Lumbosacral plexopathy and sciatic neuropathy: differential diagnosis and treatment

Author(s): Karen Barr, MD

Originally published:09/20/2014

Last updated:09/20/2014

1. DISEASE/DISORDER:

Definition

Lumbosacral plexopathy: an injury to the nerves in the lumbar or sacral plexus. A sciatic neuropathy is any injury to the sciatic nerve.

Etiology

There are multiple causes including the following:

  1. Trauma
  2. Childbirth
  3. Stretch injuries (eg, hip surgery)
  4. Compression of the plexus from a retroperitoneal hematoma or abscess
  5. Compression from metastatic cancer
  6. Radiation-induced nerve injury
  7. Diabetic lumbosacral radiculoplexus neuropathy
  8. Autoimmune
  9. Paraneoplastic
  10. Infectious
  11. Idiopathic

Epidemiology including risk factors and primary prevention

The prevalence of lumbosacral plexopathies is unknown and is much less common than brachial plexopathies.

Risk factors vary based on etiology.

Situations of heightened clinical suspicion for lumbosacral plexopathies include the following:

  1. High force traumas, particularly if pelvic fractures are seen.
  2. Women with prolonged labor, usually present in the first few days after delivery.
  3. Retroperitoneal bleeding (eg, anticoagulated patient), or those who have undergone transfemoral percutaneous procedures (eg, cardiac catheterization).
  4. Cancers that could invade the lumbosacral plexus, and those who have undergone radiation therapy to cancers in this area. (Most commonly, radiation plexopathy occurs 1 to 5 years after the completion of treatment but can occur anywhere between weeks and 30 or more years later.1)
  5. Diabetes, including recent very high glucose, and those with strict glucose control in a newly diagnosed diabetic.
  6. Autoimmune diseases.

Patho-anatomy/physiology

The lumbosacral plexus is made up of the lumbar plexus, which is formed from the T12, L1 through L4 nerve roots, and the sacral plexus, which is formed from the L4 to S4 nerve roots. Unlike the brachial plexus, the lumbosacral plexus does not have distinct structural components (eg, trunks, cords); instead, it is made up of a variety of branches and divisions.

The lumbar plexus lies within the psoas muscle. It is made up of the following:

  1. Direct muscular branches from the ventral primary rami of L2 and L3 (and sometimes L1 and L4), which directly innervate the psoas muscle.
  2. Several branches from T12, L1, and L2, including the iliohypogastric, ilioinguinal, and genitofemoral nerves, which provide motor and sensory function to the lower abdomen, inguinal area, and genitals.
  3. Several branches from L2 to L4, which provide motor and sensory function of the upper thigh, including lateral femoral cutaneous, obturator, and femoral nerves. Branches of the femoral nerve supply sensory branches to the lower leg.

The sacral plexus lies more inferiorly and posteriorly within the pelvic outlet. It is made up of ventral primary spinal nerve branches from L4 to S4, which form several branches including the following:

  1. Proximal branches to the pelvic musculature and buttock region, including nerves to the quadratus femoris, gemelli, obturator internus, piriformis, and superior and inferior gluteal nerves.
  2. Posterior femoral cutaneous nerve, which has multiple sensory branches to the genitals and thigh.
  3. Sciatic nerve, which is the largest nerve in the body and supplies all of the muscles of the posterior thigh, leg, and foot, all articular branches to the joints of the lower limb, and cutaneous supply to the calf, lateral leg, and foot.2

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

The clinical course depends on the etiology.

In trauma, the prognosis is generally good for at least partial recovery of function unless root avulsion has occurred. Without root avulsion, at least partial recovery is the norm, and many patients will have a full or nearly full recovery. Recovery can be prolonged, but it generally peaks about 18 months after injury.3

For compressive causes of lumbosacral plexopathy (eg, retroperitoneal hematomas), outcomes can be excellent; however, some patients have lingering symptoms.4

For diabetic lumbosacral radiculoplexus neuropathy, significant improvement with time is expected; however, some deficits may remain. They are generally not progressive or recurrent.2

For radiation-induced plexopathies, unfortunately, a slow but progressive loss of function is expected.1

Specific secondary or associated conditions and complications

Decreased function and an abnormal gait related to muscle weakness, including foot drop, and complication of insensate skin. Pain can be predominate and severe.

2. ESSENTIALS OF ASSESSMENT

History

Typical history is unilateral weakness, sensory loss, and pain.

Determining the onset and progression of symptoms are helpful if the diagnosis is unclear. Often, with trauma, the plexopathy is overlooked in the acute phase because lower extremity pain and weakness is blamed on associated traumas (eg, bone fractures).

Many causes of plexopathy have a subacute onset with progression over days to weeks. This can help distinguish them from competing neurologic diagnoses (eg, most diabetic length-dependent peripheral polyneuropathies), which generally have a more chronic time course.

Plexopathies are most often unilateral; however, bilateral disease is possible (eg, in the case of massive traumas, autoimmune diseases, or radiation-induced plexopathy).

In cases cause by cancer or autoimmune disease, systemic symptoms are often present (eg, weight loss, fever, other signs of the accompanying disease).

Physical examination

Observation of the limb may reveal decreased muscle bulk in the distribution of the affected nerves. Muscle tone is decreased in the affected muscles, and reflexes are usually absent or greatly diminished at the patellar if the lumbar plexus is affected and at the hamstrings and Achilles if the sacral plexus is involved. The areas of the plexus involved can be discerned by the pattern of weakness found in manual muscle testing of the lower extremity in combination with areas of sensory loss. These will follow a peripheral nerve pattern rather than a myotomal or dermatomal pattern. It may be difficult to differentiate multilevel radiculopathy from plexopathy based on physical exam. If bilateral plexopathy has occurred, it may be difficult to differentiate from cauda equina syndrome; however, bowel and bladder function should be normative with plexopathy.

Functional assessment

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

Laboratory studies

Blood glucose and glycosylated hemoglobin if diabetic nerve disease is suspected, sedimentation rate and white blood count if abscess is suspected, prothrombin time and platelets if hematoma is suspected, and so forth.

Imaging

Magnetic resonance imaging (MRI) and computed tomography can identify space occupying lesions (eg, cancer, hematoma, abscess) that may be compressing the plexus. MRI neurogram can be done if distribution of nerve involvement is unclear after physical exam and electrodiagnostic testing. It can also be used to evaluate if nerve root avulsion has occurred.

Supplemental assessment tools

Electrodiagnostic testing is used to localize the nerve injury and characterize the process.

Study may include the following:

  1. Fibular and tibial motor nerve conduction studies (NCS) with F waves. If the sacral plexus is involved, the expected finding in the motor study would be absent or of low amplitude with a normative distal latency unless the amplitudes are very low, in which case the fastest fibers may be no longer functioning and the distal latencies and conduction velocity in the leg may be prolonged. F waves may be absent or show poor penetrance and be slowed.
  2. Sural, saphenous, and lateral femoral cutaneous sensory NCS would be expected to be absent or of low amplitude with normative distal latency unless the amplitudes are very low, in which case there may be prolonged distal latencies. The exception to these findings would be if root avulsion is present and sensory studies are normative (though the area is insensate) because the dorsal root ganglion cell body remains intact.
  3. Often, side-by-side comparisons are helpful, and upper extremity testing may be needed if deficits are seen bilaterally to rule out a length-dependent peripheral polyneuropathy.
  4. Needle electromyography will give the most significant and useful information. Muscle sampling needs to be widespread, testing multiple muscles innervated from L2 to S1 with multiple peripheral nerves. Lumbar paraspinals should also be tested to search for radiculopathy. Sometimes testing needs to be bilateral to exclude competing diagnoses. If it has been at least 3 weeks since the onset of symptoms, it would be expected that positive sharp waves and fibrillations would be seen in the muscles innervated by the affected nerves. If the injury is more chronic, there may be evidence of terminal reorganization as signified by increased polyphasicity, duration, and amplitude of motor units along with a neuropathic recruitment pattern. If the plexus is severely damaged or in the case of root avulsion, no motor recruitment will be seen.2

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 generally has a very poor prognosis because they are not usually resectable, usually continue to grow, and are usually resistant to chemotherapy and radiation therapy.

Radiation plexopathy also has a poor prognosis with expected progression of symptoms with time.1

Traumatic plexopathies generally have a better prognosis with some improvement with time; however, some long-term deficits may remain. In 1 case series involving 72 patients with traumatic lumbosacral plexopathies, about 70% of cases recovered spontaneously, most within 18 months.3

Various case reports of compressive plexopathies from hematomas also generally report good outcomes, often to the point of near or complete resolution of symptoms.4

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.

3. REHABILITATION MANAGEMENT AND TREATMENTS

Available or current treatment guidelines

There is very little literature to guide the rehabilitation of patients with lumbosacral plexus injury; therefore, we must rely on using core rehabilitation principles as they relate to lower motor neuron nerve disease.

  1. Pain management, including medications, modalities, and in some cases spinal cord stimulators or intrathecal therapies.
  2. Physical therapy to strengthen partially affected muscles, address muscular imbalances, maintain flexibility, and improve balance and gait.
  3. 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 quadricep weakness. AFOs are generally essential in sacral plexopathies because of the predominance of foot drop.
  4. Surgery in selected cases of severe nerve injury. Surgery is the prefered treatment with root avulsions and sharp lacerations, and surgical consultation is indicated as soon as this diagnosis is made.3

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.

4. CUTTING EDGE/EMERGING AND UNIQUE CONCEPTS AND PRACTICE

5. GAPS IN THE EVIDENCE-BASED KNOWLEDGE

REFERENCES

1. Jaeckle KA. Neurological manifestations of neoplastic and radiation-induced plexopathies.Semin Neurol.2004;24:385-393.

2. Laughlin RS, Dyck JB. Electrodiagnostic testing in lumbosacral plexopathies.Phys Med Rehabil Clin N Am. 2013;24:93-105.

3. Garozzo D, Zollino G, Ferraresi S. In lumbosacral plexus injuries can we identify indicators that predict spontaneous recovery or the need for surgical treatment? Results from a clinical study of 72 patients.J Brachial Plex Peripher Nerve Inj.2014;9:1.

4. Kent KC, Moscucci M, Gallagher SG, DiMattia ST, Skillman JJ. Neuropathy after cardiac catheterization: incidence, clinical patterns, and long term outcome. J Vasc Surg.1994;19:1008-1013.

Author Disclosure

Karen Barr, MD
Nothing to Disclose

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