ABSTRACT
BACKGROUND: Hemorrhagic cerebrovascular events, either due to aneurysmal rupture or spontaneous subarachnoid hemorrhage (SAH), are not rare in COVID-19. Several mechanisms such as coagulopathy, cytokine storm, viral endotheliopathy, hypertension, and immune modulation might play a role in the pathogenesis of SAH in COVID-19. This study aimed to report the first case of spontaneous non-aneurysmal SAH associated with SARS-CoV-2 from India. We briefly discussed the possible pathogenetic mechanisms underlying this process and succinctly reviewed the relevant literature. CASE REPORT: We herein report a case of a non-comorbid young woman infected with SARS-CoV-2 presenting with thunderclap headache and eventually non-aneurysmal SAH, who recovered with conservative management. CONCLUSION: Headache, although a very common clinical feature of COVID-19 itself, must be investigated in detail to identify alternate causes that may be life-threatening. This case also incites further enquiry into the possible pathogenic mechanisms of neurovascular complications in COVID-19.
ABSTRACT
BACKGROUND AND AIMS: Initially, novel severe acute respiratory syndrome coronavirus (SARS-CoV-2) was considered primarily a respiratory pathogen. However, with time it has behaved as a virus with the potential to cause multi-system involvement, including neurological manifestations. Cerebral venous sinus thrombosis (CVT) has increasingly been reported in association with coronavirus infectious disease of 2019 (COVID-19). Here, we have shed light upon CVT and its possible mechanisms in the backdrop of the ongoing COVID-19 pandemic. METHODS: In this review, data were collected from PubMed, EMBASE and Web of Science, until March 30, 2021, using pre-specified searching strategies. The search strategy consisted of a variation of keywords of relevant medical subject headings and keywords, including "COVID-19", "SARS-CoV-2", "coronavirus", and "cerebral venous sinus thrombosis". RESULTS: COVID-19 has a causal association with a plethora of neurological, neuropsychiatric and psychological effects. CVT has gained particular importance in this regard. The known hypercoagulable state in SARS-CoV-2 infection is thought to be the main mechanism in COVID-19 related CVT. Other plausible mechanisms may include vascular endothelial dysfunction and altered flow dynamics. CONCLUSIONS: Although there are no specific clinical characteristics, insidious or acute onset headache, seizures, stroke-like, or encephalopathy symptoms in a patient with, or who has suffered COVID-19, should prompt the attending physician to investigate for CVT. The treatment of COVID-19 associated CVT does not differ radically from the therapy of CVT without the infection, i.e. urgent initiation of parenteral unfractionated heparin or low molecular weight heparin followed by conventional or mostly newer oral anticoagulants.