Abstract

Background

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is typically associated with respiratory disease and fever. Originating from Wuhan, China, COVID-19 has rapidly spread worldwide. COVID-19 commonly presents with respiratory symptoms with mild clinical features in the majority of patients. The neurological manifestations of COVID-19 include headache, stroke, seizures, encephalitis, hypogeusia and neuralgia.^1–3

Guillain-Barré syndrome (GBS) is a rare immune-mediated postinfectious neuropathy typically leading to ascending weakness. It has been reported as a possible rare sequela of COVID-19,^4–6 though the first reported case in Wuhan suggested a parainfectious presentation.⁷ We report a case of GBS associated with mild COVID-19 infection in the UK.

Case presentation

A 49-year-old man of South Asian descent with no medical history, apart from sinusitis, presented with difficulty in mobilising. There was no recent travel history. He reported a 3-week history of shortness of breath, headache and cough. He had completed two courses of antibiotics in view of his background of recurrent sinusitis. On initial presentation to the emergency department, he reported worsening cough and distal lower limb paraesthesia during the previous week, resulting in difficulty mobilising, requiring the use of a frame. He was apyrexial on presentation with a mild tachycardia of 109, normal oxygen saturation of 99% on room air and haemodynamically stable. He had an elevated lactate on venous blood gas (3.3mmol/L) and a mildly elevated C-reactive protein (20mg/L). His white cell count, sodium, potassium and renal function and liver function were normal. His oropharyngeal swabs tested positive for SARS-CoV-2 on RT-PCR. His family members were self-isolating and had no symptoms of COVID-19. He had a mildly elevated creatine kinase (CK) of 589IU/L, which led to an initial diagnosis of viral myositis and was discharged.

The patient represented 3days later with worsening lower limb paraesthesia and unable to mobilise due to ascending lower limb weakness. His repeat CK was normal (151IU/L). Four days later, he had developed facial diplegia, weakness of Medical Research Council (MRC) Muscle Scale 1/5 in his lower limbs, 3/5 proximal upper limbs and 2/5 distal upper limbs. He had distal reduced sensation to pinprick and vibration sense and was areflexic. There was no meningism, spinal cord sensory level, bladder or bowel involvement or dysautonomia. He developed dysaesthesia in his lower limbs which responded well to neuropathic medication, pregabalin.

Investigations

His cerebrospinal fluid (CSF) showed cytoalbuminologic dissociation (protein >1.25g/L, white cell count 1×10⁶/L). His CSF was negative for SARS-CoV-2. He continued to test positive for SARS-CoV-2 on oropharyngeal swabs for 4weeks after initial presentation. His neurophysiology studies showed absent sensory response of the median nerve (table 1A) and severe slowing of motor responses of the median and ulnar nerve with reduced amplitude (table 1B). He had severe neurogenic firing with normal motor units, without spontaneous activity, on electromyography (table 1C), indicating a demyelinating polyneuropathy. Meeting all domains of the Brighton criteria,⁸ a diagnosis of GBS was confirmed.

Treatment

During the initial week of admission, the patient was monitored in intensive care and required a nasogastric tube for feeding due to swallowing difficulties, without respiratory dysfunction. He received intravenous immunoglobulin (IVIG) 0.4 g/kg daily for 5days and his symptoms stabilised, avoiding the requirement of intubation.

Outcome and follow-up

The patient’s motor symptoms began to improve within the first week of IVIG administration. Four weeks later, the patient no longer had facial diplegia and his motor strength had improved to 4/5 proximally, 3/5 distally and lower limbs 3/5. Eleven weeks later, after receiving neurorehabilitation and optimisation of neuropathic medications, the patient was able to mobilise unassisted.

Discussion

The first reported case of COVID-19-associated GBS was reported from Wuhan as a suspected parainfectious disease, as the patient developed COVID-19 symptoms 7days after the onset of GBS symptoms.⁷ Here, we have presented a patient from the UK who developed GBS as a likely postinfectious complication 3weeks after the initial onset of infectious symptoms. Our case supports increasing numbers of reports of COVID-19-associated autoimmune neuropathies,^{5 6} including the Miller-Fisher variant of GBS.⁹ As with reports from Italy, our patient was highly responsive to immunoglobulin therapy,¹⁰ emphasising the importance of early recognition and treatment.

Toscano et al report five cases of COVID-19 who developed GBS 5 to 10 days post infection; all five cases had negative PCR for SARS-CoV-2 in CSF. Our patient remained positive for SARS-CoV-2 for approximately 7weeks post onset of initial COVID-19 symptoms, supporting previous reports of RT-PCR remaining positive in patients who have fully recovered from COVID-19, which raises questions about the duration of viral shedding.¹¹ Neurological manifestations of COVID-19 is often associated with severe acute respiratory distress syndrome but our patient presented with neurological sequelae following mild COVID-19 symptoms. Despite neurological sequelae, RNA may not be detected in CSF,^{4 12} as in our case; though there has been a reported case of encephalitis with SARS-CoV-2 detected in CSF but not nasopharyngeal swabs.¹² GBS has severe consequences and early recognition is vital to monitor for loss of ambulation and initiation of immunoglobulin treatment. Patients presenting with paresthesia and difficulty in mobilising after COVID-19 symptoms should not be overlooked as viral-associated myositis. GBS should be considered as a potential rare but serious complication weeks after initial COVID-19 infection.

Footnotes

References