A 42-year-old woman with invasive carcinoma of the cervix presented with progressive pain and weakness in her left lower extremity of 2 months’ duration; she was referred for an EMG.
She had a history of heart disease and had had a coronary artery bypass graft 6 years previously. She had been on warfarin therapy for 1 month because of a recent deep venous thrombosis in the left leg.
Social history revealed no tobacco, alcohol, or illicit drug use. The family history was unremarkable for neurologic complaints. On review of systems she reported some weight loss and intermittent fever.
On physical examination, she was alert and oriented. There were no cranial nerve abnormalities. Severe pain in her left lower extremity interfered with her motor examination. She was felt to have 2/5 left hip flexor strength, 4−/5 knee flexor, 5/5 knee extensor, 5/5 plantar flexion, and 3+/5 dorsiflexion. Strength was normal in the right leg and the upper extremities. There was a sensory loss in the L5 dermatome distribution in her left lower extremity. She had no left patellar and ankle reflexes; these were normal on the right lower extremity. The rest of the neurologic examination was unremarkable. There was evidence of a well-healed old midline abdominal incision.
What is the Differential Diagnosis?
This patient had uterine cancer and a history of deep venous thrombosis for which she received anticoagulation. She presented with unilateral left leg pain and weakness which followed the territories of several myotomes, with absent knee and ankle reflexes representing roots at L2–L4 and S1 and a sensory deficit that seemed to correspond to the L5 dermatome. The possibility of tumor invasion of the lumbosacral plexus was very likely, but a retroperitoneal hematoma might also have a similar presentation, particularly in patients on anticoagulation. The lack of acute abdominal pain, however, is against this diagnosis. The lack of back pain is also against the possibility of tumor invasion of the lumbosacral spine, and she did not have involvement of the other leg to suggest meningeal carcinomatosis. The distribution findings could also suggest a mononeuritis multiplex, but the involvement is only of one limb.
A complete metabolic panel and FANA were normal. Hematocrit was 32% (normal, 36%–48%), and INR was 1.4 (normal, 1.4 or less).
An EMG Test was Performed
Nerve and Site | Latency(ms) | Amplitude (mV) | Conduction Velocity (m/s) |
---|---|---|---|
Peroneal Nerve L. | Normal ≤ 5.7 | Normal ≥ 3 | Normal ≥ 40 |
Ankle | 4.1 | 1 | – |
Fibular head | 11.8 | 1 | 39 |
Knee | 14.1 | 1 | 43 |
Tibial Nerve L. | Normal ≤ 5.3 | Normal ≥ 4 | Normal ≥ 40 |
---|---|---|---|
Ankle | 4.4 | 13 | – |
Pop. fossa | 13.5 | 8 | 43 |
Nerve and Site | Latency (ms) | Amplitude (mV) | Conduction Velocity (m/s) |
---|---|---|---|
Peroneal Nerve R. | Normal ≤ 5.7 | Normal ≥ 3 | Normal ≥ 40 |
Ankle | 4.1 | 8 | – |
Fibular head | 10.5 | 7 | 46 |
Knee | 12.7 | 7 | 50 |
Ankle, before exercise | 1 | – | – |
Ankle, posttetanic | 1 | – | – |
Nerve | Latency (ms) | Normal Latency ≤ (ms) |
---|---|---|
Peroneal nerve L. | NR | 54 |
Tibial nerve L. | 51.6 | 54 |
Peroneal nerve R. | 46.5 | 54 |
H-reflex L. | NR | 34 |
H-reflex R. | 29.6 | 34 |
Nerve | Onset Latency (ms) | Normal Onset Latency ≤ (ms) | Peak Latency (ms) | Normal Peak Latency ≤ (ms) | Amp (μV) | Normal Amp ≥ (μV) | Conduction Velocity (m/s) | Normal Conduction Velocity ≥ (m/s) |
---|---|---|---|---|---|---|---|---|
Sural nerve L. | 3.1 | 3.5 | 3.6 | 4.0 | 16 | 13 | 45 | 40 |
Superficial peroneal L. | 3.4 | 3.5 | 3.9 | 4.0 | 6 | 11 | 41 | 40 |
Sural nerve R. | 3.5 | 3.5 | 4.0 | 4.0 | 16 | 13 | 40 | 40 |
Superficial peroneal R. | 2.7 | 3.5 | 3.2 | 4.0 | 23 | 11 | 52 | 40 |

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