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Table of Contents
CASE REPORT
Year : 2021  |  Volume : 12  |  Issue : 1  |  Page : 37-39

Guillain–Barré syndrome unmasking asymptomatic peripheral spondyloarthritis


Department of Neurology, St. Stephen's Hospital, New Delhi, India

Date of Submission23-Sep-2020
Date of Decision15-Oct-2020
Date of Acceptance16-Oct-2020
Date of Web Publication06-Jan-2021

Correspondence Address:
Dr. Gaurav Kumar Mittal
Department of Neurology, St. Stephen's Hospital, New Delhi - 110 054
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/injms.injms_116_20

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  Abstract 


Guillain–Barré syndrome (GBS) is an immune-mediated disease characterized by evolving ascending limb weakness, sensory loss, and areflexia. While moderate and severe back or extremity pain is frequent in patients with GBS due to polyradiculopathy, the literature does not reveal any association of acute demyelinating disorders and asymptomatic sacroiliitis, which becomes symptomatic during the episode of the demyelinating illness. We present the case of a young male patient with acute-onset quadriparesis diagnosed as GBS based on clinical evidence and electrophysiological criteria, who developed acute low backache 7 days after the onset of acute demyelinating illness. Subsequently, a diagnosis of peripheral spondyloarthritis (SpA) was confirmed based on clinical outline (past history of bilateral heel pain and acute low backache), along with magnetic resonance imaging (MRI) and computed tomography findings of focal erosions with surrounding sclerosis on iliac para-articular surface bilaterally. The patient responded well to the therapy (intravenous immunoglobulin, hydroxychloroquine, and symptomatic treatment) thereafter. It is crucial to consider the possibility of SpA when patients with GBS complain of low backache. Timely diagnosis will not only aid in the institution of early therapy but also prevent any long-term sequelae. MRI can visualize active inflammation at sacroiliac joints and spine in recent-onset disease.

Keywords: Acute demyelination, Guillain–Barré syndrome, HLA B27, low backache, peripheral spondyloarthritis


How to cite this article:
Kaur H, Mittal GK, Singhdev J. Guillain–Barré syndrome unmasking asymptomatic peripheral spondyloarthritis. Indian J Med Spec 2021;12:37-9

How to cite this URL:
Kaur H, Mittal GK, Singhdev J. Guillain–Barré syndrome unmasking asymptomatic peripheral spondyloarthritis. Indian J Med Spec [serial online] 2021 [cited 2021 Jan 16];12:37-9. Available from: http://www.ijms.in/text.asp?2021/12/1/37/306246




  Introduction Top


It has been over 100 years since the first description of Guillain–Barré syndrome (GBS), which is now recognized as the most common cause of acute postinfectious flaccid paralysis worldwide.[1] GBS is a neurologic illness where pain occupies a major clinical dimension. We wish to report a unique case of GBS developing acute-onset low backache eventually diagnosed as peripheral spondyloarthritis (SpA).


  Case Report Top


A 32-year-old married male presented to the emergency department with acute-onset progressive weakness of all the four limbs (involving the proximal and distal groups of muscles), trunk, and neck and dysphagia for 4 days. At the onset of the illness, he had weakness of the lower limbs with subsequent involvement of both the upper limbs after 12 h. On the 3rd day of illness, he had difficulty in turning sides in the bed, getting up from supine position, walking, and holding his neck, along with dysphagia. The patient denied sensory loss, pain, diplopia, vertigo, oral ulcers, sicca symptoms, and bladder or bowel incontinence at presentation. He had diarrhea lasting for a day, 1 month ago. There was a history of bilateral heel pain of moderate intensity (visual analog scale of 5) without any swelling or restriction of movements lasting for 6 weeks 2 years ago, which resolved with over-the-counter painkillers.

On examination (performed on the 4th day of the onset of symptoms), he was conscious and oriented. Muscle power in all the four limbs was 3/5 according to the Medical Research Council grading system. Truncal and neck weakness was present. Deep tendon reflexes were absent. Bilateral plantars were flexors. There was no sensory loss. Vital signs (including respiratory rate of 15/min and single breath count of 52/min) and rest of the systemic examination were normal. Systemic features associated with SpA such as uveitis, dactylitis, and skin changes were absent. Routine blood investigations including erythrocyte sedimentation rate and C-reactive protein were normal. Nerve conduction study (NCS) showed prolonged motor distal latencies in the bilateral peroneal and bilateral tibial nerves, along with a conduction block in the bilateral peroneal and bilateral tibial nerves with severely decreased conduction velocities. Bilateral median and ulnar nerves were showing partial conduction block with normal distal motor latencies and conduction velocities. F-waves were absent in the bilateral peroneal nerves with bilateral absent H-reflex. Overall, NCS was suggestive of demyelinating type of motor radiculoneuropathy, affecting all the four limbs [Figure 1]. He was treated with intravenous immunoglobulin (total 150 g over 5 days) which was initiated on the 8th day of the onset of weakness.
Figure 1: (a) Motor nerve conduction study showing demyelinating type of motor polyneuropathy involving all the four limbs along with conduction block, (b) normal sensory nerve conduction study, (c) nonrecordable F-wave in bilateral peroneal nerves and nonrecordable H reflex on both sides

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On the 7th day of illness, he complained of severe low backache. Magnetic resonance imaging (MRI) of the lumbosacral spine revealed subchondral marrow edema in the bilateral sacroiliac joints [Figure 2]a. Contrast-enhanced computed tomography (CT) of the whole abdomen showed focal erosions with surrounding sclerosis on the iliac para-articular surface bilaterally, suggestive of bilateral sacroiliitis [Figure 2]b. In view of the past history of bilateral heel pain, acute onset of low backache, MRI, and CT findings, the possibility of SpA was considered. HLA B27 (by polymerase chain reaction) was negative. He was started on sulfasalazine, and was discharged in a recovering condition.
Figure 2: (a) Magnetic resonance imaging spine short tau inversion recovery image showing subchondral hyperintensity in the right sacroiliac joint (arrow). (b) Contrast-enhanced computed tomography showing focal erosion (arrowhead) with surrounding sclerosis (arrow) on iliac para-articular surface bilaterally

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  Discussion Top


Pain may be a heralding feature of GBS (either can occur as a sentinel symptom prior to weakness or along with the onset of weakness) and has been described in patients up to 2 years after the onset of symptoms. Backache, aching muscle pain, and neuropathic pain in the extremity are highly prevalent in GBS.[2] The largest prospective study of pain in GBS reported lower back to be the second-most common location of distressing pain, peaking at 50% in the first 3 weeks and remaining nearly 35% throughout the 1st year.[3] Usually, the back pain resolves in a few days in most of the patients after the initiation of therapy. Spondyloarthritides, a heterogeneous group of inflammatory diseases, share common clinical, radiological, and genetic features. They can be axial, peripheral, or extra-articular. The spectrum of spondyloarthritides includes ankylosing spondylitis, psoriatic arthritis, arthritis related to inflammatory bowel disease, reactive arthritis, undifferentiated SpA, and juvenile SpA.[4] It is a widely known fact that demyelinating polyneuropathy can develop after administration of anti-tumor necrosis factor (TNF)-α agents for spondyloarthitides.

Available data mostly from case reports and larger prospective natural history studies have not captured any GBS patient with low backache due to the underlying asymptomatic SpA.[3],[5] Several reports exist in the literature linking the use of TNF-α agents in the management of SpA with unmasking of demyelinating events and exacerbation of symptoms in patients with longstanding neurological disorders such as multiple sclerosis.[6]

However, to the best of our knowledge, there have been no reports of patients who developed low backache soon after having presented with GBS or other demyelinating events. Furthermore, we have found no other reports of asymptomatic SpA becoming symptomatic after an episode of demyelinating events. This makes our case report the first and one of its kind regarding GBS unmasking SpA. The patient's radiological features of erosions and sclerosis suggest the chronicity of the lesions, though the onset of low backache is acute. Furthermore, the causal association between GBS and SpA in our case is difficult to prove or disprove. It is difficult to hypothesize the exact reason why GBS unmasked low backache, ultimately leading to the diagnosis of SpA in our case.


  Conclusions Top


GBS patients commonly experience severe pain, which is often overlooked due to limb weakness. Through our case, we wish to highlight the fact that not every patient is the same and a thorough evaluation of every symptom should be done so as not to miss the correct diagnosis. SpA should be considered one of the important differentials for low backache in the setting of GBS. Low threshold should be exercised in terms of adjuring dedicated imaging (MRI or CT) of the spine and sacroiliac joint in appropriate clinical setting. As such, more data and long-term monitoring of these patients will be needed to know about the disease course, as these have evolving manifestations.

Acknowledgments

The authors would like to acknowledge Dr. Sudhir Joseph, Director, St. Stephen's Hospital, Tis Hazari, Delhi.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

None.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Yuki N, Hartung HP. Guillain-Barré syndrome. N Engl J Med 2012;366:2294-304.  Back to cited text no. 1
    
2.
Farmakidis C, Inan S, Milstein M, Herskovitz S. Headache and pain in Guillain-Barré syndrome. Curr Pain Headache Rep 2015;19:40.  Back to cited text no. 2
    
3.
Ruts L, Drenthen J, Jongen JL, Hop WC, Visser GH, Jacobs BC, et al. Pain in Guillain-Barre syndrome: A long-term follow-up study. Neurology 2010;75:1439-47.  Back to cited text no. 3
    
4.
Zeidler H, Amor B. The Assessment in Spondyloarthritis International Society (ASAS) classification criteria for peripheral spondyloarthritis and for spondyloarthritis in general: The spondyloarthritis concept in progress. Ann Rheum Dis 2011;70:1-3.  Back to cited text no. 4
    
5.
Ding X, Jiang H, Hu X, Ren H, Cai H. Guillain-Barré syndrome and low back pain: Two cases and literature review. Open Med (Wars) 2018;13:503-8.  Back to cited text no. 5
    
6.
Psarelis S, Hajineocli AP, Hadjicosta E, Elliott HS, Johnson P. Is secukinumab a safe alternative treatment for ankylosing spondylitis with Guillain Barré syndrome after anti-TNF-α treatment? Case report and literature review. Clin Rheumatol 2017;36:1197-9.  Back to cited text no. 6
    


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