ABSTRACT
Cerebral small-vessels are generally located in the brain at branch points from major cerebral blood vessels and perfuse subcortical structures such as the white matter tracts, basal ganglia, thalamus, and pons. Cerebral small-vessel disease (CSVD) can lead to several different clinical manifestations including ischemic lacunar stroke, intracerebral hemorrhage, and vascular dementia. Risk factors for CSVD overlap with conventional vascular risk factors including hypertension, diabetes mellitus, and hypercholesterolemia, as well as genetic causes. As in cardiovascular disease, treatment of CSVD involves both primary and secondary prevention. Aspirin has not been established as a primary prevention strategy for CSVD among the general population; however, long-term antiplatelet therapy with aspirin alone continues to be the mainstay of secondary stroke prevention for non-cardioembolic ischemic stroke and high-risk TIA.
ABSTRACT
Hypercoagulability and virally-mediated vascular inflammation have become well-recognized features of the SARS-CoV-2 virus infection, COVID-19. Of growing concern is the apparent ineffectiveness of therapeutic anticoagulation in preventing thromboembolic events among some at-risk patient subtypes with COVID-19. We present a 43-year-old female with a history of seropositive-antiphospholipid syndrome and systemic lupus erythematosus who developed an acute ischemic stroke in the setting of mild COVID-19 infection despite adherence to chronic systemic anticoagulation. The clinical significance of SARS-CoV-2-mediated endothelial cell dysfunction and its potential to cause macrovascular events in spite of full anticoagulation warrants further investigation and likely represents another disease-defining pathology of COVID-19.
Subject(s)
Anticoagulants/therapeutic use , Antiphospholipid Syndrome/drug therapy , COVID-19/complications , Ischemic Stroke/etiology , Lupus Coagulation Inhibitor/blood , Adult , Antiphospholipid Syndrome/blood , Antiphospholipid Syndrome/complications , Antiphospholipid Syndrome/diagnosis , Biomarkers/blood , COVID-19/diagnosis , Female , Humans , Ischemic Stroke/diagnostic imaging , Ischemic Stroke/prevention & control , Risk Factors , Treatment FailureABSTRACT
Novel coronavirus SARS-CoV-2 has created unprecedented healthcare challenges. Neurologic deficits are often an important presenting symptom. To date, the only reported post-infectious COVID-19 manifestations of neurologic disease include cognitive deficits and dysfunction of the peripheral nervous system. Here we report that seizure can also be a post-COVID-19 or "long-COVID" complication. We present a 71-year-old man with hypertension, diabetes mellitus, and COVID-19 diagnosed by RT-PCR who initially presented with posterior circulation stroke-like symptoms, which completely resolved after emergent thrombolysis. Six days later, the patient returned with seizure activity, supported by radiographic and electroencephalographic studies. Notably, he was negative for SARS-CoV-2, and no other provoking factor was uncovered after a comprehensive work-up. To our knowledge, this is the first report of post-infectious seizures after a case of COVID-19, highlighting the potential importance of monitoring for neurologic symptoms in COVID-19 patients, even after convalescence.
ABSTRACT
Here we describe a case of brainstem infarction secondary to rapid thrombus formation in a giant vertebrobasilar fusiform aneurysm (GVBFA) that was preceded clinically by several months of headaches and dizziness initially attributable to mass effect. Less than a month after initial identification of the aneurysm, a large partially-occluding thrombus formed leading to infarction of the brainstem. Interestingly, this patient also had ulcerative colitis, which has been associated with acquired hypercoagulability. Balancing risk versus benefit in the management of GVBFA to prevent morbidity and mortality is very challenging; thus more information is needed to better stratify treatment options for patients, particularly those that may have an accelerating clinical course or co-morbidities that increase clotting risk.