ABSTRACT
BACKGROUND: Acute arterial-ischemic-stroke (AIS) has been reported as a rare adverse-event following COVID-19-vaccination with mRNA or viral-vector vaccines. However, data are sparse regarding the risk of post-vaccination AIS and its potential association with thrombotic-thrombocytopenia-syndrome (TTS). METHODS: A systematic review and meta-analysis of randomized-controlled clinical trials (RCTs), pharmacovigilance registries, registry-based studies, observational cohorts and case-series was performed with the aim to calculate: (1) the pooled proportion of patients presenting with AIS following COVID-19-vaccination; (2) the prevalence of AIS after mRNA and vector-based vaccination; (3) the proportion of TTS among post-vaccination AIS-cases. Patient characteristics were assessed as secondary outcomes. RESULTS: Two RCTs, three cohort and eleven registry-based studies comprising 17,481 AIS-cases among 782,989,363 COVID-19-vaccinations were included in the meta-analysis. The pooled proportion of AIS following exposure to any COVID-19-vaccine type was 4.7 cases per 100,000 vaccinations (95%CI:2.2-8.1; I2=99.9%). The pooled proportion of AIS following mRNA-vaccination (9.2 cases per 100,000 vaccinations; 95%CI: 2.5-19.3; I2=99.9%) did not differ compared to adenovirus-based-vaccination (2.9 cases per 100,000 vaccinations; 95%CI: 0.3-7.8; I2=99.9%). No differences regarding demographics were disclosed between patients with AIS following mRNA- or vector-based vaccination. The pooled proportion of TTS among post-vaccination AIS-cases was 3.1% (95%CI: 0.7-7.2%; I2=78.8%). CONCLUSIONS: The pooled proportion of AIS following COVID-19 vaccination is comparable to the prevalence of AIS in the general population and much lower than the AIS prevalence among SARS-CoV-2-infected patients. TTS is very uncommonly reported in patients with AIS following COVID-19 vaccination.
Subject(s)
Autonomic Nervous System Diseases , COVID-19 , Primary Dysautonomias , Autonomic Nervous System Diseases/etiology , COVID-19/complications , Heart Rate/physiology , Humans , Sympathetic Nervous System/physiology , Ultrasonography, Doppler, Transcranial , Vagus Nerve , Post-Acute COVID-19 SyndromeSubject(s)
Brain Ischemia , Myelodysplastic Syndromes , Thrombocytopenia , Thrombosis , Vaccines , Brain Ischemia/diagnosis , Brain Ischemia/etiology , Humans , Myelodysplastic Syndromes/complications , Myelodysplastic Syndromes/diagnosis , Thrombocytopenia/chemically induced , Vaccines/adverse effectsABSTRACT
Accumulating evidence points toward a very high prevalence of prolonged neurological symptoms among coronavirus disease 2019 (COVID-19) survivors. To date, there are no solidified criteria for 'long-COVID' diagnosis. Nevertheless, 'long-COVID' is conceptualized as a multi-organ disorder with a wide spectrum of clinical manifestations that may be indicative of underlying pulmonary, cardiovascular, endocrine, hematologic, renal, gastrointestinal, dermatologic, immunological, psychiatric, or neurological disease. Involvement of the central or peripheral nervous system is noted in more than one-third of patients with antecedent severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, while an approximately threefold higher incidence of neurological symptoms is recorded in observational studies including patient-reported data. The most frequent neurological manifestations of 'long-COVID' encompass fatigue; 'brain fog'; headache; cognitive impairment; sleep, mood, smell, or taste disorders; myalgias; sensorimotor deficits; and dysautonomia. Although very limited evidence exists to date on the pathophysiological mechanisms implicated in the manifestation of 'long-COVID', neuroinflammatory and oxidative stress processes are thought to prevail in propagating neurological 'long-COVID' sequelae. In this narrative review, we sought to present a comprehensive overview of our current understanding of clinical features, risk factors, and pathophysiological processes of neurological 'long-COVID' sequelae. Moreover, we propose diagnostic and therapeutic algorithms that may aid in the prompt recognition and management of underlying causes of neurological symptoms that persist beyond the resolution of acute COVID-19. Furthermore, as causal treatments for 'long-COVID' are currently unavailable, we propose therapeutic approaches for symptom-oriented management of neurological 'long-COVID' symptoms. In addition, we emphasize that collaborative research initiatives are urgently needed to expedite the development of preventive and therapeutic strategies for neurological 'long-COVID' sequelae.
ABSTRACT
This correspondence comments on a published article presenting a case of rhombencephalitis following SARS-CoV-2-vaccination with the mRNA vaccine BNT162b2 (Pfizer/BioNTech). We also present the case of a 47-year-old man who developed Guillain-Barré-syndrome and a fulminant encephalomyelitis 28 days after immunization with Ad26.COV2.S (Janssen/Johnson & Johnson). Based on the presented cases, we underscore the importance of clinical awareness for early recognition of overlapping neuroimmunological syndromes following vaccination against SARS-CoV-2. Additionally, we propose that that role of autoantibodies against angiotensin-converting enzyme 2 (ACE2) and the cell-surface receptor neuropilin-1, which mediate neurological manifestations of SARS-CoV-2, merit further investigation in patients presenting with neurological disorders following vaccination against SARS-CoV-2.