Radiation-Induced Lumbosacral Plexopathy 

Updated: May 24, 2019
Author: Rajesh R Yadav, MD; Chief Editor: Dean H Hommer, MD 

Overview

Practice Essentials

Lumbosacral plexopathy can result in loss of strength and sensation in the regions innervated by the femoral and obturator nerves (lumbar plexopathy) and those reached by the gluteal, peroneal, and tibial nerves (sacral plexopathy).[1] The causes of lumbosacral plexopathy include radiation, which can damage the lumbosacral plexus when directed toward management of abdominal and pelvic malignancies. The diagnosis of radiation plexopathy can be supported by diagnostic studies, such as computed tomography (CT) scanning and magnetic resonance imaging (MRI) of the pelvis. Treatment is symptomatic.

Anatomically, the lumbosacral plexus consists of lumbar (L1-L4) and sacral (L5-S5) portions, which are connected by the lumbosacral trunk (L4-L5). The L1-L4 nerve roots transverse through the psoas muscle and then coalesce into the lumbar plexus, which then divides into anterior and posterior divisions. The first three nerves (iliohypogastric, ilioinguinal, and femoral) of the seven major branches of lumbar plexus provide motor and sensory innervation to the abdominal wall. The next three nerves (lateral femoral cutaneous, femoral, and obturator) innervate the anteromedial thigh. The femoral nerve terminates in the saphenous nerve providing sensation along the medial aspect of the leg.

The sacral plexus also divides into anterior and posterior divisions, which further divide into various peripheral nerves, providing sensory motor innervation to posterior hip girdle, thigh, and anterior and posterior leg. The 5 main nerves are the superior gluteal, inferior gluteal, posterior femoral cutaneous, sciatic, and pudendal. The sciatic nerve divides into the common peroneal and tibial nerves in the thigh.

Although radiation-induced lumbosacral plexopathy is rare, its occurrence is believed to be increasing due to improvements in long-term cancer survival.[2]

Workup

The diagnosis of radiation plexopathy can be supported by diagnostic studies, such as computed tomography (CT) scanning and magnetic resonance imaging (MRI) of the pelvis. MRI is more sensitive than is CT scanning in detecting tumor recurrence.[3, 4] In addition, positron emission tomography (PET) scanning with 2-[fluorine-18]-fluoro-2-deoxy-D-glucose (FDG) may be helpful in diagnosing recurrent tumor. Electromyography (EMG) reveals myokymic discharges in most patients (57%) with radiation-induced lumbosacral plexopathy.

Management

Treatment of radiation plexopathy is symptomatic. For issues of pain, consider the use of nonopiate pharmacologic medications, such as tricyclic antidepressants or antiepileptic agents (eg, gabapentin, carbamazepine). The use of steroids and opiates, including methadone, can also be assessed.

Strengthening of lower extremity muscles, use of assistive devices for ambulation (eg, cane, walker), and gait training should be prescribed for patients with weakness and proprioceptive feedback loss. Use of orthotics also may be beneficial in certain individuals with lumbosacral plexopathy.

Related Medscape Drugs & Diseases topic:

Radiation-Induced Brachial Plexopathy

Pathophysiology

The effects of radiation are correlated with the dose, technique, and concomitant use of chemotherapy.[5] Risk particularly increases with intracavitary radiation.[6] The mechanism may be related to a combination of localized ischemia and subsequent soft-tissue fibrosis due to microvascular insufficiency. With doses above 1000 cGy, pathologic changes can be seen in Schwann cells, endoneurial fibroblasts, vascular cells, and perineural cells. Injury to anterior and posterior nerve roots in rodents has been shown with doses of 3500 Gy. However, combined modality therapy may alter predicted tolerability and potential for late effects.

Radiation-induced lumbosacral plexopathy is particularly noted with uterine, cervical, ovarian, rectal, and testicular cancers, as well as with lymphomas.[7, 8]

Epidemiology

Frequency

United States

Radiation-induced lumbosacral plexopathy is rare (0.3-1.3% of patients treated with radiation). It was noted in 1.3% of patients after abdominal irradiation and in 0.32% of patients after pelvic irradiation.

International

The international incidence of radiation-induced lumbosacral plexopathy is unknown.

Mortality/Morbidity

Generally, the symptoms of radiation-induced lumbosacral plexopathy progress gradually and with variable rapidity. Clinical manifestations of the condition have appeared 3 months to 22 years after the completion of radiation therapy.[9] Jaeckle and colleagues found that 20% of patients developed moderate or even severe weakness over 6 months.[10] Others were found to have mild weakness at 4-5 years following the onset of neurologic symptoms.

Race

No race predilection for radiation-induced lumbosacral plexopathy has been reported.

Sex

The male-to-female ratio is 1:1.2.

Age

Age at the time of presentation ranges from 34-68 years, with a median age of 47.5 years.

 

Presentation

History

With prior radiation treatment and initial symptoms, a recurrent tumor may need to be distinguished from radiation plexopathy. The median symptom-free interval for radiation-induced lumbosacral plexopathy, from treatment to the initial neurologic symptom, is 5 years, with a range of 1-31 years.[9]

  • Patients with radiation-induced lumbosacral plexopathy most commonly present with painless weakness in 1 or both legs. Pain is present initially in only 10% of patients, although ultimately it is noted in as many as 50% of patients. The incidence of initial pain is lower than that of brachial plexopathy. This pain is described in varying terms, such as aching, burning, pulling, cramping, and lancinating; however, pain rarely is a major problem.

  • Weakness is asymmetrical. At the height of illness, the ratio of bilateral to unilateral illness is 5:1. Acute lower extremity paralysis has been noted in a patient with cervical cancer 10 weeks after completion of radiation treatment.[11]

  • Sensory loss occurs in 50-75% of patients and is more severe with greater motor impairment, which can add significantly to disability.

  • Bladder or bowel incontinence may occur.[12]

Physical

See the list below:

  • In radiation-induced lumbosacral plexopathy, motor deficits in the lower extremities commonly are bilateral (80%) and asymmetrical. Diffuse limb weakness with distal predominance in L5-S1 distribution is relatively common (55% of patients). Exclusive proximal paresis in the distribution of L2-L4 is less common (10% of patients), as is femoral neuropathy (5% of patients). Moderate weakness is present in 50% of patients, with equal distribution of mild and severe weakness.

  • Deep tendon reflexes (DTRs) almost always are abnormal at the knees and/or ankles and usually are present bilaterally.

  • Sensory impairments are present in most patients (75%) and more often are bilateral. No specific sensory modality is favored. The distal lower extremities are affected more commonly than are the proximal lower extremities. Impaired deep sensation occurs with severe, superficial sensory loss.

  • Skin changes may be present in areas of radiation portals.

Causes

Radiation dosage, treatment technique, and concomitant use of chemotherapy are associated with development of radiation-induced lumbosacral plexopathy.

 

DDx

Diagnostic Considerations

Meningeal carcinomatosis, also known as leptomeningeal disease, may cause subacute motor or sensory deficits to be present with low back or leg pain. In addition, patients with meningeal carcinomatosis often also have mental status changes, headaches, cranial nerve palsies, and/or nuchal rigidity. In cancer patients with thrombocytopenia, retroperitoneal bleeding can cause plexopathy, with a rapid onset of pain and neurologic signs that usually are developed fully in 24 hours. Other associated findings include flank, thigh, or low back ecchymoses. Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), which is felt to be immune mediated, can cause severe, symmetrical, peripheral neurologic deficits. Nerve root thickening may be noted in the lumbosacral plexus, a finding that may be associated with moderate gadolinium enhancement.[13, 14]

Causes of lumbosacral plexopathy not related to cancer include aortic aneurysms, diabetes mellitus (DM), obstetric procedures, trauma, and intragluteal injections.[15, 16] With aortic aneurysms, acute pain commonly is seen, and the resultant weakness typically worsens over 1-2 weeks and then stabilizes. A pulsatile rectal or abdominal mass also can be seen in many patients. Acute thigh pain with acute or insidious onset of weakness can result from diabetic amyotrophy and can be difficult to differentiate from the aortic aneurysms. Weakness with diabetic amyotrophy usually is noted proximally, with relative sparing of distal lower extremity muscles.

Differential Diagnoses

 

Workup

Imaging Studies

Routine spine and pelvis radiographs and myelograms are unremarkable in lumbosacral plexopathy.

The diagnosis of radiation plexopathy can be supported by diagnostic studies, such as computed tomography (CT) scanning and magnetic resonance imaging (MRI) of the pelvis. MRI is more sensitive than is CT scanning in detecting tumor recurrence.[3, 4] Enhancement of nerve roots and T2-weighted hyperintensity usually suggests tumor. Unfortunately, differentiation from tumor recurrence remains difficult. Generally, radiation plexopathy does not produce nerve enhancement. Positron emission tomography (PET) scanning with 2-[fluorine-18]-fluoro-2-deoxy-D-glucose (FDG) may be helpful in diagnosing recurrent tumor.

Although PET/CT scanning can aid in differentiating tumor recurrence from radiation plexitis in oncology patients, it offers only limited resolution of the brachial or lumbosacral plexus.[17]

Other Tests

Electromyography (EMG) reveals myokymic discharges in most patients (57%) with radiation-induced lumbosacral plexopathy. Such changes occur over years; however, the absence of myokymia does not exclude radiation injury. EMG in clinically weak muscles also may reveal fibrillation potentials (ie, chronic, neurogenic motor unit changes with decreased recruitment). Paraspinal involvement occurs in 50% of cases. Compound muscle action potential (CMAP) of motor nerves may be low.[18, 19]

 

Treatment

Rehabilitation Program

Physical Therapy

Strengthening of lower extremity muscles, use of assistive devices for ambulation (eg, cane, walker), and gait training should be prescribed for patients with weakness and proprioceptive feedback loss. Use of orthotics also may be beneficial in certain individuals with lumbosacral plexopathy.

Occupational Therapy

The patient's ability to perform activities of daily living (ADL) should be assessed, and appropriate assistive device(s) should be prescribed as needed. In particular, safety with standing transfers may be impaired with more distal involvement. With more proximal involvement, sit-to-stand transfers also may be affected. Strengthening exercises, along with sensory reeducation techniques, may be employed.

Medical Issues/Complications

Treatment of radiation plexopathy is symptomatic. For issues of pain, consider the use of nonopiate pharmacologic medications, such as tricyclic antidepressants or antiepileptic agents (eg, gabapentin, carbamazepine). The use of steroids and opiates, including methadone, can also be assessed.

Other Treatment

Nonpharmacologic measures, such as transcutaneous electrical nerve stimulation (TENS), may be used for pain.

While not studied in patients with radiation-induced lumbosacral plexopathy, hyperbaric oxygen therapy has not led to the slowing or reversal of radiation-induced brachial plexopathy symptoms, although improvement was noted in warm sensory threshold.[20]

In a small population, partial recovery of motor function was noted in few patients treated with anticoagulant therapy for a period of 3-6 months.

A study by Tunio et al indicated that radiation-induced lumbosacral plexopathy can be reduced by delineating the lumbosacral plexus through imaging and administering intensity-modulated radiotherapy (IMRT) so that radiation dosages of 40, 50, 55, and 60 Gy are absorbed by less than 55%, 30%, 5%, and 0.5% of the lumbosacral plexus volume, respectively. The study involved 50 patients with cervical cancer who underwent IMRT and high-dose-rate brachytherapy. Four patients had developed grade 2/3 radiation-induced lumbosacral plexopathy by 60-month follow-up.[21]

A randomized, placebo-controlled, double-blind trial by Delanian et al indicated that although studies have reported that pentoxifylline/vitamin E (PENTO) treatment can lead to a significant decrease in radiation-induced fibrosis and that, in combination with clodronate (PENTOCLO), it permits progressive mandible osteoradionecrosis to heal and reduces some neurologic symptoms, PENTOCLO therapy has no significant benefit in radiation-induced plexopathy. However, the authors stated that more sensitive means are needed to detect whether investigational drugs can aid this condition.[22]

 

Medication

Medication Summary

Tricyclic antidepressants (TCAs), such as amitriptyline, may be used in lower doses. The use of antiepileptics may be helpful.

Tricyclic antidepressants

Class Summary

TCAs have central and peripheral anticholinergic effects, as well as sedative effects, and block the active reuptake of norepinephrine and serotonin. The multifactorial mechanism of analgesia may include improved sleep, an altered perception of pain, and an increase in pain threshold. The efficacy of these drugs can be potentiated with the concomitant use of opiates and nonsteroidal anti-inflammatory drugs (NSAIDs). Rarely should these drugs be used in the treatment of acute pain, since a few weeks may be required for them to become effective.

Amitriptyline (Elavil)

Analgesic for certain chronic and neuropathic pain. Amitriptyline has the most anticholinergic side effects of all drugs in this category.

Antiepileptic drugs

Class Summary

These drugs stabilize neuronal membranes and reduce neuronal hyperexcitability. The analgesic effect may be due to such stabilization and control of hyperexcitability, because aberrant electrical activity has been recorded with neuropathic pain.

Gabapentin (Neurontin)

Has anticonvulsant properties and antineuralgic effects; however, the exact mechanism of action is unknown. Gabapentin is structurally related to GABA but does not interact with GABA receptors.

Carbamazepine (Tegretol)

Used typically for generalized tonic-clonic seizures and partial seizures, as well as for trigeminal neuralgia. Plasma levels are between 4-12 mcg/mL for analgesic and antiseizure response.

Valproic acid (Depakene)

Generally indicated for absence seizures and generalized tonic-clonic seizures. Some relief may be noted with neuropathic pain, especially the lancinating type.

Corticosteroids

Class Summary

Glucocorticoids have anti-inflammatory, hormonal, and metabolic effects. Inflammation is suppressed with the blockage of phospholipase A2, which inhibits the formation of arachidonic acid and, thus, the prostaglandins. The analgesic effect may be due to the anti-inflammatory activity, with a decrease in edema.

Dexamethasone (Decadron, AK-Dex)

For various allergic and inflammatory diseases. Dexamethasone decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and by reducing capillary permeability.

Analgesics

Class Summary

These drugs are generally used for short-term, acute pain that is moderate to severe in nature, as well as for chronic pain (eg, cancer). They provide analgesia without antipyretic or anti-inflammatory action. The mechanism of action is the inhibition of nociceptive impulses at the dorsal horn of the spinal cord and at supraspinal sites due to interaction with opiate receptors. Structural derivatives of GABA are also used in the management of neuropathic pain.

Pregabalin (Lyrica)

Structural derivative of GABA. Pregabalin's mechanism of action is unknown. This agent binds with high affinity to the alpha2 -delta site (a calcium channel subunit). In vitro, pregabalin reduces the calcium-dependent release of several neurotransmitters, possibly by modulating calcium channel function. It is FDA approved for neuropathic pain associated with diabetic peripheral neuropathy or postherpetic neuralgia and as an adjunctive therapy in partial-onset seizures.

Methadone (Dolophine)

Used in the management of severe pain. Methadone inhibits ascending pain pathways, diminishing the perception of and response to pain.

Morphine sulfate (Duramorph, MS Contin, Astramorph)

Available in immediate (3-4 h duration) and extended release preparation (12 h). Switch over to long-acting preparations (MS Contin) once pain is controlled with short-acting preparation (MS IR). Morphine can produce drug dependence and has the potential for being abused. Tolerance may develop with repeated exposure. Abrupt cessation or sudden reduction in dose with prolonged use may result in withdrawal symptoms. Physical dependence is not of paramount importance in terminally ill patients.

 

Follow-up

Further Outpatient Care

See the list below:

  • After radiation-induced lumbosacral plexopathy has been diagnosed, follow up with patients on functional issues. Address issues of pain in a timely fashion.

Further Inpatient Care

See the list below:

  • Inpatient care for radiation-induced lumbosacral plexopathy is not required.

Complications

See the list below:

  • Radiation-induced lumbosacral plexopathy may result in pain and decreased functional status.

Prognosis

See the list below:

  • Gradual, rather than stepwise, progression of radiation-induced lumbosacral plexopathy is the rule. Eventually, patients may have significant or severe disability. Spontaneous recovery is less common.[23]

Patient Education

See the list below:

  • Educate patients about the effects of radiation and the reason for altered function, pain, and sensory deficits.