Affiliation:
1. Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suarez Ciudad de México México
2. Instituto de Biotecnología Universidad Nacional Autónoma de México (UNAM) Cuernavaca Morelos México
3. Instituto de Neurobiología UNAM‐Juriquilla Querétaro México
4. Institute for Memory Impairments and Neurological Disorders University of California‐Irvine Irvine California USA
5. Hospital General de Ticomán Secretaría de Salud de la Ciudad de México Ciudad de México México
6. Unidad de Investigación en Biomedicina Facultad de Estudios Superiores Iztacala, UNAM Tlalneplantla Estado de México México
Abstract
AbstractMore than 670 million cases of coronavirus disease 2019 (COVID‐19) have been recorded worldwide in the 3 years since the start of the severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) pandemic. About 45% of survivors of COVID‐19 develop a syndrome known as long‐term COVID, in which symptoms persist even months after the acute infection. About 76% of patients with long COVID experience neurological manifestations. Moreover, patients who have survived COVID‐19 have an increased risk of cerebral venous thrombosis. This case report describes a 41‐year‐old woman who developed neurological manifestations associated with jugular vein thrombosis 24 h after administration of the Oxford–AstraZeneca (ChAdOx1 nCoV‐19) vaccine (AstraZeneca‐Serum Institute of India). She had been infected with SARS‐CoV‐2 three months before vaccination. Although initially suspected to be a case of vaccine‐induced immune thrombotic thrombocytopenia (VITT) in view of her recent vaccination, the patient did not have any hallmarks of VITT, such as thrombocytopenia, an increased d‐dimer level, or antibodies against platelet factor‐4. Moreover, the neurological manifestations were associated with a high concentration of inflammatory cytokines, including interleukin (IL)‐6, IL‐17A, and IL‐21, and elevated neutrophil levels in cerebrospinal fluid, suggesting that inflammatory immune components had a role in the development of thrombotic events and pointing to an alternative diagnosis. In this case, the laboratory results indicated that the neurological manifestations associated with jugular vein thrombosis were not associated with VITT. Therefore, we propose that the thrombosis of the left jugular vein was a sequela of SARS‐CoV‐2 infection.