Guillain-Barre Syndrome is an important cause of severe, acute weakness in children, and Acute Inflammatory Demyelinating Polyradiculoneuropathy (AIDP) is the most common subtype [1]. GBS is characterized by a monophasic, ascending, and symmetrical paralysis that progresses over days to weeks and is associated with areflexia. AIDP is a post-infectious autoimmune process to peripheral nerves that causes inflammation and destruction of myelin. History of past infection was noticed in the majority of cases. Respiratory illness is the most common infectious trigger, but gastrointestinal illnesses, other viruses, and immunizations have also been related to GBS [2].

 In Wuhan China in late 2019, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) originated and rapidly spread around the world. It brought out a pandemic of novel coronavirus disease 2019 (COVID-19). The majority of Pediatric diseases is asymptomatic. The common symptoms of COVID-19 are fever, malaise, and respiratory symptoms, which may range from a mild cough to severe pneumonia. It presents occasionally gastrointestinal symptoms [3]. However, COVID-19 can present with a variety of other symptoms which include neurological symptoms in adult patients [4]. Anosmia is the most common neurological presentation among COVID-19 patients. However, others include encephalopathy, encephalitis, stroke, acute-disseminated encephalomyelitis, as well as Neuro-inflammatory auto-immune diseases [5].

There are scattered reports of adults with possible GBS and concurrent evidence of COVID-19 [6-10]. There are very few previously reported cases of GBS in children with evidence of COVID-19.

The patient was a previously healthy, 9-year-old male who presented in our patient department with progressive weakness in the lower limb and difficulty in walking for 10 days. He had a history of frequent falls on his buttocks before the presentation. He complained of pain in both lower limbs for 8 days. Over the next couple of days, he started experiencing bilateral lower extremity weakness that progressed and which led to his inability to walk. He was evaluated by a local family physician where lumbar spine and right ankle x-rays were normal. Over the next few days, his weakness worsened as he began to develop upper extremity weakness. The patient was transferred to a tertiary care children’s hospital for further evaluation.

The parents gave the history of illness 1months back; including fever, upper respiratory infection, and cough. The patient’s SARS-CoV-2 nucleic acid amplification was positive. The patient did not have urinary or fecal incontinence. He passes stool once in 3 days and has no reported difficulty voiding. He had no lower back pain and bilateral foot paresthesia. Other family members denied any recent respiratory or febrile illness. The father was a daily wedge worker and works outside the home. The patient had a history of playing outside the home and a visit to a local mall 3 weeks before the presentation, during which he wore a mask. The patient belonged to a containment zone for COVID-19.

At the time of admission to the Pediatric ward, the patient was afebrile with a blood pressure of 110/78 mmHg, heart rate of 90 beats per minute, respiratory rate of 20 breaths per minute, and oxygen saturation of 99 % on room air. He appeared anxious but was alert and oriented. He was able to converse and able to speak a sentence with 5-6 words at a time. Cranial nerves were intact Overall muscle power was reduced with 4/5 in the upper limbs and 3/5 in the lower extremities. Deep tendon reflexes were absent in the lower extremities bilaterally. The sensation was intact to light touch, but proprioception of the distal lower extremities was abnormal. The single breath count test was 14.

An MRI of the spine was done and it was normal. A lumbar puncture was also performed. The cerebrospinal fluid demonstrated albuminocytologic dissociation with 1 nucleated cell/cu.mm, 1 RBC/cu.mm, and a protein of 450 mg/dl. Gram stain, culture was negative.

Electro diagnostic testing including F waves was performed 10 days after symptom onset. It demonstrated nearly absent CMAP amplitude in both median nerves. Markedly reduce CMAP in both peroneal nerves. Both ulnar and tibial nerves show increased latency with reduced velocity. Conduction block was seen in the left tibial and right ulnar nerve. Sensory nerve conduction showed absent SNAPs in all sampled upper and lower limb nerves. F waves were absent in both the peroneal and median nerves. H reflex was absent bilaterally (Table 1). These findings were compatible with sensory-motor demyelinating polyneuropathy.

Table 1: Nerve conduction studies and EMG Examination.

A diagnosis of GBS, AIDP form, was made. The patient underwent infectious evaluation for the cause of the GBS. Blood, urine, and stool cultures were negative. SARS-CoV2 Ig G antibody was detected in his serum. Further workup showed WBC 14,200/cu.mm. Treatment was initiated with intravenous immunoglobulin (IVIG) on day two of hospitalization. He was given a total of 2 g/kg of IVIG over 48 hours. His exam demonstrated improvement over the next several days following IVIG with 4/5 upper extremity power and 4/5 lower extremities bilaterally. Physical therapy was initiated. At the time of publication, three weeks following IVIG, he continues to demonstrate slow improvement. He can sit and walk independently. He tested SARS-CoV-2 which came negative on admission.

This case is the first reported case of a child with GBS with a history of acute SARS-CoV-2 infection one month back in our setup. GBS in a child has been reported associated with other forms of coronavirus. The patient came with obvious symptomatology of GBS with symmetric ascending weakness with loss of reflexes. The workup subsequently was consistent with GBS, and AIDP forms. The CSF showed raised protein without pleocytosis, there was an enhancement of the posterior nerve roots in the cauda equina on MRI, and electrophysiological findings (EMG) demonstrated a demyelinating process.

The relation between COVID-19 and GBS was demonstrated previously in case reports of adults with a different variety of GBS, like demyelinating, axonal, and Miller-Fisher in connection with COVID-19 [10-12]. Typical post-infectious presentations have been seen in our report after one month [13-16].

SARS-CoV-2 and other coronaviruses, SARS and MERS specifically, have been shown to have a neurotropic nature and cause diseases of the central and peripheral nervous system [17]. The absence of SARS-CoV-2 in the CSF is a constant report as per past publications. The real course and physiology of this reason have yet to be determined.

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