ABSTRACT
Background and aims: SARS-CoV2 infection may increase stroke risk. The biological mechanisms underlying ischemic stroke occurrence during COVID-19 remains unclear. Methods: A Genome-Wide Association Study (GWAS) from MEGASTROKE was used to generate Polygenic risk scores (PRSs) across four p-value thresholds (p=0.05-p=5e-8) using PRSice-2. For all ischemic stroke (AIS) we used 34217 cases and 406111 controls, large-artery atherosclerosis (LAA) 4373 cases 297290 controls, cardioembolic (CE) 7193 cases 355468 controls and small-vessel occlusion (SVO) 5386 cases 343560 controls. For undetermined stroke etiology (UND) 984 cases and 5590 controls from a Spanish stroke cohort were used. PRSs were tested in 54 patients with an ischemic stroke that occurred after COVID-19 hospitalization (<8 days)(IS-COV). IS-COV cases were genotyped with Axiom Spain Biobank Array (11 UND, 6 CE, 6 LAA, 5 SVO, 2 infrequent cause and 24 unknown etiology). 726 population controls were also genotyped. Results: We found significant associations of IS-COV with PRSAIS (threshold= 5e-5, p= 0.04;R2= 0.01, number of SNPs= 60), PRSCE (threshold= 5e-8, p= 0.02, R2= 0.01, SNPs= 4;threshold= 0.05, p= 5.9e-4, R2= 0.03, SNPs=19308), PRSLAA (threshold= 5e-5, p= 6.5e-3, R2= 0.02, SNPs= 81;threshold= 1e-4, p= 0.02, R2= 0.01, SNPs= 146;threshold= 0.05, p =1.3e-3, R2= 0.03, SNPs= 20722) and PRSUND (threshold= 1e-4, p= 0.04, R2= 0.01, SNPs=10;threshold= 0.05, p =1.5e-6, R2= 0.06, SNPs= 3416). We did not find any association between PRSSVO and IS-COV. Conclusions: CE, LAA and UND shared genetic mechanisms with ischemic stroke cases due to COVID-19. We found no association between SVO and IS-COV.
ABSTRACT
INTRODUCTION: The COVID-19 pandemic will give rise to long-term changes in neurological care, which are not easily predictable. MATERIAL AND METHODS: A key informant survey was used to enquire about the changes expected in the specialty over the next 5 years. The survey was completed by heads of neurology departments with broad knowledge of the situation, having been active during the pandemic. RESULTS: Despite a low level of consensus between participants, there was strong (85%) and moderate consensus (70%) about certain subjects, mainly the increase in precautions to be taken, the use of telemedicine and teleconsultations, the reduction of care provided in in-person consultations to avoid the presence of large numbers of people in waiting rooms, the development of remote training solutions, and the changes in monitoring visits during clinical trials. There was consensus that there would be no changes to the indication of complementary testing or neurological examination. CONCLUSION: The key informant survey identified the foreseeable changes in neurological care after the pandemic.
Subject(s)
Coronavirus Infections , Health Care Surveys , Nervous System Diseases/therapy , Neurology/trends , Pandemics , Pneumonia, Viral , Administrative Personnel/psychology , COVID-19 , COVID-19 Testing , Clinical Laboratory Techniques , Clinical Trials as Topic/methods , Consensus , Coronavirus Infections/diagnosis , Coronavirus Infections/epidemiology , Coronavirus Infections/prevention & control , Disease Management , Distance Counseling , Forecasting , Hospital Departments/organization & administration , Humans , Nervous System Diseases/diagnosis , Neurologic Examination , Neurology/methods , Neurology/organization & administration , Pandemics/prevention & control , Patient Isolation , Pneumonia, Viral/epidemiology , Pneumonia, Viral/prevention & control , Spain/epidemiologyABSTRACT
SARS-CoV-2 infection can produce neurological features. The most common are headache, anosmia and dysgeusia but patients may also develop other central nervous system (CNS) injuries. We present a patient affected by Covid-19 who initially consulted for decreased visual acuity. The MRI showed inflammation in the right optic nerve and demyelinating lesions in the CNS. We speculate that an immune mechanism induced by SARS-CoV-2, which can activate lymphocytes and an inflammatory response, plays a role in the clinical onset of the disease. This pathogen may be associated with either the triggering or the exacerbation of inflammatory/demyelinating disease.