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| CASE REPORT |
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| Year : 2021 | Volume
: 12
| Issue : 1 | Page : 31-33 |
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Post-COVID-19 guillain-barre syndrome: A distinct neurological entity
Ritika Sud1, Jyoti Verma2, Shubham Goswami1, Niharika Aggarwal1, Anil Gurtoo1
1 Department of Medicine, Lady Hardinge Medical College & SSK Hospital, New Delhi, India
2 Department of Medicine, Bhagwan Mahavir Hospital, New Delhi, India
| Date of Submission | 04-Nov-2020 |
| Date of Acceptance | 06-Nov-2020 |
| Date of Web Publication | 06-Jan-2021 |
Correspondence Address:
Dr. Ritika Sud
Department of Medicine, LHMC, Shaheed Bhagat Singh Marg, New Delhi - 110 001
India
 Source of Support: None, Conflict of Interest: None  | 2 |
DOI: 10.4103/injms.injms_142_20
SARS-CoV-2, the causative agent for COVID-19, originated in China in the fall of 2019 and soon became a pandemic engulfing the entire world, presenting with a myriad of presentations from asymptomatic to severe disease with acute respiratory distress syndrome and multiple organ dysfunction and severe inflammatory response. Little is understood about the new virus and its pathogenesis, and it is too early to ascertain its long-term sequelae at this point in time. New associations and clinical problems keep appearing with the new virus and thus we also got to encounter three cases of acute inflammatory demyelinating polyneuropathy (AIDP) in patients following COVID-19 infection. This case series aims to convey clinicians that AIDP can be seen in patients with COVID-19, particularly during the recovery phase, and thus not to miss it as postviral fatigue and malaise.
Keywords: Acute flaccid quadreparesis, COVID-19, Guillain–Barre syndrome, intravenous immunoglobulin G
How to cite this article:
Sud R, Verma J, Goswami S, Aggarwal N, Gurtoo A. Post-COVID-19 guillain-barre syndrome: A distinct neurological entity. Indian J Med Spec 2021;12:31-3 |
How to cite this URL:
Sud R, Verma J, Goswami S, Aggarwal N, Gurtoo A. Post-COVID-19 guillain-barre syndrome: A distinct neurological entity. Indian J Med Spec [serial online] 2021 [cited 2023 Mar 31];12:31-3. Available from: http://www.ijms.in/text.asp?2021/12/1/31/306252 |
| Introduction | |  |
SARS-CoV-2, the organism that has lived up to its reputation and truly gone viral, has created a whirlwind in the field of medicine. After the first case of coronavirus disease (COVID-19) was reported in the Chinese province of Hubei in December 2019, the disease has spread rapidly, engulfing the entire world, with its high infectivity index. India as of today stands as one of the most affected nations.
The clinical manifestations of this novel infection are heterogeneous. The typical triad at the offset of the pandemic consisted of fever, dry cough, and breathlessness, but with the passage of time, symptoms involving almost all systems have been uncovered and added to the spectrum of COVID-19. The severity of symptoms ranges from mild flu-like to severe life-threatening acute respiratory distress syndrome, multiorgan dysfunction, and death. Little is known at this juncture about the pathogenesis and long-term sequelae of this mysterious pathogen. Reports of neurological manifestations in COVID-19 patients are on the rise, with presentations varying from a mild headache to more severe manifestations such as seizure, polyneuropathy, encephalopathy, and stroke.[1],[2] Recently, cases of Guillain–Barre syndrome (GBS) have been described as a complication of COVID-19.[3],[4] We report a series of three cases which are clinically in agreement with a diagnosis of acute inflammatory demyelinating polyneuropathy (AIDP), associated with SARS-CoV-2 infection.
| Case Reports | | |
Case 1: The classical presentation
A 50-year-old female, diagnosed with COVID-19 confirmed based on reverse transcription-polymerase chain reaction (RT-PCR), was admitted to the COVID ward of LHMC with mild disease and after the initial evaluation over the next 48 h, the patient was sent with an undertaking to be home isolated. She presented to the emergency department a week later with quadriparesis.
The patient after apparently remaining asymptomatic for 5 days during home isolation noticed mild tingling and weakness in her lower limbs that progressed to involve the upper limbs over the next 36 h with no bowel or bladder involvement. Motor examination revealed a power of 2/5 in the proximal and 3/5 in the distal groups of the lower limbs and 4/5 in the proximal and distal groups of the upper limbs on admission. The weakness progressed to 0/5 in both the lower limbs and 1/5 and 2/5 in the proximal and distal groups, respectively, of the upper limbs, over the next 4–5 days with global areflexia and unremarkable sensory and cranial nerve examination. She received 0.4 g/kg/day of intravenous immunoglobulin G (IVIG) for 5 days and could be discharged from the ward 2 weeks later with slight improvement [Table 1].
Case 2: Guillain–Barre syndrome masquerading as post-COVID fatigue
An 80-year-old male with no known comorbidities presented to the emergency department with undue fatigue and inability to carry out his activities of daily living for the past 6 weeks. The patient had been admitted to another institution for a fortnight with RT-PCR-confirmed COVID-19 infection 8 weeks prior to presentation. He was conscious and oriented with normal vitals yet wheelchair bound. Examination revealed flaccid quadriparesis and a power of 3/5 in the lower limbs with areflexia, but there was no definite sensory level, cranial nerve, or bladder bowel involvement. The inflammatory and prothrombotic markers were elevated, indicative of a multi-inflammatory syndrome. On electrophysiological studies, acute motor sensory axonal neuropathy-like pattern of the lower limbs was recorded. Bilateral peripheral nonhomogenous peripheral opacities in the middle and lower zones were seen on chest X-ray, with contrast-enhanced computed tomography chest showing a small patchy area of ground-glass opacities peripheral in distribution (CORAD 6).
Although the exact time of the onset of GBS could not be ascertained, the patient was given IVIG (0.4 g/kg/day) for 5 days. The patient on his follow-up visit 4 weeks later walked into the outpatient department without support.
Case 3: A fatal encounter with post-COVID Guillain–Barre syndrome
A 28-year-old healthy male, a multi-task worker at a tertiary care hospital, presented to the emergency department of SSKH with ascending quadriparesis and distal dysesthesias. Weakness started with symmetrical involvement of both lower limbs that ascended to the upper limbs over a period of 4 days. The weakness was accompanied by facial diplegia, difficulty in swallowing, inability to speak, blurring of vision, and headache, which had developed a few hours prior to admission. The patient on presentation had an oxygen saturation of 94%, needing supplemental oxygen. He had no urinary or fecal incontinence. Incidentally, his COVID-19 IgG antibody done during a routine hospital survey 15 days prior was positive.
On examination, he was conscious and oriented, with a blood pressure of 160/100 mmHg and a pulse rate of 120 beats/min. Examination showed weakness in all the four limbs with a power of 0/5 in both lower extremities (proximal and distal groups) and 1/5 in the upper extremities (proximal and distal groups) with bulbar involvement and bilateral 7th nerve involvement. There were global areflexia and absence of fine touch and vibration in both lower limbs. Within the next 2 h, there was worsening of respiratory effort and fall in oxygen saturation, warranting intubation and mechanical ventilation.
Noncontrast computed tomography head, chest X-ray, and fundus examination were normal. RT-PCR test for COVID-19 was negative though serological IgG antibody test for COVID-19 was positive, indicating an asymptomatic COVID illness in the recent past.
Complementary tests to support the diagnosis of AIDP given the rapid progression and critical condition of the patient could not be done. However, the clinical picture of acute areflexic flaccid ascending quadriparesis and distal dysesthesia with bulbar involvement supported the diagnosis of GBS. IVIG was initiated at a dose of 0.4 g/kg/day. An initial apparent response was noted, but ventilatory support could not be withdrawn. It is worth noting that there were persistent and wide variations in the heart rate and blood pressure recordings of the patient. Much to our dismay, the patient died on the 4th day of admission due to respiratory failure.
| Discussion | | |
Starting from 1 April until September 2020, cases of numerous patients with SARS-CoV-2 infection and GBS have been reported mostly from Italy and the rest of Europe along with some from all over the world, including India. Despite the multiple reports, the exact temporal association between the two has yet to be ascertained. The mechanism by which SARS-CoV-2 causes neurologic damage is multifaceted and includes direct damage to specific receptors, cytokine-related injury, secondary hypoxia, and retrograde travel along nerve fibers. Understanding the neurological manifestations in infectious diseases such as MERS and SARS-CoV-2 is important, as they are rarely evaluated thoroughly during the course of the illness and may hamper prognosis or require treatment modification.[5]
COVID-19 may be oligosymptomatic or asymptomatic with a variable incubation period going up to 14 days, making it difficult to estimate the time interval between the infection and the development of GBS.[6] The most severe form of SARS-CoV-2 evolves through three stages namely early infection, pneumonia, and hyperinflammatory response.[7]Active viremia occurs during the earlier stages, whereas immunological and inflammatory complications have been observed in the hyperinflammatory phase. In critical patients, predictability of the time and phase in which GBS is likely to occur is nearly impossible. Moreover, respiratory symptoms, as well as radiological abnormalities, tend to persist beyond the phase of acute infection.
In our series of GBS patients infected with COVID-19, one of the patients followed a rather catastrophic course with the sole evidence of a preceding infection being indirect, in the form of COVID antibodies. Most of the earlier reported cases[8],[9] had documented preceding infection except two cases where diagnosis was made in retrospect based on COVID antibodies. The other two patients, like the majority of cases reported so far, developed GBS following a confirmed diagnosis of COVID, but only in one could the exact onset of GBS be ascertained. Most of the previous case reports have documented an interval of 5–24 days between the appearance of symptoms of SARS-CoV-2 and GBS.[10],[11]
Antiganglioside antibodies were detected in two of our patients, supporting the postinfectious mechanism of GBS and a suggested cross-reactivity between the viral protein gangliosides and peripheral nerve gangliosides. Antiganglioside antibodies have been detected in 12% of the post-COVID GBS reports analyzed earlier, hinting that novel autoantibodies mediate the COVID-associated GBS.
IVIG was given to all the patients, with each one responding in a variable manner. One with an initial apparent response succumbed to the illness, whereas the other two responded well and were ambulatory after 4–6 weeks. Previous case reports have shown mixed treatment responses with IVIG treatment, with some reporting very good recovery, whereas others reporting minimal or delayed responses.[11],[12]
A general drawback of the present evidence in literature is that the cases, understandably, have been investigated on an extemporized and retrospective basis; other preceding infections related to GBS could not be excluded and loss or rather impending long-term patient follow-up has left the clinical outcome to our imagination.
| Conclusion | | |
While large research studies are underway, it does appear that GBS is a serious phenomenon possibly linked to COVID-19. The Global Consortium Study of Neurological Dysfunctions in COVID-19 is in progress to find the extent of neurological involvement in hospitalized COVID-19 patients. Although post-COVID Guillain-Barré syndrome appears to be a distinct neurological entity, a chance occurrence cannot be ruled out emphatically, since no validated serological or polymerase chain reaction cerebrospinal fluid tests are commercially available to demonstrate the neurotoxicity of the virus.
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.
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[Table 1]
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