Ischemic Monomelic Neuropathy Workup

Updated: Jan 17, 2019
  • Author: Michael T Andary, MD, MS; Chief Editor: Dean H Hommer, MD  more...
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Approach Considerations

The proper diagnosis of ischemic monomelic neuropathy (IMN) as a vascular lesion can avoid incorrect classification of the injury as a plexus or a root lesion from trauma, as well as avoid incorrect positioning during surgery.

Depending on the clinical presentation, vascular studies that detect acute arterial occlusion may be useful. Because IMN usually is not the presenting problem but is instead a complication that occurs after previous arterial occlusion, work up and/or treatments (eg, arteriogram, surgeries) already have been completed. In chronic IMN, results from vascular studies are abnormal and show arterial occlusion in 1 leg.

In confusing clinical situations, imaging studies sometimes are necessary to rule out upper motor neuron problems (eg, stroke, spinal cord injury). Other imaging studies that can be helpful, depending on history, include arteriograms and venous or arterial Doppler studies. These tests can help to include vascular occlusion in or to exclude it from the diagnosis. With an arteriovenous fistula in the upper extremity, a Doppler study to assess for vascular patency can be helpful.

Hours to days after the onset of IMN, an elevated creatine kinase level can be noted from muscle necrosis.

Occasionally, compartment pressure measurements are indicated immediately following the ischemia if there is a concomitant compartment syndrome.

A study by Shin and Park indicated that because IMN is a potential complication of arterial occlusion, neurologic and electrophysiologic assessment can be used to evaluate peripheral arterial occlusive disease (PAOD). In the study, which involved 38 patients with PAOD, primary outcomes took the form of neurologic symptom and impairment scores for the lower extremities, and secondary outcomes were represented by nerve conduction study results. Among the findings, the investigators determined that neurologic symptom and impairment scores tended to be worse in female patients with old age, hypertension, a low body weight, a low body mass index, a reduced ankle-brachial index, and a poorer Fontaine classification (for peripheral arterial disease). [9]

IMN does not require any direct procedures, although various procedures may be needed to treat associated conditions. Tissue biopsies rarely are taken after IMN and are not reported to be helpful in its diagnosis.



Electrodiagnosis establishes the pattern of peripheral nerve injury. If the findings are not consistent with IMN, additional diagnostic studies may be warranted.

Upper extremity evaluation

Abnormalities are seen in a distal-to-proximal pattern, and the distal nerve supply is affected much more than any other. Radial, median, and ulnar sensory nerve action potentials (SNAPs) usually are absent from the respective digits. More proximal SNAPs (medial antebrachial cutaneous, lateral antebrachial cutaneous) are likely to be present.

Motor nerve conduction from the median and ulnar nerves to the hand muscles is absent or has a low amplitude. Nerve conduction velocities, when present, are spared to a relative extent.

Needle electromyography shows evidence for axonal loss with positive sharp waves and fibrillation potentials in the hand muscles (median and ulnar innervation). If the lesion is severe, there may be no recruitment or evidence of decreased (neuropathic) recruitment. Evidence for reinnervation can be seen months to years after the nerve injury, including large motor unit action potentials (MUAPs) and/or polyphasic motor units. In complete injuries, there is scarring in the muscle, with decreased insertional activity. Needle electromyography is typically normal or less severe in proximal muscles (forearm and upper arm). This clear distal-to-proximal gradient is in contrast to a brachial plexopathy.

For the diagnosis of IMN to be clear, one arm needs to demonstrate significantly more injury than the other arm. In cases of severe diabetic neuropathy, in which both arms are affected equally, it is essentially impossible to make the diagnosis of an IMN that is superimposed on a severe polyneuropathy. For example, it can be difficult to differentiate a lower trunk plexopathy from an IMN in the hand. A lower trunk plexopathy generally shows severe abnormalities in the intrinsic muscles of the hand on electromyography, low compound motor action potentials (CMAPs) from the median and ulnar nerves, and an absent SNAP.

The major differentiation in the hand is that, in a lower trunk plexopathy, the radial SNAP and median SNAPs to the fingers probably are spared, while the medial antebrachial cutaneous SNAP is absent. In IMN, the median and radial SNAPs are absent, and the medial antebrachial cutaneous SNAP is spared. With a lower trunk plexopathy, needle electromyography abnormalities in the flexor carpi ulnaris, triceps, and extensor indices are expected; in IMN, the abnormalities of these proximal muscles are absent or minimal.

Lower extremity evaluation

SNAPs to the sural and superficial peroneal commonly are absent. CMAPs to the abductor hallucis and peroneal nerve to the extensor digitorum brevis are either absent or low in amplitude. Nerve conduction velocities are relatively spared, if they can be measured. In IMN, H-reflexes and CMAPs elicited from the tibial nerve at the gastrocnemius and from the peroneal nerve at the anterior tibialis are frequently normal or near normal.

Needle electromyography frequently shows marked abnormalities consistent with axon loss in foot intrinsic musculature and lesser findings in the anterior tibialis, gastrocnemius, and soleus. Abnormalities in the quadriceps, hamstrings, or gluteal muscles generally are not observed, although they have been reported.

As in the upper extremity, differentiation of the normal limb from the abnormal limb is helpful in diagnosing IMN. In severe peripheral polyneuropathies, primarily distal ones, findings can be very similar or identical to those of IMN. The diagnosis of IMN is contingent on a normal or near-normal contralateral limb. Occasionally, distal aortic occlusion with saddle emboli can cause bilateral IMN, or use of the IABP pump in both legs can contribute. In mild cases of IMN, electromyographic abnormalities (positive sharp waves and fibrillation potentials) have been seen only in the foot intrinsic muscles.

Differentiation of IMN from an L5-S1 or S2 radiculopathy or sciatic nerve neuropathy can be difficult. In IMN, the distal L5-S2 muscles have severe abnormalities, while the more proximal L5-S1 (gluteus medius, tensor fasciae lata) are likely to be normal or have minimal abnormalities. The tensor fasciae lata or gluteal muscles rarely are involved in IMN; in an L5-S2 radiculopathy, the tensor fasciae lata and/or gluteus medius should show similar abnormalities to the more distal L5-S2 muscles. This finding differentiates IMN from a plexopathy or radiculopathy.

In chronic IMN, the most common electrodiagnostic abnormality is a decreased CMAP in the tibial nerve to the abductor hallucis. Because the disease is chronic, both of a patient's legs can be affected, and the sural responses may be abnormal unilaterally or bilaterally. Quantitative sensory testing results have been reported to be abnormal in the distal foot.

Absent responses are a poor prognosis.