Guillain–Barré Syndrome With Bilateral Facial Diplegia Secondary to Severe Acute Respiratory Syndrome Coronavirus-2 Infection

A Case Report

Natalia Ramirez; David Ujueta; Luis Felipe Diaz; Lucila Emilse Folleco; Andrea Rodriguez; Ivan Gaona; Mauricio O. Nava-Mesa

Disclosures

J Med Case Reports. 2021;15(558) 

In This Article

Discussion

We presented the case of a previously healthy 50-year-old Hispanic male recently diagnosed with SARS-CoV-2 infection, who was admitted to the hospital without neurological manifestations except for symptoms and signs of bilateral facial nerve palsy. According to the history and physical examination, he was diagnosed with bilateral facial diplegia, an uncommon variant of GBS. Albuminocytologic dissociation was found on CSF study. Brain images were assessed with no pathological findings. Interestingly, the GBS-related symptoms he presented were only facial, but in contrast with previous reports, we included a neurophysiology study that reported severe acute axonal neuropathy of the right and left facial nerves with prolongation of latency and severe reduction of the amplitude in all the motor potentials recorded bilaterally.

Guillain–Barré syndrome (GBS) is an inflammatory disease of the peripheral nervous system. Its manifestations typically involve weakness and sensory symptoms that begin in the lower extremities and progressively ascend until the arms and face are compromised.[14] It has been proposed that a previous infection generates an immune response, which in turns cross-reacts with peripheral nerve components because of its molecular mimicry, resulting in acute polyneuropathy with axonal and/or myelin involvement.[14,15] Diagnosis is made taking into account the patient's clinical history and neurological examination, and is associated with changes in the CSF such as albuminocytologic dissociation (CSF protein > 0.55 g/L with no increase in white blood cell count) or electrophysiology studies, including F-wave and H-reflex suggesting peripheral nerve compromise. These features are important for the differentiation of different subtypes of GBS.[14]

In addition to the typical clinical presentation described previously, other less frequent GBS variants have been described, including bilateral facial nerve palsy,[16] as in the case of the above-mentioned patient. Up to 10% of GBS patients present facial weakness as the main clinical manifestation of this disease,[17] and 20–60% of the cases with motor symptoms have reported bilateral facial involvement.[18] Other manifestations documented in patients with GBS and bilateral facial palsy were sensory symptoms including paresthesias and reduced perception of pinprick, and motor involvement with areflexia and weakness.[6,7] Less common symptoms were positive Romberg sign and hypogeusia.[6]

As mentioned previously, around 73 cases of GBS related to SARS-CoV-2 infection have been reported,[5–9] mostly with respiratory symptoms prior to neurological impairment. Other variants included Miller Fisher, acute motor axonal neuropathy (AMAN), and bilateral facial nerve palsy, as in the case of our diagnosed patient. Seventeen cases of facial involvement variants have been reported in the literature. Of these, one presented bifacial weakness as the only neurological manifestation[10] while others were described as motor or sensory symptoms followed by facial diplegia.[6] In one case, facial palsy preceded motor symptoms,[19] and in the others, the facial palsy and weakness or paresthesias developed at the same time.[6,11] Recently, a case of Bell's palsy on the left side of a 65-year-old woman in China associated with SARS-CoV-2 infection was reported, though without preceding fever, cough, or any other respiratory symptoms. The patient recovered after antiviral treatment; however, no neurophysiological or CSF test was performed.[20]

It is already known that GBS could be triggered by prior bacteria or virus infections, such as Campylobacter jejuni, influenza virus, cytomegalovirus, or Epstein–Barr virus.[14] Taking into account the revised literature and the temporal relationship between the infection and the onset of symptoms described in our case, it is possible that the pathophysiology of SARS-CoV-2 causing GBS via inflammatory reaction through immune mimicry is similar to that proposed for other pathogens.[21,22] However, this should be further characterized with the continuing and growing evidence on the implications of COVID-19 in this pathology.

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