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EMG for Sacral Plexopathy
Abstract & Commentary
By Michael Rubin, MD, Professor of Clinical Neurology, NewYork-Presbyterian Hospital, Weill Cornell Medical Center. Dr. Rubin is on the speaker's bureau for Athena Diagnostics, and does research for Pfizer and Merck.
Synopsis: EMG studies are helpful in a minority of patients with suspected sacral plexopathy. Clinical examination and imaging provide more useful information.
Source: Tavee J, et al. Pitfalls in the electrodiagnostic studies of sacral plexopathies. Muscle Nerve. 2007;35;725-729.
Are electrodiagnostic studies useful in the diagnosis of sacral plexopathy, allowing one to differentiate the former from sciatic neuropathy or radiculopathy? Retrospective review of 171 cases of suspected sacral plexopathy, seen at the Cleveland Clinic Foundation between 1975-2005, was undertaken to address this question. Each patient had been evaluated clinically, and electrodiagnostically by nerve conduction studies and needle electromyography (EMG). All patients experienced leg weakness, usually manifested as foot drop, hip, leg, or back pain, and occasionally distal sensory loss. Electrodiagnosis of sacral plexopathy was confirmed by EMG if patients demonstrated: (a) absent or reduced sural or superficial peroneal sensory amplitudes, (b) denervation potentials in muscles innervated by the sacral plexus but not by the sciatic nerve, and (c) normal paraspinal muscle EMG.
Using the above EMG guidelines, 60 patients (35%) had abnormalities localizing to the sacral plexus, most often due to cancer, usually gynecologic, colorectal, or prostatic, and including direct tumor invasion, radiation, or chemotherapy associated injury. Trauma, including motorcycle or motor vehicle accidents, gunshot wounds, and falls, was the 2nd most common cause of plexopathy, followed by idiopathic (n = 10, 17%) and iatrogenic (n = 8, 14%) etiologies. Vasculitis, viral, and autoimmune disorders were suspected to underlie the former, while the latter were seen following lumbar laminectomy, and aortic or cardiac surgery. Intrapartum injury (n = 4, 8%), diabetes (n = 2, 3%), herpes zoster (n = 1, 2%), or unknown (n = 4, 5%) was seen in the remainder.
Among the remaining 111 cases, lumbosacral radiculopathy or sciatic neuropathy could not be excluded based on electrodiagnostic studies, and no firm sacral plexus localization was possible. Plexus could not be differentiated from root disease in 52 (30%), most often due to the bilateral absence of sensory responses, either sural (69%) or superficial peroneal (63%). Paraspinal muscle fibrillation potentials (50%) and normal gluteal muscle EMG (67%) also prevented precise localization. Plexus could not be differentiated from high sciatic nerve in 32 (19%) due to normal gluteal muscle EMG in 79%. In 27 (16%), root vs. plexus vs. sciatic neuropathy were equal possibilities due to the variable combination of abnormalities on EMG. Definitive localization of sacral plexopathy is often impossible using EMG.
Truth be told, if a single test were warranted for the investigation of all cases of suspected lumbosacral radiculopathy, magnetic resonance imaging would be that test. Needle electromyography (EMG) records the physiologic extent of nerve injury, but usually does not affect decision making, as clinical evaluation suffices. Even in radiographic or surgically documented lumbar disc herniation, needle EMG shows no paraspinal abnormalities in approximately 50%, although estimates vary from 26% to 86%. It is not surprising that EMG often cannot localize sacral plexopathy, or separate it from radiculopathy or high sciatic neuropathy.