Several principles of electrodiagnosis in lumbosacral plexopathy are similar to those described in the evaluation of brachial plexus lesions. The anatomy of the lumbosacral plexus is more straightforward; again, considering lumbar and sacral plexus separately is helpful. In general, lesions tend to affect either one but rarely both the lumbar and sacral plexus. In cases of lumbar plexopathy, the patient generally presents with quadriceps weakness and the differential diagnostic considerations are femoral neuropathy versus high lumbar radiculopathy (L2-3). The involvement of obturator-innervated muscles localizes a lesion outside of the femoral nerve territory; to distinguish lumbosacral plexopathy from radiculopathy, the saphenous SNCS should be performed and paraspinal EMG is important.
A patient with a lesion of the sacral plexus will often present with foot drop (inability to dor-siflex the foot) or a flail foot (inability to dorsiflex or plantar flex the foot), and the differential diagnostic considerations include peroneal neuropathy, sciatic neuropathy, and lumbosacral radiculopathy. Weakness outside of the ankle dorsiflexors and foot evertors (involving tibial-innervated muscles such as tibialis posterior and gastrocnemius) indicates a lesion proximal to the peroneal nerve while weakness of gluteal muscles indicates a lesion proximal to the sciatic nerve, involving either plexus or nerve roots.
Routine MNCS of the peroneal and tibial nerves evaluate only the sacral plexus. As lumbosacral plexopathies may superficially resemble peroneal neuropathy, it is important to exclude focal lesions of this nerve, most commonly occuring at the fibular neck. This includes peroneal MNCS recording tibialis anterior if no CMAP is obtainable from extensor digitorum brevis.
Because of their proximal location, the muscles innervated by the lumbar plexus are technically difficult to evaluate with MNCS. A CMAP may be recorded from quadriceps, stimulating femoral nerve at the level of the inguinal ligament. Side-to-side comparison is the most reliable means of obtaining a relative normal value for amplitude. While this may be helpful in demonstrating axonal loss, one can obtain evidence for this from the needle EMG of the quadriceps; thus, femoral MNCS is not commonly performed in the evaluation of lumbar plexus lesions.
As in brachial plexopathy, SNCS are a key tool in the assessment of lumbosacral plexus lesions; however, there are important issues which complicate both the performance and the interpretation of SNCS in the lower extremities. First, it is technically difficult and almost impossible to elicit responses from some of the nerves arising from the lumbar plexus, such as the iliohypogastric, genitofemoral, and ilioinguinal nerves. While sensory responses from the lateral femoral cutaneous and saphenous nerves can be obtained, it is often with significant difficulty, even in normal subjects; as previously emphasized, side-to-side comparison is necessary. Sensory responses representing sacral plexus dermatomes (i.e., superficial peroneal and sural) are more easily obtainable and extremely helpful in the evaluation of sacral plexus lesions.
Another complicating issue which frequently influences the electrodiagnostic evaluation of this region is the presence of underlying polyneuropathy, a common finding in the population of patients seen in the EMG laboratory. Abnormalities due to polyneuropathy will affect SNCS most significantly; in some cases, SNAPs are absent, significantly hindering lesion localization. However, when milder polyneuropathy is present, the finding of an asymmetrically reduced SNAP in the involved lower extremity is a useful, localizing finding.
As in brachial plexopathy, late responses may provide information about proximal conduction in the tibial and peroneal nerves; however, abnormalities are not specific for localization to the plexus. Still, F-response abnormalities may be an early finding in lumbosacral plexopathy.
EMG is one of the most important electrodiagnostic tests in the evaluation of lumbosacral plexopathy. As in the upper extremity, a plexus lesion will produce abnormalities in multiple nerve and root territories, largely sparing related paraspinal muscles. Therefore, muscles from different myotomes supplied by different peripheral nerves need to be evaluated, and the sampling should include those innervated by both the lumbar and sacral plexus. When evaluating the lumbar plexus it is useful to examine muscles innervated by the femoral nerve and obturator nerves, as well as the iliopsoas and the high lumbar paraspinal muscles (Table 1). Lumbar plexus lesions are differentiated from femoral neuropathy by the presence of EMG abnormalities in the obturator-innervated adductor longus muscle, in addition to the quadriceps. The finding of abnormalities restricted to the iliopsoas and quadriceps is considered evidence of a femoral neuropathy, because the nerves innervating these muscles run in very close proximity one another, even though, strictly speaking, the branch to iliopsoas comes directly from the lumbosacral plexus rather than the femoral nerve.
In the evaluation of the sacral plexus, the electromyographer examines muscles innervated by peroneal and tibial divisions of the sciatic nerve in multiple myotomes both below and above the knee, followed by gluteal-innervated muscles, and followed finally by lower paraspinal muscles. For example, to distinguish between peroneal neuropathy and more proximal lesions causing foot drop, i.e., sciatic neuropathy or lumbosacral plexopathy, EMG abnormalities are sought in the short head of the biceps femoris (peroneal division of the sciatic nerve, above the knee) in addition to the tibial-innervated tibialis posterior. Additional abnormalities in gluteal-innervated muscles then help localize the lesion to the sacral plexus, proximal to the sciatic nerve.
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