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Table of Contents    
Year : 2018  |  Volume : 66  |  Issue : 4  |  Page : 1189-1190

Ischemic polyradiculoneuropathy with an aortic aneurysm masquerading Guillain–Barré syndrome

Department of Neurology, Narayana Institute of Neurosciences, Bengaluru, Karnataka, India

Date of Web Publication18-Jul-2018

Correspondence Address:
Dr. Lobo M Alexander
Department of Neurology, Narayana Institute of Neurosciences, Mazumdar Shaw Medical Center, 258/A, Bommasandra Industrial Area, Anekal Taluk, Hosur Road, Bengaluru, Karnataka - 560 099
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.237030

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How to cite this article:
Alexander LM, Philip VJ, Gosar A. Ischemic polyradiculoneuropathy with an aortic aneurysm masquerading Guillain–Barré syndrome. Neurol India 2018;66:1189-90

How to cite this URL:
Alexander LM, Philip VJ, Gosar A. Ischemic polyradiculoneuropathy with an aortic aneurysm masquerading Guillain–Barré syndrome. Neurol India [serial online] 2018 [cited 2020 Nov 23];66:1189-90. Available from:


Peripheral neuropathy associated with occlusive atherosclerotic peripheral vascular disease, otherwise called ischemic neuropathy, is infrequently reported.[1] However, it is important to recognize and treat this condition early as it is a cause of significant morbidity. Electrophysiologically, patients may present with multifocal motor neuropathy.[2] Pseudoconduction blocks have been reported in vasculitic neuropathy, the mechanism being axonal damage between proximal and distal stimulation sites.[3],[4]

A 63-year old gentleman presented to our institution with complaints of acute-onset, proximal more than distal, progressive paraparesis with mild asymmetry over 4 days. He also had associated paresthesias in both feet and had a low backache. He had no upper limb or cranial nerve abnormalities, and had no bowel or bladder symptoms. He was on treatment for hypertension and diabetes mellitus for the past 6 years. There was a significant history of smoking 6 cigarettes per day. The patient was ambulatory with the support of two persons but would buckle at his knees after walking for a few meters. He had bilateral foot drop. His proximal lower limb power was grade 3 (based on the Medical Research Council scoring), and distally, it was grade 1–2. The knee reflexes were bilaterally sluggish and his ankle reflexes could not be elicited. He had no sensory deficits and his bilateral plantar reflexes were equivocal. His dorsalis pedis pulses on both the sides were feeble to palpate but other peripheral pulses were well palpable. He was a farmer by occupation. There was no exposure to any neurotoxins. There was no history of any preceding viral illness.

Based on his clinical presentation, the possibility of an infective arachnoiditis versus an inflammatory polyradiculopathy was considered. A lumbar puncture and nerve conduction study were performed. The lumbar puncture showed no cells, normal glucose, and mildly elevated proteins. Cerebrospinal fluid (CSF) and serum venereal disease research laboratory (VDRL) test were nonreactive. The nerve conduction study showed conduction blocks across the peroneal and tibial nerves in both lower limbs, with absent sural sensory nerve conduction amplitudes bilaterally but with normal median sensory conduction amplitudes [[Figure 1], right panel]. The absence of sural sensory nerve action potentials (SNAPs) was attributed to subclinical diabetic neuropathy. He was considered to have acute inflammatory demyelinating polyradiculopathy and was started on plasma exchange.
Figure 1: Right, Motor nerve conduction studies showing bilateral tibial and peroneal conduction blocks with normal upper limb motor conductions. Left, CT angiogram showing complete occlusion and fusiform dilatation of infrarenal abdominal aorta extending to bifurcation

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After the third cycle of plasma exchange, the patient complained of severe left lower limb pain and worsening of weakness of both lower limbs to grade 1–2. Examination revealed absent popliteal and posterior tibial pulses in both lower limbs with feebly palpable femoral pulses. An urgent computed tomography (CT) angiogram of the abdominal aorta with lower limb vessels was performed. It revealed complete occlusion of the vessels and mild fusiform aneurysmal dilatation of the infrarenal abdominal aorta extending up to the bifurcation, with diffuse atheromatous changes in the thoracic and abdominal aorta, and bilateral lower limb arteries. There was absent contrast flow in bilateral mid- and distal anterior tibial artery, bilateral distal posterior tibial artery, and bilateral dorsalis pedis arteries [[Figure 1], left panel]. The patient was taken up for axillary bifemoral bypass and after 3 weeks could walk with support. On review, a repeat nerve conduction study showed absent compound muscle action potentials (CMAPs) in both peroneal and tibial nerves.

The patient presented with acute-onset paraparesis resembling an autoimmune inflammatory polyradiculopathy.[5],[6] He was initiated on plasma exchange, the hemodynamic effects of which probably led to acute thrombosis of a preexisting abdominal aortic aneurysm. The presentation of an infrarenal aortic aneurysm with ischemic polyradiculoneuropathy and pseudoconduction blocks is hitherto unreported.

This case highlights the need to be vigilant about the possibility of ischemic polyradiculopathy as a differential diagnosis for acute paraparesis, especially in patients with other vascular risk factors.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient has given his consent for images and other clinical information to be reported in the journal. The patient understands that name and initial will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Derksen A, Ritter C, Athar P, Kieseier BC, Mancias P, Hartung HP, et al. Sural sparing pattern discriminates Guillain-Barré syndrome from its mimics. Muscle Nerve 2014;50:780-4.  Back to cited text no. 1
Nukada H, van Rij AM, Packer SG, McMorran PD. Pathology of acute and chronic ischaemic neuropathy in atherosclerotic peripheral vascular disease. Brain J Neurol 1996;119(Pt 5):144-60.  Back to cited text no. 2
England JD, Ferguson MA, Hiatt WR, Regensteiner JG. Progression of neuropathy in peripheral arterial disease. Muscle Nerve 1995;18:380-7.  Back to cited text no. 3
Sandbrink F, Klion AD, Floeter MK. “Pseudo-conduction block” in a patient with vasculitic neuropathy. Electromyogr Clin Neurophysiol 2001;41:195-202.  Back to cited text no. 4
Nagappa M, Netto AB, Taly AB, Kulkarni GB, Umamaheshwara Rao GS, Periyavan S, et al. Electrophysiological observations in critically ill Guillain–Barre syndrome. Neurol India 2016;64:914-20.  Back to cited text no. 5
[PUBMED]  [Full text]  
Mehndiratta MM, Wadhwa A. Electrophysiological features of Gullian Barre syndrome: Newer insights. Neurol India 2016;64:921-2.  Back to cited text no. 6
[PUBMED]  [Full text]  


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