, lumbosacral plexopathies arise from various disease processes, primarily: neoplasm, infection, trauma, radiation treatment of pelvic neoplasm, hematoma and other vascular lesions in the retroperitoneal or pelvic areas, mechanical or stretch injury (especially after hip surgery), ischemia, inflammation, infiltration (amyloid), and idiopathic causes.

The clinical course of lumbosacral plexopathies depends on the etiology.


Neoplasm has been reported to be the most common cause of nontraumatic lumbosacral plexopathy5. 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 affected6. 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 thighs7. The major differential diagnoses of neoplastic lumbosacral plexopathy include local pelvic bone infection (osteitis pubis), avascular necrosis of the hip, and radiation-induced plexopathy8.

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 bladder8
  • 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)
  • 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 case of LSP caused when 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 resection1


Both local and systemic infection has been found to cause lumbosacral plexopathy (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 LSP9. 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 lymphoma10. 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.


The trauma that causes a lumbosacral plexopathy 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 brim1. Etiologies include high-velocity car accident, gunshot wound, and traumatic dislocation of the hip – which can cause lumbosacral plexopathy predominantly involving its lower portion, particularly at the major branches of the sciatic nerve (most commonly fibular, followed by tibial), and is seen in up to 20% of case11.

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 injury12.

Intrapartum lumbosacral plexopathy has rarely been seen during labor.  Acute foot drop is the usual presentation (believed to be caused by compression of the lumbosacral plexus from the fetal head against the pelvic brim) – and is most often seen in women of short stature giving birth to large newborns12.

Radiation Treatment of Pelvic Neoplasm

Radiation of pelvic neoplasms (e.g. colon, ovarian, cervical, testicular, prostate, Hodgkin) 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 inflammation13. 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 large total dose of radiation, a large dose per fraction of radiation, have a large 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.

Hematomas and other vascular lesions in the Retroperitoneal and Pelvic area

Vascular lesions, such as a retroperitoneal hematomas whether traumatic or non-traumatic or an iliac artery aneurysms, can cause structural damage to the lumbosacral plexus14,6. 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 limb1. Symptoms often resolve after evacuation of the hematoma if ischemic changes have yet to occur.


Lumbosacral plexopathies caused by inflammatory/microvasculitic changes are seen in diabetic lumbosacral radiculoplexus neuropathy, nondiabetic lumbosacral radiculoplexus neuropathy, postsurgical inflammatory neuropathy, sarcoidosis, and in some cases, intrapartum lumbosacral plexopathy1. 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 lumbosacral radiculoplexus neuropathies occur most frequently in patients with a mild form of Type 2 Diabetes Mellitus after weight loss, initiating an exercise regimen or tightening glycemic control15. 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, worsen at first then improve 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 lumbosacral radiculoplexus neuropathies present similarly to diabetic lumbosacral radiculoplexus neuropathies, however the patients do not have diabetes mellitus1. 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 neuropathies15,16. These neuropathies can present as focal (involving only one nerve), multifocal or generalized, with pain again seen as the major symptom1. Continued progression of these symptoms post-operatively, distinguishes it from a typical traumatic postoperative lumbosacral plexopathy 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 lumbosacral neuropathy or polyradiculopathy1. 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.



A thorough history and physical exam are key to diagnosis and determining the underlying cause of a lumbosacral plexopathy. 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.

It is important to know the location and severity of the pain. Lumbosacral plexopathies caused by neoplasms often present with back, hip or buttocks pain, while other causes often present with lower extremity pain1. 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, however flank pain could be associated with a lumbosacral hematoma. Laterality is also an important qualifier as plexopathies are often unilateral, however, bilateral involvement can be seen in massive traumas, autoimmune diseases, diabetic lumbosacral radiculoplexus neuropathies 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 lumbosacral radiculoplexus neuropathies, as well as autonomic symptoms such as erectile dysfunction, blood pressure changes and sweating17.

Physical examination

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 based on physical exam alone. If bilateral plexopathy has occurred, it may be difficult to distinguish it from cauda equine syndrome; however, bowel and bladder function should be normal with a plexopathy. Comparing strength, assessing for increased muscle tone or spasticity is necessary. Decreased muscle tone with absent or diminished lower extremity weakness on the affected side are usually seen in lumbosacral plexus 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, 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 assessment

Functional history focuses on the lower extremity, gait, transfers, and dressing.

Laboratory studies

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 lumbosacral plexopathy (e.g. diabetic lumbosacral radiculoplexus neuropathy, lumbosacral radiculoplexus neuropathy, 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 lumbosacral plexopathy from sarcoidosis, both protein and cell count can be elevated in the CSF.  In lumbosacral plexopathy from lymphoma, cytology may confirm the malignancy.


Neuroimaging studies of the lumbosacral plexus are invaluable tools in the workup and diagnosis of a lumbosacral plexopathy.  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 plexus18. MRI of the lumbar spine and the  lumbosacral plexus 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 interventions19. Higher field strength MRIs (e.g. 3 Teslas vs. 1.5 Teslas) are preferable for its greater signal to noise ratio20. 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”)21.

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 neuromas21. In diabetic lumbosacral radiculoplexus neuropathy, lumbosacral radiculoplexus neuropathy, or postsurgical inflammatory neuropathy causing lumbosacral plexopathy, an MRI of the lumbosacral plexus may show abnormal images with increased T2 signal in STIR of the involved plexus or a normal result20.  MRI of the lumbosacral plexus is also of value in distinguishing neoplastic from radiation-induced lumbosacral plexopathy.

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 characterize the process, and are seen as an extension of the physical exam22. The electrophysiological definition of a lumbosacral plexopathy is involvement of muscle from at least two lumbosacral root levels from at least two peripheral nerves in a pure lumbosacral plexopathy1.

Typically, a nerve conduction study will yield decreased amplitudes of compound action potentials and sensory nerve action potentials asymmetrically1. Conduction velocities are usually normal as myelin is preserved. A prolonged late response (F wave) may also be seen. Needle EMG demonstrate fibrillation potentials as well as neurogenic motor unit potentials in those muscle that are involved. Testing the lumbosacral paraspinal muscles is important. Fibrillation potentials can be seen in both lumbosacral radiculoplexus neuropathies and lumbar radiculopathies, however they are absent in a pure lumbosacral plexopathy.

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 seen4. In radiation induced plexopathies, myokymic discharges are seen on EMG. In diabetic lumbosacral radiculoplexus neuropathies, 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.

A nerve biopsy can be useful in diagnosing inflammatory/microvasculitic causes such as diabetic and nondiabetic lumbosacral radiculoplexus neuropathies. Evidence of ischemic injury and perivascular inflammation would be seen.

Please see Table 2 for the diagnostic workup for lumbosacral plexopathy.

Table 2: Diagnostic Workup for Lumbosacral Plexus

  • Nerve conduction studies and EMG
  • Blood tests
    • Complete blood count
    • Metabolic profile
    • Glycosylated hemoglobin
    • Sedimentation rate
    • Rheumatoid factor
    • SSA/SSB
    • Antinuclear antibody
    • Antineutrophil cytoplasmic antibody
    • Lyme titer
    • Angiotensin-converting enzyme
    • HIV
    • Immunofixation for monoclonal proteins
    • Paraneoplastic antibody panel
  • CSF studies
    • Cell count
    • CSF protein
    • CSF glucose
    • CSF viral studies (particularly cytomegalovirus)
    • CSF cytology
    • CSF ACE
    • CSF Lyme
  • MRI of lumbosacral plexus
  • MRI of lumbosacral spine
  • Positron emission tomography (PET)/CT (for neoplasm)
  • Nerve biopsy

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.  The best predictors are based on the etiology of the plexopathy.  Neoplastic plexopathy 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 time23.

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 months24. Presence of root avulsions noted on imaging is indicative of a poor outcome.

Diabetic lumbosacral radiculoplexus neuropathies significant improvement in symptoms is expected with time, on average lasting up to 18 months; however, some deficits may remain1. Compared to typical diabetic mellitus type II patients, patient with DLRNs often have less long-term complications of hyperglycemia25. In general, diabetic lumbosacral radiculoplexus neuropathy, lumbosacral radiculoplexus neuropathy, and postsurgical inflammatory neuropathy have a better prognosis1.

Various case reports of compressive plexopathies from hematomas also generally report good outcomes, often to the point of near or complete resolution of symptoms26.

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.


Current management and treatment guidelines

Specific management of lumbosacral plexopathy depends on the underlying etiology and has been alluded to in previous sections. Despite the diverse spectrum of root cause pathology, the greatest morbidity from lumbosacral plexopathy remain pain and functional impairment1. 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, stretching, medications (NSAIDs, neuropathic agents such as gabapentin/ pregabalin/duloxetine/amitriptyline/venlafaxine, or opioids), 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, treatment can involved chemotherapy, surgery, and radiation, and depends on the underlying malignancy.  Management of benign tumors such as perineurioma is observation.

Surgery is the preferred treatment for root avulsions and sharp lacerations, and surgical consultation is indicated as soon as this diagnosis is made26. Microbial infections require appropriate antibiotics, and abscesses require drainage.

Diabetic lumbosacral radiculoplexus neuropathy, lumbosacral radiculoplexus neuropathy, and postsurgical inflammatory neuropathy may be treated with immunotherapies to stop inflammatory etiology/damage.  Despite the lack of evidence for improving neurological deficits or impairment status, the authors of this article include treatment with corticosteroids in their management of patients with this condition27.

A controlled trial of IV methylprednisolone did not improve impairments, however it did improve pain and other neurological symptoms in diabetic lumbosacral radiculoplexus neuropathy. The authors of this article include corticosteroids in their management of patients with diabetic lumbosacral radiculoplexus neuropathy, lumbosacral radiculoplexus neuropathy, and postsurgical inflammatory neuropathy causing lumbosacral plexopathy28. There is no standard on dose, however the authors of these report typically using a dose of 1 g of IV methylprednisolone weekly for 12 weeks.

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.



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 research1.


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Original Version of the Topic

Karen Barr, MD. Lumbosacral plexopathy and sciatic neuropathy: differential diagnosis and treatment. Publication Date: 9/20/18

Author Disclosure

Christian Custodio, MD
Nothing to Disclose

William Douglas, DO
Nothing to Disclose

Kristian von Rickenbach, MD
Nothing to Disclose