Ischemic monomelic neuropathy obscured by diabetes and stroke after thoracic endovascular aortic repair ======================================================================================================= * Ahmad J. Abdulsalam * Biju Gopinath * Buthaina M. Alkandari * Diaa Shehab * Salem A. Alkandari **A** 58-year-old male was transferred to the emergency department with back pain after a traffic accident. On arrival, his heart rate was 80 beats per minute, blood pressure was 115/65 mmHg, and oxygen saturation was 97%. His level of consciousness, based on the Glasgow Coma Scale, was E 2, V 4, M 6. He showed slight confusion but could communicate and interact. Past medical history revealed that he was a smoker and hypertensive, with poorly controlled diabetes. He had no known history of vascular disease. Chest computed tomography (CT) showed a large saccular aneurysmal dilatation in the thoracic aorta, just distal to the left subclavian artery (LSA) (type B). Minutes after the CT scan, the patient went into frank shock (arterial pressure: 50/30 mmHg). Therefore, he was placed under general anesthesia in the angiography room and underwent an emergency thoracic endovascular aortic repair (TEVAR). During the repair, due to a non-sufficient length of the proximal landing zone, the LSA was covered. The proximal landing zone was set to be between the left common carotid artery and the LSA. A stent graft was subsequently fully deployed (Valiant Captivia Medtronic Proximal Freeflo, straight, 22 mm×152 mm). An angiogram showed persistent slow filling of the LSA from the arch, with no evidence of endoleak or antegrade flow (Figure 1A). Late flow was noted into the LSA from the left vertebral artery. ![Figure 1](http://nsj.org.sa/https://nsj.org.sa/content/nsj/26/3/300/F1.medium.gif) [Figure 1](http://nsj.org.sa/content/26/3/300/F1) Figure 1 - Post-TEVAR CT MIP images demonstrating a) proper apposition of the graft, b,c,d) MRI brain (diffuse weighted images) revealing small high signal intensity lesions of both cerebral hemispheres. Subsequent to the procedure, the patient was shifted to the ICU due to hypotension (arterial pressure: 80/50 mmHg). One day later, the patient complained of left-sided weakness, numbness, and pain in the upper limb, along with reduced grip strength and arm and wrist movement. Examination revealed a 3/5 reduction in motor power in the left upper limb including shoulder abductors, elbow flexors, elbow extensors, wrist flexors, wrist extensors, with finger flexors, finger extensors. In the left lower limb, including the hip flexors/abductors, knee flexors and extensors and ankle plantar and dorsiflexors, the motor power was 4/5. Deep tendon reflexes were brisk on the left side and the plantar reflexes were upgoing. Sensation was also impaired in the whole left upper limb, accompanied by a stocking-glove pattern in all four limbs. A brain CT showed multiple ill-defined hypodensities. A follow-up MRI revealed three acute lacunar infarctions in the right parietal and left occipital lobes (Figure 1B, C, D). The patient was therefore diagnosed with a stroke after the TEVAR. The stocking-glove pattern and decreased sensation in the left upper limb prompted electromyography and nerve conduction studies (NCSs) 1 month later (Table 1). The findings were severe sensory motor axonal neuropathy of the left upper limb, with a distal to proximal gradient. The right upper limb had evidence of sensory motor axonal polyneuropathy. These findings were correlated as ischemic neuromuscular injury to the left upper limb, with superimposed axonal distal polyneuropathy (diabetes). Therefore, he was diagnosed with both diabetic neuropathy and ischemic monomelic neuropathy (IMN). View this table: [Table 1](http://nsj.org.sa/content/26/3/300/T1) Table 1 - Motor conduction study showed absent CMAP for left median nerve. Left ulnar nerve showed markedly reduced CMAP amplitude with mild reduction in conduction velocity. After a one-year follow-up, his motor weakness improved mildly. Despite being on a high dose of gabapentin, he still complained of neuropathic pain. His left arm also had a slightly lower blood pressure (95/65mmHg) when compared to the right arm (130/80mmHg). We present a patient with diabetic neuropathy who developed a stroke and IMN after TEVAR. TEVAR is known to cause complications like stroke, which is thought to be mainly associated with covering of the LSA during the procedure.1,2 By contrast, IMN due to TEVAR has been described only once before in the literature.3 The IMN is a type of peripheral neuropathy that develops as a rare complication after shunting of blood flow or due to acute non-compressive occlusion of the major proximal limb artery after vascular surgery; both of these blood-flow disruptions cause ischemia.4,5 Notably, IMN tends to occur in patients with pre-existing microvascular disease, like our patient who had uncontrolled diabetes.4,5 View this table: [Table 2](http://nsj.org.sa/content/26/3/300/T2) Table 2 - Sensory conduction study showed absent SNAP for left median, radial and ulnar nerves. Right side showed low amplitude SNAP. View this table: [Table 3](http://nsj.org.sa/content/26/3/300/T3) Table 3 - Needle EMG of upper limb showed denervation potentials in the left biceps and bilateral first dorsal interosseous. Left upper limb showed neurogenic polyphasic MUAPs in all sampled muscles. Recruitment pattern was reduced with more reduction in distal muscles. Right side showed few polyphasic in extensor digitorum and first dorsal interosseous. Right deltoid was mostly unremarkable. Many clinicians have difficulty diagnosing IMN. In general, neurologic motor and sensory deficits appear immediately after the vascular procedures.3 However, many patients present with other comorbidities, such as severe neuropathic pain and allodynia, which can overshadow the motor function losses. Since our patient had diabetic neuropathy, along with hemiparesis from the stroke, clinically it was very difficult to detect and suspect this rare neuropathy. As in our case, electrodiagnostic studies are helpful for differentiating IMN from other conditions.3-5 The NCSs usually show axonal loss and reduced motor and sensory nerve conduction velocities in the median, radial, and ulnar nerves.3-5 Needle electromyography primarily reveals acute denervation and reduced motor unit recruitment of the upper limbs.3-5 In conclusion, we note to physicians that IMN occurs not only in dialysis patients but also in those with other vascular accesses, like TEVAR. Hence, improved awareness of this disease entity and clinical suspicion of neurologic deficit in the immediate post-operative period can provide early diagnosis and treatment. Last but not least, nerve conduction examinations are important for clarifying the obscurity of IMN in the presence of comorbidities like stroke and diabetes. Illustrations, Figures, Photographs All figures or photographs should be submitted in a high resolution (minimum 300 DPI) electronic version saved in jpeg or tiff format. Original hard copies of all figures may be requested when necessary. Photographs will be accepted at the discretion of the Editorial Board. All lettering, arrows, or other artwork must be done by an artist or draftsman. If arrows are used please ensure they appear in a different color to the background color, preferably black with a white border, or white with a black border. If arrows distinguish different items on the figure then different arrow styles should be used ie. long, short, wide, narrow. Written informed consent for publication must accompany any photograph in which the subject can be identified. Written copyright permission, from the publishers, must accompany any illustration that has been previously published. * Received March 4, 2021. * Accepted February 16, 2021. * Copyright: © Neurosciences Neurosciences is an Open Access journal and articles published are distributed under the terms of the Creative Commons Attribution-NonCommercial License (CC BY-NC). Readers may copy, distribute, and display the work for non-commercial purposes with the proper citation of the original work. ## References 1. 1.Klocker J, Koell A, Erlmeier M, Goebel G, Jaschke W, Fraedrich G. Ischemia and functional status of the left arm and quality of life after left subclavian artery coverage during stent grafting of thoracic aortic diseases. J Vasc Surg 2014; 60: 64–69. [CrossRef](http://nsj.org.sa/lookup/external-ref?access_num=10.1016/j.jvs.2014.01.060&link_type=DOI) [PubMed](http://nsj.org.sa/lookup/external-ref?access_num=24657299&link_type=MED&atom=%2Fnsj%2F26%2F3%2F300.atom) 2. 2.Zamor KC, Eskandari MK, Rodriguez HE, Ho KJ, Morasch MD, Hoel AW. Outcomes of thoracic endovascular aortic repair and subclavian revascularization techniques. J Am Coll Surg 2015; 221: 93–100. [CrossRef](http://nsj.org.sa/lookup/external-ref?access_num=10.1016/j.jamcollsurg.2015.02.028&link_type=DOI) [PubMed](http://nsj.org.sa/lookup/external-ref?access_num=25872688&link_type=MED&atom=%2Fnsj%2F26%2F3%2F300.atom) 3. 3.Lee JW, Lee S, Kim DW. Ischemic monomelic neuropathy after thoracic endovascular aortic repair (Tevar): Case report. J Korean Assoc EMG Electrodiagn Med 2017; 19: 36–41. 4. 4.Kirksey L. Ischemi monomelic neuropathy: an underapprecisated cause of pain and disability following vascular acess surgery. J Vasc Access 2010; 11: 165–168. [PubMed](http://nsj.org.sa/lookup/external-ref?access_num=20175065&link_type=MED&atom=%2Fnsj%2F26%2F3%2F300.atom) 5. 5.Miles A. Vascular steal syndrome and ischaemic monomelic neuropathy: two variants of upper limb ischaemia after hemodialysis vascular access surgery. Nephrol Dial Transplant 1999; 4: 297–300.