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Lumbosacral plexopathy is a neurological disorder resulting from injury or dysfunction of the lumbosacral plexus, a nerve network formed by the anterior rami of spinal roots L1 to S4, which may result in symptoms, eg, lower back and leg pain, motor weakness, sensory deficits (numbness, paresthesia), and in some cases, sphincter dysfunction. Though less common than brachial plexopathy, lumbosacral plexopathy can be debilitating and challenging to diagnose. This course examines this neurological condition, including the etiologies, pathophysiology, differential diagnoses, and various clinical presentations. Symptom onset may be acute or chronic, and physical findings vary depending on the severity and location of involvement, ranging from foot drop to specific patterns of muscle weakness and sensory loss. Prompt recognition and targeted therapy are essential to mitigate morbidity and improve patient outcomes. This activity for healthcare professionals is designed to enhance the learner's competence in identifying lumbosacral plexopathy, performing the recommended evaluation, and implementing an appropriate interprofessional approach when managing this condition. Objectives: Identify the etiologies associated with lumbosacral plexopathy. Assess the characteristic clinical features of lumbosacral plexopathy. Implement the optimal management approach for a patient with lumbosacral plexopathy. Apply interprofessional team strategies to improve care coordination and outcomes in patients with lumbosacral plexopathy. Access free multiple choice questions on this topic.

The lumbosacral plexus is a network of nerves formed by the anterior rami of the lumbar and sacral spinal cord, involving the L1 to S4 nerve roots. Lumbosacral plexopathy is an injury to the lumbar and sacral plexus nerves. Lumbosacral plexopathy is not an uncommon condition, but it can be difficult to diagnose and manage.[1] However, this condition is far less common than brachial plexopathy. Patients with lumbosacral plexopathy usually present with low back and leg pain. Patients may also experience motor weakness, other sensory symptoms of numbness, paresthesia, and sphincter dysfunction.[2][3] Lumbosacral plexopathy can be caused by multiple etiologies, with diabetes mellitus, traumatic injury, neoplasms, penetrating trauma, and pregnancy being a few of the primary causes. Treatment is often limited and varies significantly depending on the underlying pathology.[4] Lumbosacral plexopathy can be debilitating, severely affecting a patient's quality of life. Therefore, early identification and initiation of effective management are critical in reducing morbidity and mortality.[5]

Anatomical Overview The lumbosacral plexus is a combination of lumbar and sacral plexuses and encompasses the anterior rami of the L1 through S4 nerve roots of the peripheral nervous system, with a small contribution from T12 as well. The lumbar plexus lies above the pelvic brim and forms from L1 through L4 nerve roots, while the S1 through S4 nerve roots make up the sacral plexus, which lies below the pelvic brim. Lumbar plexus The lumbar plexus is formed by the anterior rami of the first 4 lumbar nerves, which descend through the psoas muscle and bifurcate into anterior and posterior divisions. These divisions subsequently branch out to form the individual nerves of the plexus. Specifically, the femoral nerve originates from the posterior divisions of the L2 to L4 nerve roots, whereas the obturator nerves are derived from their anterior counterparts. Additional components of the lumbar plexus include the iliohypogastric nerve (T12-L1), ilioinguinal nerve (L1), genitofemoral nerve (L1-L2), and lateral femoral cutaneous nerve of the thigh (L2-L3). The sciatic nerve, a major nerve of the lower limb, incorporates fibers from both the anterior and posterior divisions of the lumbosacral trunk, along with the S1 and S2 anterior rami. Sacral plexus The sacral plexus is primarily composed of the superior gluteal (L4-S1), inferior gluteal (L5-S2), posterior femoral cutaneous of the thigh (S1-S3), and pudendal nerve (S1-S4). The vascular supply to the lumbosacral plexus is provided by 5 lumbar arterial branches from the abdominal aorta, complemented by the deep circumflex iliac artery, the iliolumbar artery, and the gluteal branches of the internal iliac artery. This anatomical configuration is extensively documented and illustrated in several studies.[3][6][7] Lumbosacral Plexopathy Etiologies Since the lumbosacral plexus is present near abdominal and pelvic organs, various pathologies and injuries contribute to lumbosacral plexopathy, including: Direct trauma Posterior hip dislocation Sacral fracture After lumbar plexus block Metabolic, inflammatory, and autoimmune causes [8][9][10] Diabetes (more likely in those with type II diabetes, ie, diabetic amyotrophy) [11] Amyloidosis Sarcoidosis Post Sars CoV-2 infection (has been reported for brachial, but clinically has been seen in the lumbosacral plexus) [12] Infections and local abscess [13] Vertebral osteomyelitis Chronic infections (eg, tuberculosis, fungal infections)

Diabetes (more likely in those with type II diabetes, ie, diabetic amyotrophy) [11] Amyloidosis Sarcoidosis Post Sars CoV-2 infection (has been reported for brachial, but clinically has been seen in the lumbosacral plexus) [12] Infections and local abscess [13] Vertebral osteomyelitis Chronic infections (eg, tuberculosis, fungal infections) Other infections, eg, Lyme disease, HIV/AIDS, herpes zoster, COVID-19 Psoas abscess with extension (Please see StatPearls' companion resource, "Psoas Syndrome", for further information on psoas abscess) Radiation therapy of the abdominal and pelvic malignancies [14][14] Pregnancy-related causes (mostly occur in the third trimester and after delivery due to birth trauma) [15] Femoral vessel catheterization Ischemia from direct compression (eg, arterial pseudoaneurysms, aortic dissection, and retroperitoneal hematoma) [16] Psoas muscle metastatic disease (endometrioid adenocarcinoma) mimicking a psoas abscess with resultant lumbosacral plexopathy [17] [17]Damage to the vasculature innervating the lumbosacral plexus Postoperative plexopathy (scar tissue formation and hematomas may occur following gynecological and other pelvic surgeries) [18] Cocaine with rhabdomyolysis [19] Toxicities from antineoplastic drugs (ie, ladiratuzumab vedotin) [20]

Lumbosacral plexopathy presents a complex epidemiological profile due to its varied etiologies, influencing both the age of onset and overall prevalence. Typically, the median age at diagnosis across all causes is approximately 65 years. Women are disproportionately affected by lumbosacral plexopathy, largely attributed to risk factors, eg, pregnancy and gynecological cancers. Diabetic amyotrophy specifically shows an incidence rate of 4.2 per 100,000 annually [1], affecting 0.8% of individuals diagnosed with diabetes mellitus.[21] Among these patients, the median duration of diabetes before the onset of amyotrophy is 4 years, with a median hemoglobin A1c value of 7.5% at diagnosis.[9][22] Neoplastic cases of lumbosacral plexopathy predominantly involve the L4 to S1 segments in over 50% of cases, with the L1 to L4 segments affected in 31%, and panplexopathy in approximately 10% of cases.[23] In 73% of these cases, the plexopathy is associated with local compression or invasion by an abdominopelvic malignancy. Notably, lumbosacral plexopathy manifests within a year of diagnosing primary tumors in over one-third of the affected patients, and in 15% of these cases, the plexopathy itself leads to the cancer diagnosis.[24][25] Traumatic incidents also contribute to lumbosacral plexopathy incidence, with about 0.7% following traumatic pelvic fractures, and increasing to 2% following postsacral fractures.[26] Additionally, lumbosacral plexopathy occurs in approximately 1 in 2000 to 6400 deliveries.[27] Furthermore, the incidence of retroperitoneal hematoma following femoral artery catheterization stands at only 0.5%. However, about 20% of these cases develop subsequent femoral neuropathy, and 9% progress to lumbosacral plexopathy.[28]

The pathophysiology of lumbosacral plexopathy varies based on the following etiologies: Trauma (ie, injury or traction on the plexus) Tumor, eg, infiltration by the tumor or metastasis, intraneural lymphomatosis, the perineural spread of prostate cancer Radiation (endothelial damage leading to chronic inflammatory cell migration and a state of fibrosis, followed by an irreversible state of microvascular injury and ischemic damage) Hematoma due to compression of the nerve plexus Diabetic and nondiabetic lumbosacral plexopathy caused by inflammatory or microvascular changes Vascular endoleak complication after an endovascular aneurysm repair [29]

In cases of malignancy extending to and causing plexopathy, the histopathology of the malignancy would be determined by biopsy, potentially receptor tested, and treated based on the oncologic standard of care for that case.

A comprehensive clinical history and meticulous physical examination are essential for diagnosing lumbosacral plexopathy. Typically, patients report low back pain that radiates to 1 side, often exacerbated in a supine position. However, bilateral lumbosacral plexopathy has been reported in sarcoidosis as well as pregnancy.[30] Clinical History The clinical presentation can vary secondary to the underlying etiology. Patients with diabetic lumbosacral plexopathy usually experience unilateral pain in the proximal thigh, accompanied by numbness, paresthesias, or dysesthesias in the lower limbs, predominantly on 1 side. Conversely, lumbosacral plexopathy resulting from radiotherapy often manifests without pain. Furthermore, the symptom onset can range from acute (eg, motor vehicular collisions) to chronic, as seen after radiotherapy. In severe cases, muscle weakness and atrophy may be noted. While sphincter dysfunction is uncommon, its presence could indicate cauda equina syndrome.[31] Systemic symptoms, eg, fever, chills, night sweats, fatigue, and weight loss, may indicate underlying malignancy or infection. Pertinent history may include exposure to factors, including road traffic accidents, abdominopelvic neoplasms, radiotherapy, abdominal surgery, diabetes mellitus, bleeding disorders, or recent pregnancy, which can guide the identification of the etiology of lumbosacral plexopathy. Physical Examination Physical examination findings vary; mild cases may appear normal, whereas trauma cases might show bruises. The straight leg raise test is often positive in over half the patients. Asymmetric lower limb muscle weakness and correspondingly diminished or absent deep tendon reflexes may be noted, with the knee jerk reflex commonly impacted in lumbar plexopathy and the ankle jerk reflex in sacral plexopathy. Muscle weakness involving hip flexion, knee extension, or adduction could indicate damage to the lumbar plexus. During a physical exam, acute or chronic foot drop is the most common initial sign of ALS.[32]

Physical examination findings vary; mild cases may appear normal, whereas trauma cases might show bruises. The straight leg raise test is often positive in over half the patients. Asymmetric lower limb muscle weakness and correspondingly diminished or absent deep tendon reflexes may be noted, with the knee jerk reflex commonly impacted in lumbar plexopathy and the ankle jerk reflex in sacral plexopathy. Muscle weakness involving hip flexion, knee extension, or adduction could indicate damage to the lumbar plexus. During a physical exam, acute or chronic foot drop is the most common initial sign of ALS.[32] Sensory loss may follow a dermatomal pattern for proximal lumbosacral plexopathy involving nerve roots or a nerve distribution pattern. Sensory alterations in the medial thigh, anterior thigh, and medial leg suggest lumbar plexus involvement, whereas changes in the posterior thigh, dorsum of the foot, and perineum point to sacral plexus involvement. Spinal point tenderness is notable in cases of sacral fracture or infection. During examination, a rectal exam is advisable to assess rectal tone. Although rare, saddle anesthesia and bowel or bladder incontinence may also occur, complicating differentiation from cauda equina and conus medullaris syndromes. The inguinal region should be palpated for potential hematomas.

Neuroimaging, specifically magnetic resonance imaging (MRI) of the lumbosacral spine, and electrodiagnostic studies, eg, nerve conduction study and electromyography, are essential in the confirmation of the diagnosis of lumbosacral plexopathy. Imaging Studie MRI with gadolinium contrast is the best test for the evaluation of the lumbosacral plexus. When contraindications to MRI (eg, a noncompatible pacemaker) are identified, a computed tomography (CT) scan with contrast can be utilized.[33][34] MR neurography is a useful modality compared to traditional MRI in lumbosacral plexopathy evaluation. Neurography helps identify extraspinal injuries responsible for neuropathic leg pain.[34] Recently, high-resolution ultrasounds have also been shown to be an excellent alternative for dynamic evaluation and visualization of the nerve architecture, and can be used as an affordable first step for diagnosticians trained in ultrasound imaging.[35] In cases of malignancy, differentiating direct compression from metastatic disease can be challenging. Thus, advanced imaging is often needed.[36] MRI is often ordered for the initial evaluation of neoplasm-associated lumbosacral plexopathy. Positron emission tomography (PET) is used to determine the full extent of malignancy.[25] PET scans also help in staging the disease, subsequent treatment, and prognosis. Electrodiagnostic Studies Electrodiagnostic studies, eg, electromyography (EMG), help differentiate lumbosacral plexopathy from other types of neuropathy or radiculopathies. Electromyography helps in the localization of neurological injury. EMG can also help differentiate malignancy from radiation-induced plexopathy.[37][38] Myokymic discharges occur in cases of radiation-induced plexopathy but do not occur in cases of neoplasm. Myokymia is the spontaneous burst of an individual motor unit. These bursts occur several times per second and rhythmically. Denervation of the paraspinal muscles is commonly seen in radiculopathy and helps to differentiate from lumbosacral plexopathy.[2] Magnetic nerve root stimulation can aid in the diagnosis of patients with contraindications to EMG (eg, bleeding disorders). The use of magnetic root stimulation for a more extensive analysis of nerve root damage has been reported in challenging cases of lumbosacral plexopathy.[39] Laboratory Investigations

Electrodiagnostic studies, eg, electromyography (EMG), help differentiate lumbosacral plexopathy from other types of neuropathy or radiculopathies. Electromyography helps in the localization of neurological injury. EMG can also help differentiate malignancy from radiation-induced plexopathy.[37][38] Myokymic discharges occur in cases of radiation-induced plexopathy but do not occur in cases of neoplasm. Myokymia is the spontaneous burst of an individual motor unit. These bursts occur several times per second and rhythmically. Denervation of the paraspinal muscles is commonly seen in radiculopathy and helps to differentiate from lumbosacral plexopathy.[2] Magnetic nerve root stimulation can aid in the diagnosis of patients with contraindications to EMG (eg, bleeding disorders). The use of magnetic root stimulation for a more extensive analysis of nerve root damage has been reported in challenging cases of lumbosacral plexopathy.[39] Laboratory Investigations Recommended blood tests to identify the etiology in patients with lumbosacral plexopathy should include a complete blood count with an erythrocyte sedimentation rate, C-reactive protein, coagulation studies, autoantibodies testing (eg, antinuclear antibodies, antineutrophil cytoplasmic antibodies, anti-Sjögren-syndrome-related antigen A, and anti-Ro/anti-La antibodies), and hemoglobin A1c. Furthermore, serum protein electrophoresis, angiotensin-converting enzyme levels, human immunodeficiency virus (HIV), Lyme antibodies, rapid plasma reagin, and Epstein-Barr virus serology may be indicated for specific cases.[40] Additional Diagnostic Studies If the cause of lumbosacral plexopathy is still not identified despite the above investigations, it indicates the need for a lumbar puncture. When malignancy is found, a biopsy of pelvic organs, as well as a biopsy of the suspected affected nerve root, is needed. Sciatic nerve fascicular biopsies aid in diagnosis for complex cases and cases of suspected malignancy present in the sciatic nerve distribution.[41] Biopsy Biopsy may be indicated in indeterminate masses compressing or metastasizing to the lumbosacral plexus. This may also be for aspiration for organisms for culture and sensitivity in the case of infectious etiology, or histopathology in the cases of malignancy. Although intramuscular metastasis is rare, sporadic cases have been documented.

The treatment of lumbosacral plexopathy primarily comprises therapy tailored to the specific underlying cause and symptomatic relief. Supportive Treatments Supportive therapies typically involve the administration of analgesics and muscle relaxants, including non-steroidal anti-inflammatory drugs (NSAIDs), pregabalin, gabapentin, duloxetine, amitriptyline, and opioids. For patients experiencing foot drop, ankle-foot orthoses may be beneficial. In cases of infection, appropriate antibiotics and antifungals are necessary. Etiology-Specific Therapies Diabetic amyotrophy, often transient, generally improves with effective glycemic control. Neuropathic pain management strategies are recommended for symptomatic relief in these patients.[4][42] Treatment options that may be considered in persistent, severe cases include steroids, intravenous immunoglobulin (IVIG), cyclophosphamide, and plasma exchange.[40] In malignancy-associated lumbosacral plexopathy, excision or appropriate management of the primary tumor is critical. For severe symptomatic cases, dorsal rhizotomy may be performed, which has been shown to significantly reduce pain and decrease opioid dependence in terminally ill patients.[43] Radiation-induced plexopathy, often manifesting as painless weakness and sensory changes, usually occurs bilaterally and can appear years following radiation exposure.[44] No effective treatments for radiation-induced plexopathy have been established; thus, physiotherapy and rehabilitation are emphasized, and any further radiotherapy should be avoided. Surgical intervention, eg, nerve repair techniques and nerve grafting, has shown promising results in improving muscle function following pelvic fractures. A small study involving 10 patients with traumatic lumbosacral plexopathy reported significant muscle function improvement at a 38-month followup after undergoing nerve grafting.[45][46] For patients with a retroperitoneal hematoma, conservative management typically includes blood transfusions and bed rest. Surgical intervention may be necessary if the hematoma worsens or if neurological function deteriorates.[47]

Differential diagnoses that should also be considered when evaluating lumbosacral plexopathy include: Cauda equina syndrome Conus medullaris syndrome Hereditary sensory and motor neuropathy (also called Charcot-Marie-Tooth disease) Lumbosacral radiculopathy Mononeuropathies (eg, Femoral neuropathy, sciatic neuropathy, and common femoral neuropathy) Polyneuropathy (eg, diabetic neuropathy, chronic inflammatory demyelinating neuropathy, and drug-related neuropathy) Spinal canal stenosis Spinal cord tumors Malingering Somatization disorder Vascular Arterial Insufficiency

Prognosis depends upon the underlying etiology, its response to treatment, and the timing of therapeutic intervention. Prognosis is good for patients with lumbosacral plexopathy secondary to pregnancy, retroperitoneal hematoma, and diabetic amyotrophy. The majority of patients with pregnancy-related lumbosacral plexopathy have a complete resolution of their symptoms 2 to 6 months following delivery.[15][48] Progressive neurological deterioration is common in patients with lumbosacral plexopathy secondary to malignancy. Prognosis is abysmal in neoplastic instances, with a mean survival of 6 months. Lymphoma has been demonstrated to be the most responsive tumor to therapy.[23] At 42-month follow-up, 86% of patients diagnosed with lumbosacral plexopathy secondary to malignancy had died. Traumatic lumbosacral plexopathies are generally considered to have an unfavorable prognosis, but a case series of 72 patients with traumatic lumbosacral plexopathies demonstrated that more than two-thirds (about 70%) of patients recovered spontaneously within 18 months.[49]

Complications associated with lumbosacral plexopathy include: Progressive neurological deterioration Intractable pain, eg, chronic pain syndrome Bedsores Recurrent infections Joint contractures Depression Arterial vascular insufficiency Reflex sympathetic dystrophy

The patient should be educated about the nature of the disease and the underlying etiology. As previously discussed, lumbosacral plexopathy secondary to pregnancy, retroperitoneal hematoma, and diabetic amyotrophy are usually transient and improve with time. Patients with malignancy should be counseled and advised for further workup and management. Symptoms can worsen over time, requiring the patient to have assistance with ambulation and activities of daily living.

Lumbosacral plexopathy may mimic dermatomal distributions. The initial presentation may be foot drop. More ominous pathologies (eg, malignancy and Lou Gehrig’s disease) are in the differential. Women are at greater risk than men. A thorough history of previous malignancies as well as risk factors for current malignancy should be performed in addition to risk factors for abscess, including intravenous drug use, previous spine injections, especially discograms. The clinician should have a low threshold for MRI with contrast. Treatment should be directed at the primary ideology. Rehabilitation efforts will be directed at the impairment and attempts to minimize disability as a result of the impairment.

Effective management of lumbosacral plexopathy hinges on the collaborative efforts of a diverse interprofessional team. Physicians, including primary care clinicians, neurologists, and pain specialists, play a central role in diagnosing the condition, identifying its etiology, and formulating a comprehensive treatment plan tailored to the patient's clinical presentation. Radiologists contribute to the interpretation of advanced imaging modalities, eg, MRI and MR neurography, to localize nerve involvement. Advanced practitioners and nurses are instrumental in monitoring symptom progression, administering therapies, and providing ongoing education to patients and families. Their responsibilities include promoting adherence to medication regimens, coordinating follow-up care, and monitoring for complications such as falls or worsening neurological function. Pharmacists ensure safe and effective use of medications, particularly when managing complex pharmacological regimens for pain control, including opioids, anticonvulsants, and antidepressants. Physical and occupational therapists are essential in improving functional outcomes by developing personalized rehabilitation programs that promote mobility and independence in daily activities. Mental health professionals, eg, psychiatrists and counselors, address psychological sequelae like depression and anxiety, which often arise from chronic pain and disability. Ongoing interprofessional communication is critical in aligning goals, sharing patient progress, and adjusting care plans proactively. Care coordination not only improves patient safety and outcomes but also enhances team performance by fostering a unified, patient-centered approach that prioritizes quality of life and long-term function.