The lumbosacral plexus is formed from the L1–S3 nerve roots. It is divided into an upper component (the lumbar plexus), which innervates hip flexion, hip adduction, and knee extension, and a lower component that innervates hip extension, hip abduction, knee flexion, and all ankle and toe movements. Lumbosacral plexus syndromes are an uncommon cause of leg weakness and numbness. As a general rule, it is much more likely that a patient with these symptoms has a lumbosacral radiculopathy (or multiple radiculopathies) or multiple mononeuropathies. Nevertheless, lumbosacral plexus syndromes are important to identify, as the causes and evaluation differ from that with radiculopathy or mononeuropathy.
While an L5 or S1 radiculopathy can usually be distinguished from a lower lumbosacral plexus lesion based on the clinical examination, an upper lumbosacral plexus lesion (lumbar plexus) usually cannot be differentiated from an L3 or L4 radiculopathy. Nerve conduction studies and needle electromyography (NCS/EMG) are necessary to confirm the localization to the lumbosacral plexus. NCS shows normal sensory responses in the setting of radiculopathy, whereas in a lumbosacral plexus lesion the amplitude of the saphenous sensory response is reduced when the upper portion is involved and the amplitudes of the sural and superficial peroneal sensory responses are reduced when the lower portion is involved.
An ischemic lumbosacral plexopathy should be considered following any surgical procedure that requires cross-clamping of the aorta, such as aortic aneurysm repair or kidney transplant.
Radiation plexopathy typically arises months to years after local radiation therapy. Symptoms progress slowly for years, and these patients often have minimal or no pain, which distinguishes it from other causes of plexopathy. The finding of myokymia on needle EMG is seen in some cases, though the absence of myokymia does not exclude radiation plexopathy.
Malignancies most often involve the lumbosacral plexus by direct tumor extension. The most commonly involved tumors arise from local tissues: colorectal, ureteral, bladder, cervical, uterine, ovarian, vaginal, testicular, penile, and prostate carcinomas and retroperitoneal or pelvic sarcomas. Distant malignant spread can also occur with common cancers, such as breast and lung carcinoma. Lymphoma can directly infiltrate the plexus or cause compression injury.
Inflammatory serologies should include Sjogren’s Syndrome anti-RO/anti-LA antibodies (SSA/SSB), antinuclear antibody (ANA), and anti-neutrophil cytoplasmic autoantibody (ANCA); erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), angiotensin-converting enzyme (ACE), and serum protein electrophoresis (SPEP) with immunofixation should also be tested. Testing for human immunodeficiency virus (HIV), Epstein-Barr virus (EBV), cytomegalovirus (CMV), varicella-zoster virus (VZV), syphilis, Lyme disease (if in an endemic area), and tuberculosis should be considered. Cerebrospinal fluid (CSF) should be evaluated, including cytology and flow cytometry.
Diabetic amyotrophy, also known as diabetic radiculoplexus neuropathy or Bruns-Garland syndrome, typically presents as severe asymmetric pelvic and leg pain followed by weakness in the proximal leg, though symptoms may also involve distal muscles. It is often seen in diabetic patients with recent improvement in glycemic control or who have had weight loss. Symptoms usually progress over several weeks and may spread to involve the contralateral limb. Improvement is gradual and incomplete in most patients. While the underlying mechanism is uncertain, some evidence suggests nerve damage due to ischemic microvasculitis. CSF protein may be elevated in patients with diabetic amyotrophy, though mild CSF protein elevation can also be seen in unaffected diabetic patients. There are no proven treatments for diabetic amyotrophy, though brief corticosteroid tapers are used by some providers to address severe neuropathic pain. Neuropathic pain agents are often used, and brief treatment with narcotic analgesics may be considered in the acute phase of the illness.
Rarely, atypical presentations of inflammatory disorders, direct infection, or latent effects of infectious agents may cause lumbosacral plexopathy. Such inflammatory disorders include vasculitides and sarcoidosis or, even less commonly, Sjögren syndrome, systemic lupus, and mixed connective tissue disease. Amyloidosis has also been implicated in rare cases. Infectious etiologies include HIV, EBV, CMV, VZV, Lyme disease, tuberculosis, and syphilis. Local abscess formation can also lead to direct compressive effects on the lumbosacral plexus.
Idiopathic lumbosacral radiculoplexus neuropathy is similar to diabetic amyotrophy with respect to its pathophysiology, clinical features, prognosis, and management. CSF protein may be elevated in some, though not all, cases.