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Título

Cerebral vasospasm: How far do the sequels of SARS-cov-2 infection go?

RESUMO

Case report: Female, 22 years-old, referred by SAMU, was admitted to the neurological emergency service after an episode of generalized tonic-clonic epileptic seizure, lasting about 20 minutes, and drowsiness after the crisis. She denied sphincter release. On admission, the patient was feverish, pale, drowsy, GCS 14, without focal deficits. No neck stiffness. Complementary investigation showing hypokalemia and leukocytosis. Brain Computed Tomography (CT) did not show any changes. Before, she reported hospitalization for a month due to a SARS-Cov-2 infection, requiring mechanical ventilation for 17 days. Considering the hypothesis of infectious encephalitis, the patient received empirical treatment with Acyclovir and Meropenem. After two days of hospitalization, she presented a new episode of generalized tonic-clonic epileptic seizure. The investigation proceeded: negative serology, no hypovitaminosis, negative COVID swab, electroencephalogram without changes. Magnetic resonance imaging (MRI) of the skull with hyperintense lesions in the occipital region. Positive Cerebrospinal Fluid (CSF) Analysis for herpes simplex virus 2, with negative bacterioscopy. Electroneuromyography without significant changes. The patient evolved with better clinical improvement. New CSF study: red blood cells: 120, leukocytes: 1 cell (neutrophils: 2%, lymphocytes: 93% monocytes: 5%) proteins: 28. glucose: 57, LDH: 27 ADA: 0.1, VDRL: negative. A new MRI was performed, which showed an increased signal at the cortico-subcortical T2 and Flair sequences in bilateral parieto-occipital lobes and right frontal lobe with contrast enhancement. Vessel wall with microconstrictions inferring a reversible cerebral vasospasm pattern.
Discussion: Here we present a case of cerebral vasospasm in a young patient with no previous comorbidities. It is known that COVID-19 has been associated with immune dysregulation of the host that can increase the risk of infections such as herpes virus, but this mechanism is still not well understood. In addition, Sars-cov-2 has been showing a vast amount of sequelae in those affected, including cerebral vasospasm .
Final comments: The literature shows to an endothelial inflammation caused by the coronavirus as a contributor to the development of cerebrovascular disease, which includes, in addition to vasospasm, stroke, headaches and other changes in the central nervous system, and it may even aggravate other infections .

Palavras Chave

Cerebral vasospasm; Reversible cerebral vasoconstriction syndrome pos covid; Neurocovid; COVID 19; herpes virus type 2