Fall 2022

Contributed by: Olga Fedirchyk, MD, Lidia Cabañes-Martínez, MD, FACNS, Estrella Barrero Ruiz, MD, Clara Fernández Cortés, MD, Marta Del Alamo De Pedro, MD, Ignacio Regidor, MD, PhD

Case Presentation

Acute limb ischemia presenting as foot drop

Our patient is a 39 year-old man who went to Emergency Room (ER) in July 2021 with acute right drop foot.

Both his father and grandfather had premature death from coronary disease. Also, he has personal history of obesity (with BMI 34.2 kg/m2), arterial hypertension, coronary heart disease (lateral STEMI at age of 23) and high serum anticardiolipin antibodies (suspected, but not confirmed antiphospholipid syndrome). He denied smoking and alcohol consumption. He was receiving treatment with simvastatin, acetilsalycilic acid, clopidogrel, carvedilol, enalapril and pregabalin. Also, since 2019 he had two episodes of lumbar pain with irradiation to the right lower limb and was diagnosed with bilateral L5-S1 foraminal stenosis that was managed conservatively.

In March 2021 he returned to the ER due to acute and intense bilateral calf pain, which made it difficult for him to walk, that was preceded with a subtle bilateral foot paresthesia and weakness (two days before). His physician did not find any signs of deep venous thrombosis. An urgent blood analysis showed high C-reactive protein (63.3 mg/L). Other parameters, including creatine kinase (CK) levels, were all normal. He required opioid analgesia, but at the view of the positive response he was discharged with diagnostic of unspecific myalgia.

In July 2021 he was derived from outpatient Neurosurgery because of a right foot drop that started three days before. At admission his physical examination showed positive right straight leg rise (Lasègue sign) at 30º hip flexion and a significant weakness (2/5) on right ankle dorsal flexion. All reflexes were normal. An urgent MRI confirmed previous findings (bilateral L5-S1 right foraminal stenosis) and showed new findings: L4-L5 disc herniation and signs of local instability (L5 body anterolishesis) (figure nº1, left image).

The patient was hospitalized because of a need of dynamic lumbar spine complementary examinations in order to determine the urgency of the surgical treatment. In addition, his neurosurgeon requested an NCS/EMG study for to exclude other peripheral causes of foot drop. In our EMG lab, we first performed NCS. We did not obtain any sensory or motor evoked potentials (EP) on the right limb (right deep peroneal and suralis nerve EPs were absent and we obtained only a very low amplitude response from the right tibialis posterior nerve). All motor and sensory conductions on his left lower limb were completely normal (figure nº2).

We completed our exam with quantitative EMG, which revealed mild signs of denervation (fibrillation potentials and polyphasic MUPs) in right tibialis anterior and gastrocnemius medialis muscles, with reduced recruitment. We also performed needle EMG of right vastus medialis muscle and all parameters were normal. As these neurophysiological findings would not be completely explained by his lumbar stenosis, and would be more likely explained by a complete distal sciatic acute neuropathy, we performed a more detailed physical examination. We found a bilateral absence of pedis pulse with a subtle coldness of lateral dorsum of his right foot and 4º and 5º right toes. When we detected these signs suggestive of an ongoing vascular dysfunction, we called the neurosurgeon and vascular surgeon immediately and we decided that a more comprehensive EMG study was not necessary. The vascular surgeon performed a vascular Doppler without delay. He found a complete occlusion of right deep femoral, femoral superficial and popliteal arteries. In addition, there was a complete occlusion of his left popliteal artery. After that, an abdominal CT-angiography confirmed these findings (figure nº1, right image) and revealed subacute ischemia of the right renal inferior pole in addition to peripheral ischemia.

Finally, our patient was diagnosed with acute right limb and subacute left limb bilateral ischemia. 24 hours later he underwent a surgical right femoral thrombectomy. A few hours after surgery his right ankle mobility started to improve, but today he still needs physical therapy and a mild weakness (4/5) of his ankle dorsal flexor muscles persists. Acenocumarol was added to his treatment. At this time, the patient is under close follow-up by Rheumatology and Hematology, but the cause of his hypercoagulability is still unknown (serum levels of anticardiolipin and other frequent antibodies were now normal).

Foot drop syndrome is defined as a weakness of the dorsiflexor muscles of the foot. It is a frequent neurologic condition usually caused by peroneal neuropathy; other causes include L5 radiculopathies, sciatic neuropathy and lumbar plexopathy. Acute limb ischemia is a rapid decrease in the blood flow to the lower limb due to arterial occlusion, presenting with five “P”: pain, pulselessness, pallor, paresthesia and paralysis. Occlusion may be caused by an embolism or thrombosis, and without treatment it can lead to irreversible damage to the nerves and muscle tissue.  An accurate diagnosis is paramount to avoid irreversible changes due to ischemia. NCS/EMG studies are essential in the diagnosis of these patients, and this case illustrates that NCS and EMG can be very useful to characterize lesions even in not purely neurological conditions.

 

Figure 1 Label: Left image: spinal MRI (T2) shows L4-L5 disc herniation that involves right L5 spinal root, and L5-S1 foraminal stenosis. Anterolisthesis of L5 vertebral body. Right image: angioCT of lower limbs. Late venous phase shows no flow through femoral (above) and popliteal (below) arteries.

Figure 1 Image:

 

Figure 2 Label: NCS study that shows absence of sensory and motor EPs in right lower limb.

Figure 2 Image:

 

Question 1: Which of the following neurological conditions does not cause

1. L4-L5 foraminal stenosis
2. Ipsilateral lumbar traumatic plexopathy
3. Posterior cerebral artery stroke
4. Peroneal (deep fibular) neuropathy.