eMedicine Specialties > Physical Medicine and Rehabilitation > Plexopathy
Radiation-Induced Lumbosacral Plexopathy
Updated: Oct 17, 2008
Introduction
Background
Lumbosacral plexopathy can result when radiation, used in the treatment of various neoplasms, is directed toward management of abdominal and pelvic malignancies.
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 3 nerves (iliohypogastric, ilioinguinal, and femoral) of the 7 major branches of lumbar plexus provide motor and sensory innervation to the abdominal wall. The next 3 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.
Related eMedicine topics:
Radiation-Induced Brachial Plexopathy
Pathophysiology
The effects of radiation are correlated with the dose, technique, and concomitant use of chemotherapy. Risk particularly increases with intracavitary radiation.1 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, and testicular cancers, as well as with lymphomas.
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.2 Jaeckle and colleagues found that 20% of patients developed moderate or even severe weakness over 6 months.3 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.
Clinical
History
With prior radiation treatment and initial symptoms, a recurrent tumor may need to be distinguished from postradiation 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.2
- 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.4
- 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.5
Physical
- 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.
Differential Diagnoses
Chronic Inflammatory Demyelinating
Polyradiculoneuropathy
Diabetic Lumbosacral Plexopathy
Lumbar Degenerative Disk Disease
Mononeuritis Multiplex
Neoplastic Lumbosacral Plexopathy
Other Problems to Be Considered
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.6
Causes of lumbosacral plexopathy not related to cancer include aortic aneurysms, diabetes mellitus (DM), obstetric procedures, trauma, and intragluteal injections.7,8 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.
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.9,10 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.
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.11,12
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 postradiation 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 considered.
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.13
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.
Medication
Tricyclic antidepressants (TCAs), such as amitriptyline, may be used in lower doses. The use of antiepileptics may be helpful.
Tricyclic antidepressants
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.
Dosing
Adult
10-100 mg PO qhs
Pediatric
Not established
Interactions
Phenobarbital may decrease effects; coadministration with CYP2D6 enzyme system inhibitors (eg, cimetidine, quinidine) may increase levels; inhibits hypotensive effects of guanethidine; may interact with thyroid medications, alcohol, CNS depressants, barbiturates, and disulfiram
Contraindications
Documented hypersensitivity; use of MAOIs in past 14 d; history of seizures, cardiac arrhythmias, glaucoma, and urinary retention
Precautions
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Caution in cardiac conduction disturbances and history of hyperthyroidism, and renal or hepatic impairment; avoid use in elderly patients
Antiepileptic drugs
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.
Dosing
Adult
300-3600 mg/d PO divided tid/qid
Pediatric
Not established
Interactions
Antacids may significantly reduce bioavailability of gabapentin (administer at least 2 h following antacids); may significantly increase norethindrone levels
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in severe renal disease
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.
Dosing
Adult
100-200 mg PO bid initial dose; titrate up by 100-200 mg q3-7d; usual dosage for pain control is 400-800 mg/d; increase to tid/qid with larger dose; not to exceed 1200 mg; in rare instances, up to 1600 mg/d
Pediatric
Not established
Interactions
Serum levels may increase significantly within 30 days of danazol coadministration (avoid whenever possible); do not coadminister with MAOIs; cimetidine may increase toxicity, especially if taken in first 4 wk of therapy; carbamazepine may decrease primidone and phenobarbital levels (their coadministration may increase carbamazepine levels)
Contraindications
Documented hypersensitivity; history of bone marrow depression; administration of MAOIs within last 14 d
Precautions
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Serious reactions include leukopenia and agranulocytosis; risk is 5-8 times higher than in control population; overall risk per 1,000,000 population per year is 2 patients for aplastic anemia and 6 patients for agranulocytosis; prior to treatment, obtain CBC counts and differentials, along with LFTs; repeat blood count in 2-3 wk and then monthly for 3 mo; if no evidence of bone marrow suppression, then biannual counts should follow; WBC counts below 4000 are contraindication to treatment; discontinue if WBC falls <3000 after treatment, significant thrombocytopenia, abnormality in other blood elements, or significant abnormality in LFTs; other rare drug adverse effects include cardiovascular effects, such as congestive heart failure, arrhythmias, and orthostatic hypotension; hepatotoxicity; inappropriate secretion of antidiuretic hormone (IASDH); severe dermatologic reactions, including Stevens-Johnson syndrome (extremely rare); caution with other TCAs
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.
Dosing
Adult
15 mg/kg/d PO initial dose in 2 or more divided doses; titrate by 5-10 mg/kg/d until pain relief is achieved or adverse effects occur; pain relief at levels less than required for antiepileptic activity (50-150 mcg/mL)
Pediatric
Not established
Interactions
Coadministration with cimetidine, salicylates, felbamate, and erythromycin may increase toxicity; rifampin may significantly reduce valproate levels; in pediatric patients, protein binding and metabolism of valproate decrease when taken concomitantly with salicylates; coadministration with carbamazepine may result in variable changes of carbamazepine concentrations with possible loss of seizure control; valproate may increase diazepam and ethosuximide toxicity (monitor closely); valproate may increase phenobarbital and phenytoin levels while either one may decrease valproate levels; valproate may displace warfarin from protein binding sites (monitor coagulation tests); may increase zidovudine levels in HIV-seropositive patients
Contraindications
Documented hypersensitivity; hepatic disease/dysfunction
Precautions
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Idiosyncratic reactions include hepatotoxicity (fatalities have been reported), dermatitis, alopecia, encephalopathy, and rare hyperammonemia syndrome; obtain baseline LFTs followed at frequent intervals for first 6 months; monitor serum ammonia, since it can be elevated without corresponding elevation in LFTs
Corticosteroids
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.
Dosing
Adult
4-16 mg/d PO
Pediatric
Not established
Interactions
Decreased blood levels with phenytoin, phenobarbital, ephedrine, and rifampin; watch for development of hypokalemia with administration of potassium-depleting diuretics
Contraindications
Documented hypersensitivity; systemic infections, especially fungal
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in DM, hypertension, renal impairment, osteoporosis, peptic ulcer disease, ocular herpes simplex, cirrhosis, hypothyroidism, and psychotic tendencies; concurrent use of NSAIDs not recommended due to GI toxicity; adverse effects can include hyperglycemia, hypertension, fluid retention, myopathy, osteoporosis, nausea, cataracts, glaucoma, peptic ulcers, convulsions, behavioral disturbances, increased susceptibility to infections, thromboembolism, change in leukocyte/lymphocyte count, malaise, impaired wound healing, increased appetite, and dermatologic effects
Analgesics
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.
Dosing
Adult
50 mg PO tid initially; if needed, may increase to 100 mg tid within 1 wk
Pediatric
Not established
Interactions
May cause additive effects on cognitive and gross motor functioning when coadministered with drugs that cause dizziness or somnolence
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Discontinue gradually (over a minimum of 1 wk) to minimize increased seizure frequency in patients with seizure disorders; may cause insomnia, nausea, headache, or diarrhea with abrupt withdrawal; common adverse effects include dizziness, somnolence, blurred vision, weight gain, and peripheral edema; may elevate creatinine kinase level, decrease platelet count, and increase PR interval; doses >300 mg/d associated with higher rate of adverse effects and treatment discontinuation; decrease dose with renal impairment (ie, CrCl <60 mL/min)
Methadone (Dolophine)
Used in the management of severe pain. Methadone inhibits ascending pain pathways, diminishing the perception of and response to pain.
Dosing
Adult
2.5-10 mg PO/IM/SC q3-8h prn; increase to a maintenance dose of 5-20 mg q6-8h
Pediatric
Not established
Interactions
Phenytoin, rifampin, and pentazocine may decrease blood levels of methadone; phenothiazines, tricyclic antidepressants, MAOIs, and CNS depressants may increase the toxicity of methadone
Contraindications
Documented hypersensitivity; bronchial asthma or increased intracranial pressure
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in severe liver disease; due to its relatively long half-life, titrate dose slowly
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.
Dosing
Adult
30 mg PO q3-4h initial dose in opiate-naive patients (no exposure to opiates) or with limited opiate exposure; may be titrated upward by 50% if pain control is inadequate after first 24 h; balance between analgesia and adverse effects
Pediatric
0.3 mg/kg PO q3-4h initial dose
Interactions
Phenothiazines may antagonize analgesic effects of opiate agonists; TCAs, MAOIs, and other CNS depressants may potentiate adverse effects of morphine
Contraindications
Documented hypersensitivity; hypotension; potentially compromised airway where establishing rapid airway control would be difficult
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Elderly patients; hepatic or renal dysfunction; respiratory disease, obstructive and restrictive (eg, COPD, asthma, kyphoscoliosis); patients with severe obesity or cor pulmonale; head injury and increased intracranial pressure; history of drug abuse; circulatory shock; adverse effect profile includes nausea/vomiting, constipation, sedation, respiratory depression (which occurs more so with opiate-naive patients and with significant pulmonary disease), cardiovascular abnormalities (eg, bradycardia, hypotension), and urinary retention
Follow-up
Further Inpatient Care
- Inpatient care for radiation-induced lumbosacral plexopathy is not required.
Further Outpatient Care
- After radiation-induced lumbosacral plexopathy has been diagnosed, follow up with patients on functional issues. Address issues of pain in a timely fashion.
Complications
- Radiation-induced lumbosacral plexopathy may result in pain and decreased functional status.
Prognosis
- 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.14
Patient Education
- Educate patients about the effects of radiation and the reason for altered function, pain, and sensory deficits.
Miscellaneous
Medicolegal Pitfalls
- Failure to diagnose and treat radiation-induced lumbosacral plexopathy may result in medicolegal liability.
References
Pettigrew LC, Glass JP, Maor M, et al. Diagnosis and treatment of lumbosacral plexopathies in patients with cancer. Arch Neurol. Dec 1984;41(12):1282-5. [Medline].
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Jaeckle KA, Young DF, Foley KM. The natural history of lumbosacral plexopathy in cancer. Neurology. Jan 1985;35(1):8-15. [Medline].
Abu-Rustum NR, Rajbhandari D, Glusman S, et al. Acute lower extremity paralysis following radiation therapy for cervical cancer. Gynecol Oncol. Oct 1999;75(1):152-4. [Medline].
Iglicki F, Coffin B, Ille O, et al. Fecal incontinence after pelvic radiotherapy: evidences for a lumbosacral plexopathy. Report of a case. Dis Colon Rectum. Apr 1996;39(4):465-7. [Medline].
Jaeckle KA. Neurological manifestations of neoplastic and radiation-induced plexopathies. Semin Neurol. Dec 2004;24(4):385-93. [Medline].
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Abdellaoui A, West NJ, Tomlinson MA, et al. Lower limb paralysis from ischaemic neuropathy of the lumbosacral plexus following aorto-iliac procedures. Interact Cardiovasc Thorac Surg. Aug 2007;6(4):501-2. [Medline]. [Full Text].
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Bradley WG, Fewings JD, Cumming WJ, et al. Delayed myeloradiculopathy produced by spinal X-irradiation in the rat. J Neurol Sci. Jan-Feb 1977;31(1):63-82. [Medline].
Cavanagh JB. Prior x-irradiation and the cellular response to nerve crush: duration of effect. Exp Neurol. Oct 1968;22(2):253-8. [Medline].
Dahele M, Davey P, Reingold S, et al. Radiation-induced lumbo-sacral plexopathy (RILSP): an important enigma. Clin Oncol (R Coll Radiol). Jun 2006;18(5):427-8. [Medline].
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Keywords
radiation-induced lumbosacral plexopathy, radiation induced lumbosacral plexopathy, plexopathy, plexus, lumbosacral, lumbar sacral, lumbosacral plexus, spine lumbosacral, radiation therapy, radiation plexopathy, motor deficits, limb weakness
Contributor Information and Disclosures
Author
Rajesh R Yadav, MD, Assistant Professor, Section of Physical Medicine and Rehabilitation, MD Anderson Cancer Center, University of Texas at Houston
Rajesh R Yadav, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation
Disclosure: Nothing to disclose.
Medical Editor
Robert J Kaplan, MD, Associate Professor, Department of Physical Medicine and Rehabilitation, University of Kansas School of Medicine and Medical Center
Robert J Kaplan, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, Association of Academic Physiatrists, International Spine Intervention Society, and Physiatric Association of Spine, Sports and Occupational Rehabilitation
Disclosure: Nothing to disclose.
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Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
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Managing Editor
Michael T Andary, MD, MS, Residency Program Director, Professor, Department of Physical Medicine and Rehabilitation, Michigan State University College of Osteopathic Medicine
Michael T Andary, MD, MS is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, American Medical Association, and Association of Academic Physiatrists
Disclosure: allergan Honoraria Speaking and teaching
CME Editor
Kelly L Allen, MD, Regional Medical Director, IMX-Medical Management Services
Disclosure: Nothing to disclose.
Chief Editor
Robert H Meier III, MD, Director, Amputee Services of America; Active Medical Staff, Presbyterian/St Luke's Hospital, Spalding Rehabilitation Hospital, Select Specialty Hospital; Consulting Staff, Kindred Hospital
Robert H Meier III, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation and Association of Academic Physiatrists
Disclosure: Nothing to disclose.
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