Updated: Dec 4, 2008
Neoplastic lumbosacral plexopathy (NLP) is an infrequent complication associated with advanced systemic cancer due to local or regional progression of the primary tumor. NLP is characterized by significant pain and sensorimotor deficits.
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 psoas muscle and then coalesce into the lumbar plexus, which then divides into anterior and posterior divisions. The first 3 nerves (iliohypogastric, ilioinguinal, 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, obturator) innervate the anteromedial thigh. The femoral nerve terminates into 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 that provide sensory motor innervation to the 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 nerves. The sciatic nerve divides into the common peroneal and tibial nerves in the thigh.
NLP associated with pelvic, abdominal, and retroperitoneal tumors often results in significant pain, sensory disturbance, weakness, and disability. Plexus involvement occurs as a result of tumor extension or invasion and heralds a progressive disease course. Plexopathy is part of the initial presentation of cancer in 15% of patients.
Related eMedicine topics:
Diabetic Lumbosacral Plexopathy
Radiation-Induced Lumbosacral Plexopathy
Lumbosacral plexus involvement occurs most commonly due to intra-abdominal tumor extension (73% of cases); it occurs less commonly with growth from metastases, lymph nodes, or bone structures. A tumor can invade the plexus directly or track along the connective tissue or epineurium of nerve trunks.
The most prevalent types of tumors are colorectal tumors (20%), sarcomas (16%), breast tumors (11%), lymphoma (9%), and cervical tumors (9%). Other tumors, including multiple myeloma, account for another 37% of cases. The most common distant metastatic lesions are caused by breast cancer. In one study, the lumbosacral plexus was involved in 50 of 2261 cases of cervical cancer; however, it was involved in 38 of the 74 patients (51%) in the subgroup with proven retroperitoneal metastatic disease.
The lower (sacral) plexus is involved most frequently (approximately 50%), followed by upper plexus involvement (more than 30%) and panplexopathy (18%).[1 ]Bilateral plexopathy occurs in 25% of cases and is usually caused by breast cancer metastases. Lower plexus involvement occurs generally with colorectal and cervical neoplasms. Involvement of the sacral sympathetic nerves is less common (10%).
Malignant psoas syndrome (MPS) was first described in 1990 by Stevens and refers to severe and difficult pain due to proximal lumbosacral plexopathy, painful fixed flexion of the ipsilateral hip, and radiologic or pathologic evidence of malignant involvement of the ipsilateral psoas major muscle.[2 ]
The incidence of neoplastic lumbosacral plexopathy is 0.71%.
Significant morbidity from neoplastic lumbosacral plexopathy occurs due to associated pain, weakness, and sensory deficits.[3 ]One study noted median survival of 5.5 months after diagnosis. In patients with prostate cancer,[4 ]symptoms may persist for years and survival may be longer.
No known correlation is recognized between the incidence of neoplastic lumbosacral plexopathy and race.
One study noted a male-to-female ratio for neoplastic lumbosacral plexopathy of 1.3:1, although the investigation involved just a small number of patients.
In one study, age at the time of presentation of neoplastic lumbosacral plexopathy ranged from 19-80 years, with a median age of 65.5 years.
Tumor invasion, either local or metastatic, can lead to lumbosacral plexopathy.
Leptomeningeal Carcinomatosis
Radiation-Induced Lumbosacral Plexopathy
Other causes of lumbosacral radiculopathy
Primary plexus tumors
Epidural cord compression
Chemotherapy toxicity associated with intra-arterial treatment
Aortic aneurysms
Diabetes mellitus
Diabetic amyotrophy
Obstetric procedures
Trauma
Intragluteal injections
Meningeal carcinomatosis or leptomeningeal disease also may cause low back or leg pain with subacute motor or sensory involvement; however, patients with these conditions often demonstrate mental status changes, headaches, cranial nerve palsies, and/or nuchal rigidity.
In cancer patients with thrombocytopenia, retroperitoneal bleeding can cause plexopathy accompanied by a rapid onset of pain and neurologic signs that usually are fully developed in 24 hours. Other associated findings include flank, thigh, or low back ecchymoses. A retroperitoneal bleed usually involves the femoral nerve and occasionally will spread to other parts of the plexus.
Other causes of lumbosacral plexopathy to consider are idiopathic in nature, aortic aneurysms, diabetes mellitus, obstetric procedures, trauma, anticoagulation therapy, retroperitoneal hematomas, surgical intervention for mesenteric thrombosis, kidney transplantation, tuberculosis, and intragluteal injections.[6,7,8,9,10,11,12 ]
Acute pain is common with aortic aneurysm, and the resultant weakness typically worsens over 1-2 weeks and then stabilizes. A pulsatile rectal or abdominal mass frequently is observed.
Acute thigh pain with acute or insidious onset weakness can result from diabetic amyotrophy and can be difficult to differentiate from the pain associated with an aortic aneurysm. In diabetic amyotrophy, weakness is more often noted proximally, with relative sparing of distal lower extremity muscles.
For physical rehabilitation, the likely progression of neurologic weakness needs to be considered. If the patient is noted to have associated weakness after acute pain has subsided, one may recommend active range-of-motion (AROM) exercises, with advancement to low resistance exercises. Assistive devices, such as a cane, walker, or wheelchair, may be required for ambulation in patients with weakness of the hip extensors, abductors, or quadriceps, with or without loss of joint position sense. Use of an ankle-foot orthosis (AFO) and, in rare cases, a knee-ankle-foot orthosis (KAFO) may be beneficial for mobility.
The occupational therapist should assess activities of daily living (ADL) and prescribe appropriate adaptive equipment. In particular, be aware that standing-transfer safety may be impaired in cases in which involvement is more distal than proximal. With more proximal involvement, sit-to-stand transfers also may be affected. Equipment may be used specifically to facilitate dressing and bathing activities involving the lower extremity.
Patients with more severe and recalcitrant pain may respond to the use of epidural catheter drug delivery and/or neurostimulatory/neuroablative surgical approaches. Cordotomies have been reported to have good outcomes in Europe. However, pain relief has been noted to be transient. Such ablative procedures carry the risk of sensory and motor deficits. The mortality rate has been significant at 5%.
Occasional relief of chronic pain has been achieved with plexus dissection and neurolysis.
Pain is a significant issue in most patients and studies have shown that pain is often poorly controlled in these patients. A multidisciplinary approach is needed. Consider early consultation with pain service, given the patient's short life expectancy following diagnosis. These patients may benefit from opiate analgesics, continuous infusion pumps, and procedures such as local and regional blocks, sympathectomy, and rhizotomy.
Nonpharmacologic measures, such as transcutaneous electrical nerve stimulation (TENS) or Anodyne therapy, may be used for neuropathic pain.
Tricyclic antidepressants, such as amitriptyline (10-100 mg qhs), may be helpful at low doses. Antiepileptics, such as gabapentin (300-3600 mg/d in 3-4 divided doses) also can be tried. Opiates, especially methadone and steroids, can be considered as well. Mexiletine, a class 1b antiarrhythmic, at 200 mg bid, has been used for the management of significant neuropathic pain due to neoplastic plexus infiltration.[17 ]Low- (0.1 g/kg/d) and higher-dose (0.2-2 g/kg/d) intravenous immunoglobulin therapy has, in limited cases, been successfully used for idiopathic brachial and lumbosacral plexopathy. However, its effectiveness in neoplastic plexopathy is unproven. A single dose (500 mg or 1 g) of intravenous magnesium sulfate has been used with success in a small sample of patients with neuropathic pain due to neoplastic plexopathy.[18 ]
These agents have central and peripheral anticholinergic effects, as well as sedative effects, and block the active reuptake of norepinephrine and serotonin.
Analgesic for certain chronic and neuropathic pain.
10-100 mg PO qhs
Not established
Phenobarbital may decrease effects; coadministration with CYP2D6 enzyme system inhibitors (eg, cimetidine and quinidine) may increase amitriptyline levels; amitriptyline inhibits hypotensive effects of guanethidine; may interact with thyroid medications, alcohol, CNS depressants, barbiturates, and disulfiram
Documented hypersensitivity; patient has taken MAO inhibitors in past 14 d; has history of seizures, cardiac arrhythmias, glaucoma, and urinary retention
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Caution in cardiac conduction disturbances and history of hyperthyroidism, renal or hepatic impairment; avoid using in elderly patients
Pain control is essential to quality patient care. Analgesics ensure patient comfort, promote pulmonary toilet, and have sedating properties, which are beneficial for patients who experience pain.
Generally used for short-term, acute pain, moderate to severe in nature, as well as for chronic pain (eg, that associated with cancer). Morphine sulfate is available in immediate (3-4 h duration) and extended-release preparation (12 h). Switch over to long-acting preparations (MS Contin) once the pain is controlled with short-acting preparation (MS IR). Morphine can produce drug dependence and has the potential to be abused. Tolerance may develop with repeat exposure. Abrupt cessation of the drug or a sudden reduction in dose with prolonged use may result in withdrawal symptoms. Physical dependence is not of paramount importance in terminally ill patients.
30 mg PO q3-4h initial dose in opiate-naive patients (no exposure to opiates) or in those with limited opiate exposure; may be titrated upward by 50% if pain control inadequate after first 24 h; balance between analgesia and adverse effects
Not established
Phenothiazines may antagonize analgesic effects of opiate agonists; tricyclic antidepressants, MAOIs, and other CNS depressants may potentiate adverse effects of morphine
Documented hypersensitivity; hypotension; potentially compromised airway where establishing rapid airway control would be difficult
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in hypotension, respiratory depression, nausea, emesis, constipation, urinary retention, atrial flutter, and other supraventricular tachycardias; has vagolytic action and may increase ventricular response rate
Used in the management of severe pain. Methadone inhibits ascending pain pathways, diminishing the perception of and response to pain.
2.5-10 mg PO/IM/SC q3-8h prn; increase to maintenance dose of 5-20 mg q6-8h
Not established
Phenytoin, rifampin, and pentazocine may decrease blood levels of methadone; phenothiazines, tricyclic antidepressants, MAOIs, and CNS depressants may increase toxicity of methadone
Documented hypersensitivity; bronchial asthma or increased intracranial pressure
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in severe liver disease; due to its relatively long half-life, titrate dose slowly
These agents inhibit events involved in muscle contraction.
Reduces nerve impulse transmission from the spinal cord to skeletal muscle.
1.5 g PO qid for 2-3 d and decrease to 4-4.5 g/d in 3-6 divided doses
Administer as in adults
Increases toxicity of CNS depressants
Documented hypersensitivity; renal impairment
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in history of seizures
Antiepileptics are used to manage severe muscle spasms and to provide sedation in neuralgia.
Structural derivative of GABA. The mechanism of action is unknown. Pregabalin binds with high affinity to the alpha2 -delta site (a calcium channel subunit). In vitro, it reduces the calcium-dependent release of several neurotransmitters, possibly by modulating calcium channel function. Pregabalin is FDA approved for neuropathic pain associated with diabetic peripheral neuropathy or postherpetic neuralgia and as an adjunctive therapy in partial-onset seizures.
50 mg PO tid initially; if needed, may increase to 100 mg tid within 1 wk
Not established
May cause additive effects on cognitive and gross motor functioning when coadministered with drugs that cause dizziness or somnolence
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
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)
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.
300-3600 mg/d PO divided tid/qid
Not established
Antacids may significantly reduce bioavailability of gabapentin (administer at least 2 h following antacids); may increase norethindrone levels significantly
Documented hypersensitivity; antacids may significantly reduce bioavailability of gabapentin (administer at least 2 h following antacids); may increase norethindrone levels significantly; caution in severe renal disease
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Antacids may significantly reduce bioavailability of gabapentin (administer at least 2 h following antacids); may increase norethindrone levels significantly; caution in severe renal disease
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neoplastic lumbosacral plexopathy, plexus, lumbosacral, breast cancer, sciatic nerve, colorectal cancer, psoas, neoplastic, psoas muscle, femoral nerve, iliopsoas, iliopsoas muscle, ilioinguinal nerve, obturator nerve, abdominal cancer, cervical cancer, pelvic tumor, retroperitoneal tumor, NLP, lumbosacral plexus, lumbosacral plexopathy, proximal lumbosacral plexopathy, malignant psoas syndrome, MPS, malignant lumbosacral plexopathy, lumbosacral carcinomatous, neuropathy tumor-induced lumbosacral plexopathy, tumor, lumbar plexus, sacral plexus
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.
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.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.
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
Kelly L Allen, MD, Regional Medical Director, IMX-Medical Management Services
Disclosure: Nothing to disclose.
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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