Third cranial nerve palsy due to COVID-19 infection.

We report a case of a previously healthy man in his 40s who presented with mild SARS-CoV-2 infection (COVID-19) concomitant with acute onset of left third cranial nerve palsy with restricted supraduction, adduction and infraduction. Our patient did not present any history of hypertension, hyperlipidaemia, diabetes mellitus or smoking. The patient recovered spontaneously without any antiviral treatment. To our knowledge, this is the second report of third cranial nerve palsy spontaneously resolved without any risk factors of vascular disease, specific image findings, nor any possible causes other than COVID-19. In addition, we reviewed 10 other cases of third cranial nerve palsy associated with COVID-19, which suggested that the aetiology varies greatly. As a clinician, it is important to recognise COVID-19 as a differential diagnosis for third cranial nerve palsy. Finally, we aimed to encapsulate the aetiologies and the prognosis of the third cranial nerve palsy associated with COVID-19.

A case report of unilateral cervical lymphadenopathy and multiple cranial neuropathies following mRNA-COVID-19 vaccination.

BACKGROUND: We report a rare case of ipsilateral multiple cranial neuropathy and ipsilateral lymphadenopathy following mRNA-COVID-19 vaccination. CASE PRESENTATION: A 41-year-old male visited our emergency room complaining of dysphagia and hoarseness that started a week after receiving COVID19 mRNA vaccination (in his right arm). During his hospitalization, he also complained of right side hearing loss and diplopia. Neurological examination depicted a right IV nerve palsy, ipsilateral facial paresthesia and peripheral facial paresis. Otorinolaryngological examination revealed right vocal cord paralysis. A brain magnetic resonance imaging showed enhancement of the right VII and VIII cranial nerves in the auditory canal. The lumbar puncture revealed increased protein concentration and lymphocytic pleocytosis in the cerebrospinal fluid (CSF). Additionally, a neck computed tomography (CT) scan showed a swollen right supraclavicular lymph node. We hypothesize that the ipsilateral cranial neuropathies of IV, VI, VII, VIII and X, associated with cervical lymphadenopathy, was possible caused by a post-vaccination immune-mediated reaction. The patient was treated with a 5-day course of intravenous methylprednisolone (1000 mg/day), and a gradual improvement was observed. CONCLUSIONS: Similarly, to other vaccines, it is possibly that also mRNA vaccines may act as triggers of non-specific autoimmune neurological syndromes.

Lower Cranial Nerve Palsies in the COVID-19 Pandemic: A 10-Case Series of Intensive Care Unit Patients.

INTRODUCTION: A number of neurological complications of COVID-19 have been identified, including cranial nerve paralyses. We present a series of 10 patients with lower cranial nerve involvement after severe COVID-19 infection requiring hospitalization in an intensive care unit. METHODS: We conducted a retrospective, observational study of patients admitted to the post-intensive care unit (p-ICU) of Besançon University Hospital (France) between March 16 and May 22, 2020. We included patients with confirmed COVID-19 and cranial neuropathy at admission to the p-ICU. All these patients were treated by orotracheal intubation, and all but one underwent prone-position ventilation therapy. RESULTS: Of the 88 patients admitted to the p-ICU, 10 patients (11%) presented at least 1 cranial nerve palsy. Of these 10 patients, 9 had a hypoglossal nerve palsy and 8 of these also had a deficit in another cranial nerve. The most frequent association was between hypoglossal and vagal palsies (5 patients). None of the patients developed neurological signs related to a global neuropathy. We found no correlation between the intensity of the motor limb weakness and the occurrence of lower cranial nerve palsies. All but 2 of the patients recovered within less than a month. CONCLUSION: The mechanical compressive hypothesis, linked to the prone-position ventilation therapy, appears to be the major factor. The direct toxicity of SARS-CoV-2 and the context of immune dysfunction induced by the virus may be involved in a multifactorial etiology.

Dysphagia, dysphonia and a deviated tongue: diagnosing Collet-Sicard syndrome.

A healthy middle-aged man presents with symptoms of dysphagia and dysphonia following an upper respiratory infection, and is diagnosed and treated for complications of pharyngitis. He presents for evaluation at a tertiary care hospital after symptoms fail to resolve, with the final diagnosis being a carotid artery dissection with compressing pseudoaneurysm. This patient's constellation of symptoms and physical examination findings are consistent with Collet-Sicard syndrome, a rare disorder caused by cranial nerve compression at the skull base. Understanding the morbidity of missing, or delaying, a diagnosis of carotid artery pathology, such as Collet-Sicard syndrome, underscores the importance of an accurate diagnosis. A review of cranial nerve anatomy, surrounding structures and potential mechanism of injury to the carotid artery are emphasised as key learning points.

Guillain-Barre syndrome associated to COVID-19 infection: a review of published case reports. / Síndrome de Guillain-Barré asociado a infección por COVID-19: revisión de casos publicados.

INTRODUCTION: The coronavirus disease 2019 (COVID-19) pandemic is a major worldwide health disorder. There is an increasing number of neurological complications recognized with COVID-19 including patients with GBS and its variants. DEVELOPMENT: A review of the clinical cases of GBS associated to COVID-19 infection published in the last months has been developed. We included 48 patients (31 men, mean age 56.4 years). The most common COVID-19 symptoms were cough (60.4%) and fever (56.3%). Mean time from COVID-19 symptoms to neurologic manifestations was 12.1 days, but in nine patients (18.8%) developed GBS within seven days. Eleven patients (22.9%) presented cranial nerve involvement in the absence of muscle weakness; 36 presented the classic sensory motor variant (75%) and one had a pure motor variant (2.1%). The electrodiagnostic pattern was considered demyelinating in 82.4% of the generalized variants. The presence of hyposmia/dysgeusia was associated with a latency shorter than seven days to GBS onset of symptoms (30% vs 15.6%), and cranial nerve involvement in the absence of weakness (30.8% vs 17.1%). Most patients (87.5%) were treated with intravenous immunoglobulin. Neurological outcome was favorable in 64.6%; 29.2% had respiratory failure and 4.2% died shortly after being admitted. CONCLUSIONS: GBS in patients with SARS-CoV-2 infection resembles clinically and electrophysiology the classical forms. Further studies are necessary to understand whether GBS frequency is actually increased due to SARS-CoV-2 infection and explore pathogenic mechanisms.

TITLE: Síndrome de Guillain-Barré asociado a infección por COVID-19: revisión de casos publicados.Introducción. La pandemia por la enfermedad por coronavirus 2019 (COVID-19) es un importante problema para la salud mundial. Hay un incremento en las complicaciones neurológicas reconocidas por la COVID-19, incluyendo el síndrome de Guillain-Barré (SGB) y sus variantes. Desarrollo. Se realizó una revisión de los casos publicados en los últimos meses de SGB asociado a infección por COVID-19. Incluimos a 48 pacientes (31 hombres; edad media: 56,4 años). Los síntomas de COVID-19 más comunes fueron tos (60,4%) y fiebre (56,3%). El tiempo promedio entre los síntomas de COVID-19 y el SGB fue de 12,1 días, pero nueve pacientes (18,8%) desarrollaron SGB en menos de siete días. Once pacientes (22,9%) presentaron afectación de los nervios craneales en ausencia de debilidad muscular, 36 presentaron la variante clásica sensitivomotora (75%) y uno tuvo una variante motora pura (2,1%). El patrón electrofisiológico se consideró desmielinizante en el 82,4% de las variantes generalizadas. La presencia de hiposmia/disgeusia estuvo asociada con una latencia menor a los siete días hasta el inicio de los síntomas del SGB (30 frente a 15,6%) y a la afectación de los nervios craneales en ausencia de debilidad (30,8 frente a 17,1%). La mayoría de los pacientes (87,5%) fueron tratados con inmunoglobulina endovenosa. La evolución neurológica fue favorable en el 64,6%, el 29,2% tuvo insuficiencia respiratoria y hubo un 4,2% de muertes. Conclusiones. El SGB en pacientes con infección por SARS-CoV-2 es similar clínica y electrofisiológicamente a las formas clásicas. Se requieren más estudios para comprender si la frecuencia del SGB realmente aumentó debido a la pandemia por COVID-19 y explorar los mecanismos patógenos involucrados.

A case of COVID-19 with multiple cranial neuropathies.

Various neurological manifestations involving the central and peripheral nervous system have been reported in association with COVID-19. Most common associations reported are encephalopathy, headache, ischemic, hemorrhagic stroke and transient ischemic attack, Miller Fisher syndrome, cranial neuropathies and Guillain-Barre syndrome. Of the cranial neuropathies, anosmia, and dysgeusia are the most common reported symptoms. This is a case of COVID-19 with ipsilateral fifth and seventh cranial nerve involvement with complete resolution of symptoms over a period of 3 weeks. The neurological symptoms started within 5 days of respiratory symptoms. We conclude that isolated cranial neuropathies can be the manifestations of SARS-CoV-2 infection.

Neurological complications of coronavirus infection; a comparative review and lessons learned during the COVID-19 pandemic.

INTRODUCTION: Coronavirus disease-19 (COVID-19) pandemic continues to grow all over the world. Several studies have been performed, focusing on understanding the acute respiratory syndrome and treatment strategies. However, there is growing evidence indicating neurological manifestations occur in patients with COVID-19. Similarly, the other coronaviruses (CoV) epidemics; severe acute respiratory syndrome (SARS-CoV-1) and Middle East respiratory syndrome (MERS-CoV) have been associated with neurological complications. METHODS: This systematic review serves to summarize available information regarding the potential effects of different types of CoV on the nervous system and describes the range of clinical neurological complications that have been reported thus far in COVID-19. RESULTS: Two hundred and twenty-five studies on CoV infections associated neurological manifestations in human were reviewed. Of those, 208 articles were pertinent to COVID-19. The most common neurological complaints in COVID-19 were anosmia, ageusia, and headache, but more serious complications, such as stroke, impairment of consciousness, seizures, and encephalopathy, have also been reported. CONCLUSION: There are several similarities between neurological complications after SARS-CoV-1, MERS-CoV and COVID-19, however, the scope of the epidemics and number of patients are very different. Reports on the neurological complications after and during COVID-19 are growing on a daily basis. Accordingly, comprehensive knowledge of these complications will help health care providers to be attentive to these complications and diagnose and treat them timely.

Miller Fisher syndrome and polyneuritis cranialis in COVID-19.

OBJECTIVE: To report 2 patients infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) who presented acutely with Miller Fisher syndrome and polyneuritis cranialis, respectively. METHODS: Patient data were obtained from medical records from the University Hospital "Príncipe de Asturias," Alcalá de Henares, and the University Hospital "12 de Octubre," Madrid, Spain. RESULTS: A 50-year-old man presented with anosmia, ageusia, right internuclear ophthalmoparesis, right fascicular oculomotor palsy, ataxia, areflexia, albuminocytologic dissociation, and positive testing for anti-GD1b-immunoglobulin G antibody. Five days previously, he had developed a cough, malaise, headache, low back pain, and fever. A 39-year-old man presented with ageusia, bilateral abducens palsy, areflexia, and albuminocytologic dissociation. Three days previously, he had developed diarrhea, a low-grade fever, and poor general condition. Oropharyngeal swab test for SARS-CoV-2 by qualitative real-time reverse transcriptase PCR assay was positive in both patients and negative in the CSF. The first patient was treated with IV immunoglobulin and the second with acetaminophen. Two weeks later, both patients made a complete neurologic recovery, except for residual anosmia and ageusia in the first case. CONCLUSIONS: Our 2 cases highlight the rare occurrence of Miller Fisher syndrome and polyneuritis cranialis during the coronavirus disease 2019 (COVID-19) pandemic. These neurologic manifestations may occur because of an aberrant immune response to COVID-19. The full clinical spectrum of neurologic symptoms in patients with COVID-19 remains to be characterized.