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A traumatic lumbosacral plexopathy is an injury to the lumbosacral plexus that results in pain to the low back and/or leg, weakness, paresthesia, and/or sphincter dysfunction.1 It is defined as involvement from at least two different root levels from at least two different peripheral nerves.2 Symptoms are dependent upon the involved portion of the plexus. It can be difficult to diagnose and manage.1,3


Traumatic lumbosacral plexopathies are less common than traumatic brachial plexus injuries due to its location within the pelvic brim.1-3 Because it is situated in a bony enclosure, significant forces are required to injure the plexus.2 Trauma accounts for only a small percentage of lumbosacral plexopathies.3 Most are the result of penetrating trauma (i.e. gunshot wounds or stabbing wounds) or high velocity injuries (i.e. motor vehicle accident, pedestrian vehicle accident, or fall from large height).2-3 Traumatic plexopathies are frequently associated with pelvic or hip joint injuries, such as fractures or dislocations.3 Other injuries can occur from sports, post-operatively, or during childbirth.1,2 Post-operative injury occurs due to a mechanical or stretch injury, especially after hip surgery.2 Injury during childbirth is thought to be due to compression of the plexus from the fetal head against the pelvic brim.2 Less commonly seen, plexopathy can occur from compression by a large retroperitoneal hematoma, abscess, or large aneurysm.3

Epidemiology including risk factors and primary prevention

Age of presentation and prevalence varies due to diverse etiologies of lumbosacral plexopathies.1 The median age for diagnosis of lumbosacral plexopathies for all causes is around 65 years of age.1 Lumbosacral plexopathies occur in roughly 0.7% of cases following a traumatic pelvic fracture, whereas incidence increases to 2% following a sacral fracture.1 Lumbosacral plexopathies due to childbirth occur in 1 in 2000-6400 deliveries.1 Patients who are on anticoagulation therapy or have history of bleeding disorders may be at risk of developing an iatrogenic hemorrhage that can result in plexopathy.3


The lumbosacral plexus is derived from the ventral rami of the L1-S4 nerve roots and is divided into the upper lumbar plexus and lower lumbosacral plexus.1-3 The upper portion ascends from the L1-L4 nerve roots with occasional involvement of the T12 nerve root; while the lower portion comes from the L4-S4 nerve roots.1-3 The lumbosacral plexus is found within the psoas major muscle and emerges laterally from the muscle.2

The upper portion of the plexus:1-3

  • iliohypogastric nerve (T12-L1)
  • ilioinguinal nerve (L1)
  • genitofemoral nerve (L1-L2)
  • lateral femoral cutaneous nerve (L2-L3)
  • femoral nerve (L2-L4)

The lower portion of the plexus:1-3

  • superior gluteal nerve (L4-S1)
  • inferior gluteal nerve (L5-S2)
  • sciatic nerve (L4-S3)
  • posterior femoral cutaneous nerve (S1-S3
  • pudendal nerve (S1-S4)

The lumbosacral plexus supplies both motor and sensory functions to the lower limb and pelvic girdle on the ipsilateral side.2 The upper portion supplies motor function to the lower and anterior abdominal muscles, hip flexion and adduction, and knee extension; whereas the lower portion supplies motor function for hip abduction and extension, knee flexion, all ankle movement, and to the urinary and anal sphincters.2 The upper portion supplies sensory perception to the groin; anterior, medial, and lateral thigh; and the medial part of the leg down to the ipsilateral ankle; whereas the lower portion provides sensory to the posterior thigh, buttocks, perineal region, and the lower extremity below the knee (excluding the medial part of the lower leg).2

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

Trauma can result in compression, stretching, or laceration of plexus components, perineural fibrosis, or avulsion of nerve roots from the spinal cord.4 The type and degree of nerve injury within the lumbosacral plexus depends on the mechanism and severity of injury.3 The degree of nerve injury can be classified into one of three stages: neuropraxia, axonotmesis, or neurotmesis.3 Neuropraxia occurs when a nerve is compressed where distortion of the myelin may be the only pathologic alteration.3 Nerve conduction studies may show focal slowing, conduction block or increased temporal dispersion across the site of compression.3 The axons are not damaged so recovery may occur swiftly if the compression is removed, resulting in a favorable prognosis.3 Most injuries to the plexus are more severe and injure the axons and other supporting structures, called axonotmesis or neurotmesis. Recovery is variable in these cases.

As previously stated, significant forces are required to cause a traumatic lumbosacral plexopathy and often is associated with pelvic fractures and other significant injuries due to its location within the retroperitoneal space.1 This can occur with high-velocity car accidents, gunshot wounds, and traumatic hip dislocations.5 Traumatic dislocation of the hip tends to involve the lower portion of the plexus, mainly the branches of the sciatic nerve.5

A traumatic lumbosacral plexopathy initially begins with acute to subacute onset and progression of pain in the thigh, leg, buttock, and/or back, which is unilateral but may spread to the contralateral limb.3 The pain has been described as an achy, sharp, or burning sensation, and may subside spontaneously.3 Weakness and atrophy usually follows pain and leads to debilitation.3 Paresis is common in the distribution of the common fibular nerve, followed by the gluteal, tibial, and obturator nerves.6 In major trauma, diagnosis of a lumbosacral plexopathy may be delayed due to other life risking injuries. When due to childbirth, a foot drop is seen acutely.6

Specific secondary or associated conditions and complications 

Since most lumbosacral plexopathies due to trauma occur from significant or violent injuries, there are often other associated injuries to local blood vessels, bony structures, and pelvic organs, such as urinary bladder dysfunction, intestinal perforation, or vascular injury.2,6 Complications from traumatic lumbosacral plexopathies includes progressive neurological deterioration, intractable pain, bedsores, recurrent infections, and/or joint contractures.1

Essentials of Assessment


A comprehensive history and physical examination should be obtained in patients with suspected traumatic lumbosacral plexopathy. The history should include the timing of onset of symptoms and course of progression, recent trauma, and general medical conditions.3 History of trauma or recent surgery or pregnancy may help narrow down the etiology.1 Patients will typically present with low back pain radiating down one leg.1 The pain may be positional, worsening when lying supine; and may be associated with numbness, paresthesia, or dysesthesias of the lower limbs.1 In cases of trauma, the pain occurs acutely and the symptoms are usually unilateral.1 Muscle weakness and atrophy may occur.1 The distribution of motor and sensory findings can help localize the injury to the lumbar or sacral plexus, or both.3 Bowel and bladder disturbances are less common but can occur.1

Physical examination

Patients will present with asymmetric lower limb weakness with reduced or absent deep tendon reflexes.1 The patellar tendon reflex will be affected in lumbar plexopathies, and the Achilles tendon reflex and hamstrings reflex may be affected in sacral plexopathies. Strength should be assessed along with muscle tone or spasticity. A comparison from side to side should always be done. Motor and sensory deficits are determined by the portion of the plexus is injured. For example, hip flexion, knee extension or adduction weakness along with sensory changes to the medial thigh, anterior thigh, and medial leg suggests a possible injury to the lumbar plexus. More than half the patients with a lumbosacral plexopathy will have a positive straight leg raise.1 Provocative hip maneuvers should also be performed to assess hip integrity.7 Point tenderness over the spine as well as bruising may be seen in traumatic presentations. Saddle anesthesia and bowel and bladder dysfunction are rare but may be present and can be difficult to distinguish between cauda equina syndrome and conus medullaris syndromes.1 Rectal tone should also be assessed.

Clinical functional assessment: mobility, self-care, cognition/behavior/affective state

It’s important to assess for specific deficits that affect mobility, transfers, gait, activities of daily living, occupation and recreational activities, as well as the need for adaptive equipment or assistive devices.

Laboratory studies

There are no required laboratory analyses in the work-up of traumatic lumbosacral plexopathy, however, basic laboratory assessments may be helpful in ruling out alternative causes of weakness, pain, paresthesia, or bowel and bladder dysfunction. Recommended blood tests may include a complete blood count, erythrocyte sedimentation rate, C-reactive protein, coagulation studies, autoantibodies testing, and hemoglobin A1c.1,2


Magnetic resonance imaging (MRI) of the lumbosacral spine and plexus can be useful in the assessment of a traumatic injury.1-4 MRI with gadolinium contrast is the best test for the evaluation of the plexus as it can show areas of breakdown of the blood-nerve barrier, as can be seen in posttraumatic neuromas.1,8 When MRI is contraindicated due to other comorbidities, a computed tomography scan can be used.1

Supplemental assessment tools

Electrodiagnostic testing is required for accurate location of a lumbosacral plexopathy and is seen as an extension of the physical exam. It can help differentiate between a lumbosacral plexopathy from other diagnoses such as a lumbar radiculopathy. Electrodiagnostic testing can help to define the pathophysiology and the severity of the nerve injury.3 A nerve conduction study will show decreased amplitudes of both compound action potentials and sensory nerve action potentials asymmetrically.2,3 Conduction velocities are normal or only mildly reduced.2,3 F wave prolongation may be present on the affected side.2 Needle electromyography reveals fibrillation potentials and neurogenic motor unit potentials in muscles involved in multiple lumbosacral levels.2,3 A plexopathy is defined as involvement from at least two different root levels from at least two different peripheral nerves.2 For a pure lumbosacral plexopathy, fibrillation potentials in the lumbosacral paraspinal muscles will be absent; whereas they will be present in a lumbosacral radiculoplexus neuropathy.2,3 Positive sharp waves and fibrillations will be present after 3 weeks of onset of symptoms. In chronic injuries, signs of terminal reorganization can be seen with increased polyphasicity and neuropathic recruitment pattern. If the nerve root has been avulsed, no motor recruitment will be seen.9 A nerve biopsy may be useful in diagnosing other etiologies of lumbosacral plexopathies but is not usually done in traumatic lumbosacral plexopathies.

Early prediction of outcomes

Prognosis depends upon the underlying etiology, response to treatment, and timing of therapeutic intervention.1 Traumatic lumbosacral plexopathies usually have a poor prognosis for recovery as it typically is a result of severe trauma causing nerve disruption.2 However, about 70% of patients recovered spontaneously within 18 months in a case series of 72 patients with traumatic lumbosacral plexopathies.1 Presence of root avulsion is generally indicative of a poor outcome. Needle electromyography can be useful in determining prognosis as recruitment of motor units during muscle activation is a good prognostic indicator. Prognosis is good for patients who develop a lumbosacral plexopathy secondary to pregnancy with most patients having complete resolution of symptoms two to six months following delivery.1


School or workplace modifications and assistance may be needed for patients with lumbosacral plexopathies. Avoidance of repetitive activities, extreme range of motions, and excessive activity that causes pain or weakness may be beneficial.1

Social role and social support system

Lumbosacral plexopathies can be debilitating and lead to lifelong challenges for the patient and their families.1 Quality of life may be greatly affected due to pain and functional impairment.1

Professional issues

Return to work, play, or school will require careful evaluation of time since injury, comorbid conditions, nature and extent of recovery, current deficits and functional status, and school or work environment.

Rehabilitation Management and Treatments

Available or current treatment guidelines

Treatment for lumbosacral plexopathies depends upon the underlying etiology.1,2 Pain management and physical therapy are the mainstay of treatment for traumatic lumbosacral plexopathies. Pain is the most common symptom reported in traumatic lumbosacral plexopathies. Management can include ice and/or heat modalities, stretching, and medications. Analgesics include non-steroidal anti-inflammatory drugs (NSAIDs), muscle relaxants, pregabalin, gabapentin, duloxetine, amitriptyline, venlafaxine, and opiods.1 Physical and occupational therapy is important to help regain function and work on mobility, and activities of daily living.1 Physical therapy can address muscular imbalance, work on strengthening partially involved muscles, maintain flexibility, and improve balance and gait. Orthoses such as ankle-foot orthoses may be used to assist with foot drop. Equipment such as walker, crutches, or wheelchair may be needed. Surgical nerve repair and nerve grafting can be utilized to help improve muscle function in lumbosacral plexopathies that occurred due to pelvic fractures.1 In severe cases, dorsal rhizotomy has shown to reduce pain, however, this treatment option is primarily used in terminal patients.1

Coordination of care

Managing traumatic lumbosacral plexopathies requires a multi-disciplinary team of healthcare professionals that may include a physiatrist, neurosurgeon or orthopedic surgeon, pain medicine specialist, psychologist, electrodiagnostician, neurologist, physical therapist, and an occupational therapist.1-2 Resources, including vocational rehabilitation, ergonomics, and driving training, can be included as necessary.

Patient & family education

Counseling regarding the nature of the disease, treatment options, prognosis for recovery, and prevention of secondary complications is a critical component of the plan of care. Symptoms may progress over time requiring the patient to have assistance with mobility, ambulation, and activities of daily living.1


  1. Dyck, P., and Thaisetthawatkul, P. Lumbosacral plexopathy. Continuum: Lifelong Learning in Neurology5, Peripheral Nervous System Disorders. 2014; 20(5): 1343-1358.
  2. Dydyk, A., Hameed, S. Lumbosacral plexopathy. [Updated 2021 July 12]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK556030/
  3. Rubin, D. Brachial and lumbosacral plexopathies: a review. Clinical Neurophysiology Practice. 2020; 5:173-193.
  4. Bowen, B., Seidenwurm, D. Plexopathy. Am J Neuroradiol. 2008; 29: 400-402.
  5. Cornwall, R., and Radomisli, T. Nerve injury in traumatic dislocation of the hip. Clinical Orthopaedics and Related Research. 2000; 337: 84-91.
  6. Katirji, B., Wilbourn, A., Scarberry, S., and Preston, D. Intrapartum maternal lumbosacral plexopathy. Muscle Nerve. 2002; 26(3): 340-347.
  7. Wilson, J., Furukawa, M. Evaluation of the patient with hip pain. Am Fam Physician. 2014; 89(1): 27-34.
  8. Soldatos, T., Andreisek, G., Thawait, G., Guggenberger, R., Williams, E., Carrino, J., Chhabra, A. High resolution 3-T MR neurography of the lumbosacral plexus. Radiographics. 2013; 33(4): 967-987.
  9. Van Alfen, N., and Malessy, M. Diagnosis of brachial and lumbosacral plexus lesions. Handbook of Clinical Neurology. 2013; 115: 293-310.

Author Disclosure

Clarice Sinn, DO
Nothing to Disclose