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Lumbosacral plexus syndromes

Lumbosacral plexus syndromes
Literature review current through: Jan 2024.
This topic last updated: Jul 14, 2022.

INTRODUCTION — Lumbosacral plexopathies (LSPs) represent a distinct group of disorders of the peripheral nervous system due in part to their relative rarity in comparison with other peripheral nerve disorders and also due to their wide array of etiologies. A thorough understanding of the anatomy of the lumbosacral plexus, the most common causes of LSP, and the most currently accepted diagnostic approaches is needed to manage these conditions effectively.

Other neuropathies affecting the lower limbs are reviewed separately. (See "Overview of lower extremity peripheral nerve syndromes" and "Acute lumbosacral radiculopathy: Etiology, clinical features, and diagnosis" and "Acute lumbosacral radiculopathy: Treatment and prognosis".)

ANATOMY — The lumbar and sacral plexuses make up the collective lumbosacral plexus, which is formed from the anterior (ventral) rami of the L1 through S4 nerve roots (figure 1). The anterior rami divide within the plexus into anterior and posterior divisions that in turn yield individual peripheral nerves.

The lumbar plexus is derived from the anterior rami of the L1 through L4 nerve roots. These rami pass downward and laterally along the psoas major muscle where they eventually form the plexus. While within the psoas, they divide into anterior and posterior branches. The posterior branches of anterior rami, L2 through L4, become the femoral nerve, which exits from the lateral aspect of the psoas, traveling through the iliacus and under the inguinal ligament to the anterior thigh. The anterior branches become the obturator nerve, which exits from the medial aspect of the psoas and courses over the sacral ala through the obturator foramen to the medial thigh. The lumbar plexus also gives off the lateral femoral cutaneous nerve of the thigh, iliohypogastric, ilioinguinal, and genitofemoral nerves [1].

The lumbar plexus and sacral plexus are united via the lumbosacral trunk, which is comprised of a portion of L4 nerve root anterior rami and all L5 anterior rami. The lumbosacral trunk passes over the sacral ala and joins the anterior rami of the S1 through 4 nerve roots to complete the sacral plexus [1].

The sacral plexus drapes the posterolateral wall of the pelvis and converges upon the sciatic notch. These anterior rami also divide into anterior and posterior branches. The posterior branches of the lumbosacral trunk and S1 and S2 anterior rami form the lateral or peroneal division of the sciatic nerve. The anterior branches form the medial or tibial division of the sciatic nerve. The sacral plexus also gives off the inferior and superior gluteal nerves, posterior cutaneous nerve of the thigh, and pudendal nerve [1].

The lumbosacral plexus has a rich vascular supply. It is fed by the five lumbar arteries that originate from the abdominal aorta, the deep circumflex iliac artery that branches from the external iliac artery, and the iliolumbar and gluteal branches of the internal iliac artery [2].

CLINICAL FEATURES — Lumbosacral plexopathies (LSPs) have a multitude of clinical features. They most often present with asymmetric, focal weakness, numbness, dysesthesia, and/or paresthesia in multiple contiguous lumbosacral nerve root distributions.

Patterns of weakness usually help localize the "lesion" to a more specific area within the plexus.

Lumbar plexus lesions tend to cause weakness of hip flexion and adduction and/or knee extension.

Lumbosacral trunk and upper sacral plexus lesions result in foot drop or flail foot depending on the extent of involvement and weakness of knee flexion or hip abduction.

Patterns of sensory disturbance are less reliable given the difficult clinical delineation between dermatomal and named nerve sensory loss. However, in general, sensory disturbance involving the anterior and medial thigh and medial leg typically represents lumbar plexus involvement, while sensory disturbance involving the leg, dorsum of the foot, posterior thigh, and perineum suggests a lumbosacral trunk and/or sacral plexus lesion.

DIAGNOSTIC EVALUATION — Given the wide array of etiologies for patients presenting with signs and symptoms suspicious for lumbosacral plexopathy (LSP) (table 1), an organized, thorough approach to diagnosis is a necessity. The diagnostic evaluation includes electrodiagnostic studies, laboratory investigations, and often neuroimaging.

Examination — A thorough general and neurologic examination can aid in the localization of lumbosacral plexus lesions.

Detailed assessment of functional strength, sensation, and deep-tendon reflexes of both lower limbs is compulsory.

Palpation of the greater trochanters may reveal tenderness indicating focal bursitis. Palpation of the inguinal region should be undertaken to look for mass or hematoma formation. Rectal examination is important to assess tone and to look for rectal mass.

Maneuvers such as the Patrick test and straight leg raising may provide clues to the presence of lumbosacral radiculopathy, which can sometimes mimic LSP, or a musculoskeletal lesion of the hip (eg, sacroiliitis).

The Patrick test is a maneuver in which the hip is externally rotated with the ipsilateral knee flexed at 90 degrees and placed on the opposite knee. The test is positive if it elicits hip or buttock pain. A positive test raises suspicion for hip or sacroiliac disease. However, it is nonspecific for a radiculopathy or plexopathy. (See "Musculoskeletal examination of the hip and groin", section on 'Tests for acetabular pathology'.)

The straight leg raise test is done with the patient supine. The examiner raises the patient's extended leg on the symptomatic side with the foot dorsiflexed, being careful that the patient is not actively "helping" in lifting the leg. The straight leg raise test is useful for the diagnosis of radiculopathy due to disc herniation, particularly for the L5 and S1 levels.

The reverse straight leg raise (femoral stretch) test is accomplished by placing the patient prone on the table and passively extending the hip and leg straight up off the plane of the table. This maneuver is most useful for evaluating the L2, L3, and L4 roots. However, the value of this test is limited by inadequate information on its sensitivity and specificity. A positive reverse straight leg raise test may be difficult to interpret due to supposed stretch of the femoral nerve, lumbar plexus, and lumbar spinal nerve root fibers.

Neuroimaging — Magnetic resonance imaging (MRI) is the imaging method of choice for plexus evaluation. The superior anatomic resolution offered by MRI techniques compared with computed tomography (CT) may increase the diagnostic accuracy and assist interventionalists or surgeons in preoperative planning. CT can be used in those with contraindications to MRI.

Gadolinium contrast should typically be given, as enhancement can be helpful in certain instances, such as suspected neoplasm, abscess, inflammation, or postoperative changes [3,4].

While ultrasound imaging is being used increasingly in the diagnosis of peripheral nerve disorders including in the brachial plexus, it is not routinely used in the diagnosis of LSP. It is likely useful in differentiating other peripheral lesions involving the sciatic, peroneal, and tibial nerves given their more superficial anatomic locations.

Electrodiagnostic studies — Electrodiagnostic studies can help differentiate LSP from lumbosacral radicular and individual nerve syndromes and may also provide clues to the intraplexus location and possible etiology. (See "Overview of electromyography" and "Overview of nerve conduction studies".)

Needle electromyography (EMG) should be done primarily to distinguish LSP from radiculopathy and isolated sciatic, femoral, peroneal, or tibial neuropathy and to characterize the severity of involvement. The electrodiagnostic approach will depend upon the clinical evaluation but may include the following [5]:

Tibial motor studies while recording from abductor hallucis brevis.

Peroneal motor studies while recording from extensor digitorum brevis; recording from the tibialis anterior may also be useful if the extensor digitorum brevis response is absent or quite small. It may also aid in prognosis for recovery from foot drop.

Tibial and peroneal F waves.

H reflex.

Sural, superficial peroneal, medial plantar, and saphenous sensory potentials.

Prolonged F waves and H responses, though nonspecific, can suggest more proximal lesions. Bilateral studies should be performed in nearly all cases. Upper limb nerve conduction studies should be performed to exclude polyneuropathy if symptoms are bilateral or diffuse.

Needle EMG should be done primarily to distinguish LSP from radiculopathy and characterize the severity of involvement. The electrodiagnostic approach will depend upon the clinical evaluation but may include the following [5]:

Peroneal innervated muscles (at least two)

Tibial innervated muscles (at least two)

Sciatic innervated muscles in the thigh (at least one)

Superior gluteal innervated muscles (at least one)

Inferior gluteal innervated muscles (at least one)

Femoral innervated muscles (at least two)

Obturator innervated muscles (at least one)

Lumbosacral paraspinal muscles innervated by L2, L3, L4, L5, and S1

Bilateral studies may be necessary if symptoms are bilateral or if abnormalities are modest in the limb of interest [5]. Upper limb EMG should be performed to exclude polyneuropathy if symptoms are bilateral or diffuse.

EMG of deep or paraspinal muscles is relatively contraindicated in certain patient populations, particularly those with thrombocytopenia or a bleeding disorder, and those on anticoagulation therapy. In these subgroups, magnetic stimulation of nerve roots may be helpful in the diagnosis of LSP [6].

Nerve conduction studies with abnormal motor and intact sensory responses of lower limb, along with EMG findings in a myotomal distribution with paraspinal muscle involvement, typically indicate a radicular process rather than LSP. (See "Acute lumbosacral radiculopathy: Etiology, clinical features, and diagnosis".)

There are limited options for performing nerve conduction studies in the proximal lower limb. Femoral nerve conductions while recording from rectus femoris can be attempted. However, these are often painful and difficult because of body habitus. When responses are obtained, they are best utilized with side-to-side comparisons of amplitude and may help determine prognosis.

However, EMG abnormalities favoring acute denervation and chronic reinnervation of L2-, L3-, and L4-innervated thigh muscles but sparing thigh adductors, tibialis anterior, and corresponding paraspinal muscles can differentiate an isolated femoral neuropathy from LSP or lumbar radiculopathy.

Slowed peroneal motor nerve conduction velocities across the fibular head, with or without corresponding diminished motor responses and/or superficial peroneal sensory involvement, can distinguish peroneal neuropathy from LSP.

EMG abnormalities in the hip abductors will help distinguish lumbosacral plexus lesions from sciatic nerve lesions.

Laboratory investigations — Suggested blood tests for LSP of unknown cause include a complete blood count, coagulation profile, glycated hemoglobin, sedimentation rate, C-reactive protein, antinuclear antibodies, antineutrophilic cytoplasmic antibodies, angiotensin-converting enzyme, serum protein electrophoresis with immunofixation, anti-Ro and La antibodies, and serologies for Epstein-Barr virus, varicella-zoster virus, human immunodeficiency virus (HIV), Lyme disease, and syphilis.

In the setting of a negative blood evaluation, a lumbar puncture to assess for leukocytes, protein, and cytology can be helpful to look for an occult infectious process or malignancy.

Biopsy — Pathologic investigation into patients with LSP will depend on the suspected etiology. Image-guided needle biopsies of intra-abdominal and intrapelvic organs and tissues are the gold standard for suspected neoplasm or infiltrative processes. However, for those in which the diagnosis remains elusive, there may be a role for fascicular biopsy of proximal nerves and/or nerve roots.

SPECIFIC DISORDERS — The causes of lumbosacral plexopathy (LSP) are vast and diverse (table 1). The most common presentations are idiopathic lumbosacral radiculoplexus neuropathy and diabetic amyotrophy. These are reviewed in detail separately. (See "Diabetic amyotrophy and idiopathic lumbosacral radiculoplexus neuropathy".)

The following sections will discuss some of the more common causes of LSP.

Diabetic amyotrophy — Diabetic amyotrophy, also known as diabetic radiculoplexus neuropathy, typically occurs in patients with type 2 diabetes mellitus. It is not a pure LSP because it also affects the lumbosacral nerve roots and peripheral nerves. The typical features include the acute, asymmetric, focal onset of pain followed by weakness involving the proximal leg with associated autonomic failure and weight loss. However, onset may be distal and can also involve thoracic and cervical nerves. Progression occurs over weeks and is followed by partial recovery in most patients.

Diabetic amyotrophy is discussed in detail separately. (See "Diabetic amyotrophy and idiopathic lumbosacral radiculoplexus neuropathy".)

Idiopathic lumbosacral radiculoplexus neuropathy — Idiopathic lumbosacral radiculoplexus neuropathy is similar to diabetic amyotrophy with respect to its pathophysiology, clinical features, prognosis, and management. (See "Diabetic amyotrophy and idiopathic lumbosacral radiculoplexus neuropathy".)

Neoplastic invasion — The lumbosacral plexus lies in close proximity to bone, multiple soft tissues, and organs and is susceptible to neoplastic invasion from nearby malignancy. The most frequent mechanism of LSP from neoplasm is direct extension of tumor. Other common mechanisms include meningeal dissemination, secondary extension of tumor to the sacrum, iliac wings or lumbar vertebrae, hematogenous or lymphatic spread of cells from primary tumor sites, and paraneoplastic phenomenon.

Neoplastic invasion of the lumbosacral plexus can occur in multiple forms of cancer, including the following [7-11]:

Carcinoma (colorectal, breast, lung, gastric, thyroid, renal, ureteral, bladder, testicular, penile, prostate, cervical, ovarian, uterine, vaginal)

Malignant melanoma

Lymphoma

Sacral chordoma

Sarcoma (retroperitoneal and pelvic), malignant schwannoma

LSPs may also arise from benign tumors, such as benign uterine leiomyoma, neurofibromas, and plexiform lesions [10,12].

Neoplastic invasion typically presents with severe, lancinating pain with or without radicular symptoms. Patients can have positional or mechanical exacerbation of pain, and symptoms may be aggravated by lying supine, weight-bearing, or straining to have a bowel movement. Within weeks to months, pain is usually followed by the development of progressive numbness, paresthesia, and weakness. Weakness can proceed to focal paralysis such as foot drop (weakness of dorsiflexion), flail foot (weakness of both dorsiflexion and plantar flexion), loss of hip flexion, or loss of knee flexion/extension.

One of the largest reports was published in the late 1980s and studied 85 patients with pelvic tumors and LSP, including 34 who were prospectively examined [9]. The following observations were noted:

Pain at presentation was reported in 91 percent, and pain eventually developed in 98 percent. The pain was typically aching and pressure-like and could be local, radicular, or referred; a combination of local and radicular pain was common.

Clinical signs (from most to least frequent) included leg weakness (86 percent); sensory loss (73 percent); reflex asymmetry (64 percent); focal tenderness involving the sciatic notch, lumbar, or sacral spine (55 percent); positive direct (53 percent) and reverse (45 percent) straight leg raising test; leg edema (47 percent); rectal mass (39 percent); dysesthesia (15 percent); decreased sphincter tone (12 percent); and fasciculations (12 percent). Autonomic involvement was rare. Urinary incontinence tended to be associated with epidural extension of tumor.

Bilateral plexopathy occurred in 27 percent and epidural extension was detected in 35 percent.

The most common primary tumors were colorectal, cervical, and breast cancers; sarcoma; and lymphoma. Direct invasion from intra-abdominopelvic neoplasm was reported in 73 percent; the remainder had metastasis of extra-abdominopelvic tumor.

Metastatic lesions tended to affect the lower plexus while direct intra-abdominal or intrapelvic mass extension was more likely to affect the upper plexus. Approximately 20 percent of affected patients had a panplexopathy secondary to massive tumors.

Plexopathy developed within one year of primary tumor diagnosis in one-third of patients and within three years in two-thirds. The symptoms of LSP preceded discovery of primary tumor in 15 percent of patients.

While perineural spread is not unusual in head and neck cancers, it has only rarely been described in pelvic malignancies including vaginal, cervical, prostate, bladder, and rectal cancer [7,13].

Diagnosis — The general approach to the diagnosis of LSP is discussed above. (See 'Diagnostic evaluation' above.)

In addition to other disorders discussed in this topic, the differential diagnosis of LSP in a patient with cancer includes lumbosacral radiculopathy, meningeal carcinomatosis, cauda equina syndrome, retroperitoneal hemorrhage or iliopsoas hematoma, and radiation plexopathy.

Since many patients may present radicular symptoms, lumbosacral radiculopathies are often the first diagnostic consideration. (See "Acute lumbosacral radiculopathy: Etiology, clinical features, and diagnosis".)

Meningeal carcinomatosis is frequently associated with other clinical signs such as nuchal rigidity, cranial nerve palsies, mental status changes, or headache. (See "Clinical features and diagnosis of leptomeningeal disease from solid tumors", section on 'Clinical manifestations'.)

Cauda equina syndrome is likely to be accompanied by urinary incontinence but usually not by leg edema or obvious rectal mass. (See "Clinical features and diagnosis of neoplastic epidural spinal cord compression".)

Retroperitoneal hemorrhage typically presents acutely instead of insidiously and may also be associated with ecchymoses. (See 'Retroperitoneal hematoma' below.)

When there is suspicion for neoplasm as the cause of LSP, pelvic anatomy should be evaluated with contrast-enhanced MRI (image 1) [14]. Positron emission tomography (PET)/CT can provide valuable complementary information and helps delineate the extent of malignancy in the region (image 2) [13]. MRI can often differentiate among direct compression, metastatic disease, and primary infiltration of plexus structures. However, different stages of inflammation, hemorrhage, or necrosis can still make diagnosis challenging. Perineural spread may show irregular and nodular thickening on T1-weighted images, increased intensity on T2-weighted images, and irregular, perifascicular enhancement with gadolinium [13,15].

Lymphomas affecting the plexus have variable appearances on neuroimaging, ranging from asymmetric muscle enlargement and altered signal density on CT to focal or diffuse low T1-weighted or high T2-weighted signal on MRI. Contrast enhancement is also variable and may be absent, ring-shaped, fusiform, or uniform. High-resolution magnetic resonance neurography has demonstrated significant utility in diagnostic dilemmas involving lymphoma [13,16]. PET/CT often helps to complement the interpretation of abnormalities seen on MRI.

Patients with LSP secondary to primary tumors in the abdominopelvic region tend to have a relatively focal disease process with lumbar plexus involvement due to direct extension. Thus, nerve conduction studies will most likely be normal or minimally involved. Electromyography (EMG) will demonstrate abnormalities in the hip flexors, hip adductors, and knee extensors with sparing of lumbar paraspinal muscles.

Metastatic lesions are more likely to cause lumbosacral or sacral plexus involvement, with nerve conduction studies demonstrating diminished sensory and motor responses and EMG displaying abnormalities in hip abductors, knee flexors, ankle dorsiflexors, and plantar flexors, evertors, and invertors.

Fascicular biopsy of the plexus or affected nerve root may be performed when imaging is nondiagnostic in institutions with expertise in the procedure [11,17].

Prognosis and management — In general, the prognosis for patients with LSP due to tumor appears to be poor, although data are limited. In a series from the late 1980s of patients with tumor-related LSP, there were 59 patients who had follow-up examinations, and neurologic deterioration was noted in approximately 60 percent [9]. Among 67 patients not lost to follow-up at the end of the study, 40 had died. The median survival from time of diagnosis was approximately six months (range 1 to 34 months). Response to therapy often differs according to the type of tumor, and lymphoma was the most responsive tumor in this series [9].

A small study of patients with advanced pelvic cancer found that dorsal rhizotomy was associated with a significant reduction in pain and opioid usage [18]. Radiation therapy for painful symptoms due to malignant lumbosacral plexus syndrome was associated with rapid pain relief and reduced tumor size in one small series [19]. Prospective trials are needed to determine whether radiotherapy, chemotherapy, surgery, or some combination of treatments is beneficial for tumor-related LSP.

Radiation plexopathy — Patients with radiation-induced LSP typically present with leg weakness, sometimes accompanied by sensory loss. Pain is usually absent or mild. Radiation plexopathy tends to occur months, years, or even decades after pelvic irradiation, has a predilection for the upper plexus, and is often bilateral [20].

Radiation-induced LSP is uncommon with standard external beam radiation doses and conventional fractionation schedules. However, certain specialized radiation therapy techniques provide an increased dose of radiation to the pelvis and may increase the risk of LSP. These techniques include intracavitary radiation therapy and intraoperative radiation therapy.

Radiation plexopathy is thought to be caused by tissue fibrosis with retraction of nerve trunks, direct toxicity to axons, and microinfarction of nerve axons due to radiation effects on the vasa nervorum [21].

Diagnosis — Differentiating radiation plexopathy from a recurrent tumor can be difficult, as both may have variable signal characteristics on imaging. MRI may demonstrate a thin pattern of enhancement due to disruption of the blood-nerve barrier, the so-called "tram-track" appearance, suggestive of radiation plexopathy. PET typically shows no or minimal 2-fluorodeoxyglucose (FDG) uptake in the case of radiation plexopathy; tumors often show increased uptake of FDG [13,22].

Approximately one-half of patients with radiation plexopathy have myokymia by EMG. This finding can help distinguish radiation plexopathy from recurrent tumor invasion in diagnostically challenging patients [23,24]. (See "Overview of electromyography", section on 'Myokymia'.)

Prognosis and management — Symptoms of radiation plexopathy typically progress slowly for years after radiation therapy. Rarely, spontaneous resolution or stabilization for several years can occur.

There are no effective therapies for radiation plexopathy. A small randomized trial found no benefit for hyperbaric oxygen therapy in patients with radiation-induced brachial plexopathy [25].

For patients with neuropathic pain or dysesthesia, symptomatic therapies such as gabapentin, pregabalin, duloxetine, amitriptyline, or venlafaxine may be helpful. Physical therapy is a useful adjunct to help patients cope with gait difficulties and to evaluate for equipment needs.

Trauma — Pelvic trauma occasionally causes LSP. Injuries from high-velocity flexion-abduction of the hip, posterior hip dislocation, and hyperextension of the thigh with external rotation of the fractured or dislocated portion of the pelvis may also disrupt the plexus [26].

In a retrospective review of 2054 patients treated for pelvic fractures at a single center, the estimated incidence of LSP, based upon patients who had electrodiagnostic studies, was 0.7 percent [27]. The estimated incidence of LSP was significantly higher with sacral fractures (2 percent) than with pelvic and acetabular fractures (0.7 percent). These findings probably underestimate the true incidence of LSP associated with pelvic fractures, since not all trauma patients were referred for electrodiagnostic studies. The close proximity of the plexus to the sacrum makes it more susceptible to injury from sacral fractures and dislocations [27].

Trauma-induced LSP may go unnoticed due to either patient expiration from multiorgan involvement, or from inability to adequately assess neurologic function or incomplete work-up due to the severity of trauma and pain [26,27]. A postmortem study of 42 victims of lethal trauma who sustained concomitant pelvic fracture found evidence of lumbosacral plexus damage in 20 (48 percent) [28].

Electrodiagnostic study findings in LSP related to trauma are likely to be compatible with lower lumbosacral or sacral involvement given that most are caused by sacral fractures and sacroiliac dislocation.

Management — Treatment options are limited in traumatic LSP. Although data are sparse, surgical nerve repair and nerve grafting techniques may lead to partial recovery of proximal leg muscle function [26,29]. One retrospective study reported 10 patients, most with pelvic fractures and severe injuries to the lumbosacral plexus, who were treated with nerve grafting and nerve transfer procedures at a mean of seven months after the injury (range 4 days to 36 months) [26]. Over a mean follow-up of 38 months, slow recovery was observed in nine patients, with return of unsupported standing and walking in those previously unable to do so without assistance.

Peripartum plexopathy — LSP related to pregnancy can present in the antepartum, intrapartum, and postpartum periods.

Antepartum LSP is rare. It usually involves the upper lumbar plexus from direct compression by the gravid uterus with symptoms most often occurring around 32 to 34 weeks of gestation. Typical manifestations are those of low back or groin pain, development of weakness involving hip flexion and adduction, and numbness and paresthesia confined to the anteromedial thigh.

Intrapartum and postpartum LSP result from direct compression of the lumbosacral trunk during fetal descent. The lumbosacral trunk is most susceptible to injury at its terminal portion near the pelvic brim, where it is no longer cushioned by the psoas muscle and instead lies in close contact with the bony pelvis [30]. Intrapartum/postpartum LSP is more common than antepartum but still infrequent, with an estimated incidence between 1:2000 and 1:6400 deliveries [31,32]. However, there are no prospective epidemiologic data.

Most females with intrapartum/postpartum LSP initially present with numbness and/or paresthesia of the lateral foreleg and dorsum of foot. Foot drop typically develops due to involvement of the lumbosacral trunk. Less often, there is mild weakness of hip flexion, hip abduction, knee flexion, and knee extension. Autonomic involvement is rare.

Symptoms of intrapartum/postpartum LSP may not be apparent during the time of delivery due to epidural anesthesia. In addition, complaints of numbness or pain may be dismissed as typical labor pains until more prominent symptoms of weakness develop hours later.

Possible risk factors for developing intrapartum/postpartum LSP include short maternal stature, large infant size, and prolonged or arrested labor [30,31,33-37]. Some [37,38], but not all [36], investigators have speculated that the use of forceps or other instrumentation is a possible risk factor. The number of previous pregnancies does not appear to be an independent risk factor for developing LSP [30].

Vaginal deliveries are not contraindicated in patients who develop antepartum or intrapartum LSP [39]. However, midforceps delivery is relatively contraindicated in intrapartum LSP.

Some patients with intrapartum/postpartum LSP will be mistakenly diagnosed with L5 radiculopathy or peroneal palsy at the fibular head. Thus, it is important to differentiate LSP from peroneal or femoral neuropathy due to prolonged positioning. Electrodiagnostic findings in antepartum and intrapartum/postpartum LSP will likely reflect lumbar plexus and lumbosacral plexus involvement, respectively. Cases of LSP with severe traction injury may have nerve root involvement with findings of paraspinal muscle denervation on EMG.

Prognosis and management — In modern series, nearly all patients with intrapartum/postpartum LSP have complete or near complete resolution of their symptoms within two to six months [30,40,41]. In reports published before 1960, some patients were left with persistent deficits [31,37].

The pathophysiologic correlate of intrapartum/postpartum LSP is probably a demyelinating lesion of the lumbosacral trunk as evidenced by electrodiagnostic findings of decreased motor unit action potential recruitment with relatively preserved compound muscle action potential amplitudes seen in the majority of patients and by the complete resolution of clinical symptoms over several months. Rare patients with more sustained or permanent deficits likely experienced axonal disruption.

Postoperative plexopathy — There are case reports of LSP due to gynecologic surgery, total knee arthroplasty, and lumbar spine surgery [39,42-44]. In some instances, postoperative plexopathy is probably the result of intraoperative patient positioning that leads to stretching, compression, transection, or ligation of plexus components. Postoperatively, scar or undetected hematoma formation may lead to LSP. In other cases, plexopathy appears to be caused by a postsurgical inflammatory neuropathy similar to lumbosacral radiculoplexus neuropathy by clinical and pathologic features, with findings on nerve biopsy that point to ischemic injury and microvasculitis [45-47]. (See "Diabetic amyotrophy and idiopathic lumbosacral radiculoplexus neuropathy".)

Vascular causes — Vascular etiologies of LSP include ischemia, hemorrhage, and direct compression by vascular structures. Retroperitoneal hematoma is an important vascular cause of LSP and is discussed in detail below. (See 'Retroperitoneal hematoma' below.)

Arterial pseudoaneurysms, a postoperative complication usually due to infection and/or defective vascular anastomosis in abdominal vascular surgeries, may cause LSP by direct compression of the lumbosacral plexus [48]. Aneurysm and pseudoaneurysm formation (with or without rupture) of the abdominal aorta; common, external, and internal iliac arteries; inferior and superior gluteal arteries; and hypogastric arteries have all been described as causes of LSP (image 3) [48-52]. Retroperitoneal hematoma predominantly affects the lumbar plexus, while iliac artery aneurysm or pseudoaneurysm is more likely to compress the lumbosacral or sacral plexus.

The rich vascular supply to the lumbosacral plexus makes ischemia of the plexus rather unusual. However, ischemic LSP has been reported in kidney transplantation, especially in those who have pre-existing atherosclerotic disease, due to transient hypoperfusion during arterial transposition or bypass [53,54]. Ischemic LSP has also been observed following embolization of an abdominal aortic aneurysm with persistent endoleak and surgical treatment of mesenteric artery thrombosis in the setting of pre-existing atherosclerosis and intraprocedural aortic cross-clamping [2,55]. Lastly, aortic dissection may be a cause of ischemia to the lumbosacral plexus [56].

Retroperitoneal hematoma — Retroperitoneal hematoma is an important vascular cause of LSP (image 4) [10,57,58]. Retroperitoneal hematoma typically occurs within the psoas muscle.

Smaller retroperitoneal hematomas predominantly compress the femoral nerve, while larger ones can affect the entire lumbar or upper plexus, leading to anteromedial thigh numbness and paresthesia as well as weakness of hip flexion, thigh adduction, and knee extension. Less often, a retroperitoneal hemorrhage will affect the entire lumbosacral plexus, causing a more confluent weakness and numbness of the ipsilateral leg.

LSP due to retroperitoneal hematoma may occur spontaneously but is best described as a sequela of femoral artery or vein catheterizations and concomitant anticoagulation. It has also been reported after lumbar plexus block for postoperative analgesia in hip surgery [59,60] and following femoral vein dialysis [57]. There is typically a delay of 2 to 10 days in presentation, likely due to postoperative institution of anticoagulant therapy. In addition, anticoagulant therapy alone has been associated with spontaneous retroperitoneal hematoma and LSP [61].

In a retrospective review of over 9200 femoral artery catheterizations, there were 45 cases of retroperitoneal hematoma, for an incidence of 0.5 percent [62]. Clinical manifestations of retroperitoneal hematoma included suprainguinal tenderness and fullness, severe back and lower quadrant pain, and femoral neuropathy in 100, 64, and 36 percent, respectively.

Among the 45 patients with retroperitoneal hematoma, 20 developed neuropathy, which was confined to the groin and involved cutaneous branches of the femoral nerve in four patients [63]. The remaining 16 patients had large retroperitoneal hematomas and sensory neuropathy in the femoral nerve distribution, while nine had motor deficits involving only the femoral nerve, and four had motor weakness involving femoral plus obturator nerve. Thus, among 45 patients with a retroperitoneal hematoma, a lumbar plexopathy involving femoral and obturator nerves developed in four patients (9 percent), while an isolated femoral neuropathy developed in 12 (27 percent).

Hematomas are visualized well by both CT and MRI, with CT more likely to demonstrate active bleeding sites and MRI allowing more characterization of the age of collected blood products [10].

LSP due to retroperitoneal hematoma must be differentiated from isolated femoral nerve compression due to hematoma formation at the inguinal ligament or mild retroperitoneal hematoma with fascial tracking of blood to the femoral nerve sheath. Under the inguinal ligament, the femoral nerve is more susceptible to injury due to limited extraneural space for blood products to expand and a relative paucity of microvasculature and lack of collateral blood flow. Concomitant involvement of the obturator nerve, manifested as weakness of adduction, points to a lumbar plexus lesion and excludes an isolated femoral neuropathy.

Prognosis and management — Retrospective data suggest that patients with LSP from a retroperitoneal hematoma generally have good neurologic recovery. As an example, in one study that reported 16 patients with large retroperitoneal hematomas and lumbar plexopathy, the only persistent sequelae at long-term follow-up were a mild sensory neuropathy in five patients and a mild motor deficit in one [63].

Treatment of retroperitoneal hematoma primarily consists of addressing the acute manifestations, such as hypovolemia and shock [57]. Rapid reversal of anticoagulation should be undertaken in patients with serious bleeding at any degree of anticoagulation. (See "Management of warfarin-associated bleeding or supratherapeutic INR", section on 'Serious/life-threatening bleeding'.)

Otherwise, management is usually conservative, consisting of bed rest and blood transfusion. Rarely, surgical evacuation has been performed for severe acute cases or in chronic, unresolved LSP [57]. There is no consensus regarding the utility of aggressive surgical intervention in patients with neurologic symptoms.

Infectious, inflammatory, and infiltrative causes — Other etiologies of LSP include infectious, inflammatory, and infiltrative disorders.

Infectious or parainfectious causes of LSP include direct infection or remote inflammatory effects of infection by such organisms as Borrelia burgdorferi, Mycobacterium tuberculosis, Treponema pallidum, varicella-zoster virus, HIV, Epstein-Barr virus, or cytomegalovirus [64-66].

Cytomegalovirus and HIV are typically associated with pure radicular syndromes. However, they can rarely cause a lumbosacral radiculoneuropathy that is similar to diabetic amyotrophy electrophysiologically [65]. In immunocompromised patients, a lumbosacral polyradiculoneuropathy has been observed with echovirus infection and Epstein-Barr virus reactivation.

Local abscess formation in the psoas muscles or nearby structures may lead to direct compressive effects on the lumbosacral plexus and subsequent LSP. Such cases have been reported in untreated tuberculosis and salmonella infections, but other organisms should be considered [67]. Abscesses can be adequately visualized by MRI or CT. With CT, gas collections are more easily seen, while bony destruction is more noticeable with MRI. Image-guided percutaneous drainage with CT can be used for both the diagnosis and treatment of abscess.

Inflammatory, infiltrative, or autoimmune causes of LSP are rare. However, atypical presentations of systemic and nonsystemic vasculitides, collagen-vascular disease, and sarcoid have been reported in association with LSP. Sjögren's disease, systemic lupus, and mixed connective tissue disorders do not typically cause LSP but should be considered in the differential diagnosis. They likely exert their effects on the plexus by causing a microvasculitis of the vasa nervorum. Sarcoidosis typically affects the cranial nerves and less often causes a length-dependent, symmetric polyneuropathy, but rarely may present as LSP [68]. Amyloidosis has also been implicated in rare cases of LSP [69]. Heroin injection has also been reported to cause LSP, purportedly by immunologically mediated mechanisms [70].

Initial electrodiagnostic findings in inflammatory or autoimmune causes of LSP may be normal or show only decreased motor unit recruitment on EMG.

SUMMARY

Anatomy – The lumbosacral plexus is formed from the anterior (ventral) rami of the L1 through S4 nerve roots (figure 1). The lumbar plexus is derived from the anterior rami of the L1 through L4 nerve roots, and the sacral plexus is derived from the anterior rami of the S1 through S4 nerve roots. (See 'Anatomy' above.)

The posterior branches of L2 through L4 become the femoral nerve and the anterior branches become the obturator nerve. The lumbosacral trunk is comprised of a portion of L4 nerve root anterior rami, all L5 anterior rami, and the anterior rami of the S1 through 4 nerve roots. The posterior branches of the lumbosacral trunk and S1 and S2 form the lateral or peroneal division of the sciatic nerve. The anterior branches form the medial or tibial division of the sciatic nerve. The lumbar plexus also gives off the lateral femoral cutaneous nerve of the thigh, iliohypogastric, ilioinguinal, and genitofemoral nerves while the sacral plexus also gives off the inferior and superior gluteal nerves, posterior cutaneous nerve of the thigh, and pudendal nerve. (See 'Anatomy' above.)

Clinical features – Lumbosacral plexopathy (LSP) most often presents with asymmetric, focal weakness, numbness, dysesthesia, and/or paresthesia in multiple contiguous lumbosacral nerve root distributions. (See 'Clinical features' above.)

Lumbar plexus lesions tend to cause weakness of hip flexion and adduction and/or knee extension.

Lumbosacral trunk and upper sacral plexus lesions result in foot drop or flail foot depending on the extent of involvement and weakness of knee flexion or hip abduction.

Diagnostic evaluation – The diagnostic evaluation of LSP typically includes electrodiagnostic studies, laboratory investigations, and neuroimaging.

MRI is the imaging method of choice for plexus evaluation given its versatility and anatomic detail. Electrodiagnostic studies can help differentiate LSP from lumbosacral radicular and individual nerve syndromes and may also provide clues to the intraplexus location and possible etiology. (See 'Diagnosis' above.)

Specific causes – The causes of LSP are numerous and diverse (table 1). Important considerations include the following:

Diabetic amyotrophy and idiopathic lumbosacral radiculoplexus neuropathy (see "Diabetic amyotrophy and idiopathic lumbosacral radiculoplexus neuropathy")

Neoplastic invasion (see 'Neoplastic invasion' above)

Radiation therapy (see 'Radiation plexopathy' above)

Trauma (see 'Trauma' above)

Pregnancy (see 'Peripartum plexopathy' above)

Surgery (see 'Postoperative plexopathy' above)

Vascular conditions, particularly retroperitoneal hematoma (see 'Vascular causes' above and 'Retroperitoneal hematoma' above)

Parainfectious, inflammatory, and infiltrative disorders (see 'Infectious, inflammatory, and infiltrative causes' above)

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Topic 5267 Version 23.0

References

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