[Isolated facial diplegia as an atypical variant of Guillain-Barre syndrome after suspected SARS-CoV-2 infection] / Diplejía facial aislada como variante atípica del síndrome de Guillain-Barré tras sospecha de infección por SARS-CoV-2.

Introduction: Since the SARS-CoV-2 pandemics began, multiple cases of Guillain-Barre syndrome secondary to COVID-19 have been described. Its typical presentation consists of the triad of paresthesia, ascending muscle weakness and areflexia, although there are several regional variants such as facial diplegia. Case presentation: Two weeks after a contact with a confirmed case of COVID-19, a 35-year-old woman presents with viral myopericarditis. Laboratory studies for autoimmune diseases come back negative, as well as multiple viral serologies. She presents anti-SARS-CoV-2 IgG, with negative PCR. A week after discharge she presents with palsy of both facial nerves, without other neurological abnormalities. She undergoes examination with cranial CT without findings, and an EMG which shows bilateral alteration of facial nerves. She refuses the performance of a lumbar puncture. Discussion: Facial diplegia can occur because of several illnesses, such as meningeal or brainstem tumors, infectious agents, Guillain-Barre syndrome, autoimmune diseases, trauma, metabolic causes or congenital causes. In our patient, having discarded other etiologies with imaging and analytical studies, the most probable cause is the Guillain-Barre syndrome. It is possibly secondary to SARS-CoV-2 infection given the presence of anti-SARS-CoV-2 IgG antibodies after contact with a confirmed case. Conclusion: This case supports the hypothesis that COVID-19 may trigger the Guillain-Barre syndrome, specifically as facial diplegia, which is an atypical variant that should be known to be early diagnosed and treated as part of this syndrome.

Introducción: Desde que se inició la pandemia por el SARS-CoV-2, se han descrito numerosos casos de síndrome de Guillain-Barré secundario a la COVID-19. Su presentación típica es la triada de parestesias, debilidad muscular ascendente y arreflexia, aunque hay diversas variantes regionales como la diplejía facial. Presentación del caso: Mujer de 35 años que, dos semanas después de un contacto estrecho con un caso confirmado de COVID-19, ingresa por miopericarditis probablemente viral, con estudio de autoinmunidad negativo, múltiples serologías virales negativas y positividad para IgG anti-SARS-CoV-2 con PCR negativa. Una semana tras el alta presenta paresia de ambos nervios faciales sin otras alteraciones neurológicas. Se realiza TAC craneal sin hallazgos y EMG que evidencia afectación bilateral de los nervios faciales. La paciente rechaza realización de punción lumbar Discusión: La diplejía facial puede ocurrir en el contexto de diversas patologías, como tumores meníngeos o troncoencefálicos, agentes infecciosos, síndrome de Guillain-Barré, patologías autoinmunes, traumatismos, causas metabólicas o causas congénitas. En el caso descrito tras descartar mediante pruebas de imagen y analíticamente el resto de etiologías, y dada la presentación clínica, permanece como causa más probable el síndrome de Guillain-Barré, posiblemente secundario a infección por SARS-CoV-2 dada la positividad de IgG anti-SARS-CoV-2 tras un contacto con un caso confirmado. Conclusión: Este caso apoya la hipótesis de que la COVID-19 puede desencadenar el síndrome de Guillain-Barré, específicamente en forma de diplejía facial, una variante atípica que se debe conocer para su identificación y manejo precoz como parte de este síndrome.

Filling the gaps on stroke research: Focus on inflammation and immunity.

For the last two decades, researchers have placed hopes in a new era in which a combination of reperfusion and neuroprotection would revolutionize the treatment of stroke. Nevertheless, despite the thousands of papers available in the literature showing positive results in preclinical stroke models, randomized clinical trials have failed to show efficacy. It seems clear now that the existing data obtained in preclinical research have depicted an incomplete picture of stroke pathophysiology. In order to ameliorate bench-to-bed translation, in this review we first describe the main actors on stroke inflammatory and immune responses based on the available preclinical data, highlighting the fact that the link between leukocyte infiltration, lesion volume and neurological outcome remains unclear. We then describe what is known on neuroinflammation and immune responses in stroke patients, and summarize the results of the clinical trials on immunomodulatory drugs. In order to understand the gap between clinical trials and preclinical results on stroke, we discuss in detail the experimental results that served as the basis for the summarized clinical trials on immunomodulatory drugs, focusing on (i) experimental stroke models, (ii) the timing and selection of outcome measuring, (iii) alternative entry routes for leukocytes into the ischemic region, and (iv) factors affecting stroke outcome such as gender differences, ageing, comorbidities like hypertension and diabetes, obesity, tobacco, alcohol consumption and previous infections like Covid-19. We can do better for stroke treatment, especially when targeting inflammation following stroke. We need to re-think the design of stroke experimental setups, notably by (i) using clinically relevant models of stroke, (ii) including both radiological and neurological outcomes, (iii) performing long-term follow-up studies, (iv) conducting large-scale preclinical stroke trials, and (v) including stroke comorbidities in preclinical research.