Encephalopathy in COVID-19 Patients

Abstract

The clinical presentation of coronavirus disease 2019 (COVID-19) has a wide spectrum, ranging from asymptomatic patients to severe presentations with acute respiratory distress syndrome (ARDS), kidney injury, stroke, electrolyte imbalance, and multi-organ failure. Encephalopathy and encephalitis are devastating severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) virus-associated central nervous system complications.We reported a case of a 67-year-old male who was admitted to the hospital for the management of COVID-19 pneumonia. Due to worsening hypoxia, the patient was transferred to ICU and was intubated. On examination, he was aphasic and noted to have right-sided hemiplegia with left-sided hemiparesis on day 4. CT scan of the head without contrast and MRI findings were suggestive of acute necrotizing encephalopathy secondary to intracranial cytokine storm caused by viral infection. The patient was treated with intravenous immunoglobulin (IVIG), and high dose corticosteroids, with clinical improvement in the right-sided hemiparesis on day 5. A repeat MRI brain revealed decreased edema.The pathogenesis of encephalopathy associated with COVID-19 may be multifactorial. Postulated mechanisms include hypoxic/metabolic changes produced by the intense inflammatory response due to cytokine storm and neurotropism. Cytokine storm causes hypoxia and metabolic insults that result in global dysfunction of the brain. Altered consciousness, ranging from mild confusion, delirium, to deep coma, are some of the cardinal clinical features. The most common imaging finding on MRI T2-weighted fluidattenuated inversion recovery (MRI T2/FLAIR) includes symmetric, multifocal lesions with invariable thalamic involvement. Other commonly involved locations include the brainstem, cerebral white matter, cortical and subcortical white matter, and cerebellum. In a few case reports, cerebrospinal fluid (CSF) analysis has shown the presence of the virus. Management of encephalopathy in COVID-19 patients involves supportive care including supplemental oxygen therapy and immune modulators. Immune modulation therapy including high-dose corticosteroids and IVIG have been shown to improve outcomes in these patients.

Effect of coronaviruses on blood vessel permeability: potential therapeutic targets

“…In this context, a case report demonstrated corticosteroids improved oxygenation in patients with COVID-19; 168 other case reports observed corticosteroids diminished cerebral edema in these patients. 169 , 170 It is worth mentioning that corticosteroids may present different outcomes in ARDS subjects depending on several factors, including the timing of initiation of treatment, the origin of ARDS, type and dose of corticosteroid, and among others (for a review on corticosteroids and ARDS, see Hussain et al . 171 ).…”

New‑onset neuropsychiatric sequelae and ‘long‑COVID’ syndrome (Review)

“…The hypometabolic state of different important brain areas in the frontal and temporal lobes, due to cytokine and neurotropism-related encephalopathy (55), contributes to the brain pathology and is evident as diffuse slowing in electroencephalography and bilateral frontotemporal hypoperfusion in arterial spin labelling MRI (56,57). Neuroinvasion of the virus is suspected to occur either through cranial nerves that innervate the respiratory tract (particularly the olfactory nerve), or through hematogenous spread by crossing the BBB or the blood-cerebrospinal fluid barrier (58)(59)(60).…”

Neurološke komplikacije COVID-19

“…Kliničke slike encefalopatija su uključivale letargiju, somnolenciju, konfuziju, agitaciju, delirij i komu. S obzirom da je u takvih bolesnika klinička slika uključivala i hipoksiju, elektrolitski disbalans, zatajenje bubrega, sedaciju te prateće komorbiditete, patofiziološki mehanizam nastanka encefalopatije je najvjerojatnije višefaktorski [34,35] . Za razliku od navedenih teških slučajeva COVID-19, provedene studije na bolesnicima u odsustvu teške respiratorne bolesti ukazuju na druge moguće mehanizme nastanka encefalopatije, uključujući biološke promjene i vaskularnu disfunkciju [36,37] .…”