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A little consideration for “Rare presentations of COVID-19: PRES-like leukoencephalopathy and carotid thrombosis"

      Highlights

      • Acute kidney injury may be associated with PRES.
      • Immunomodulatory drugs may trigger PRES.
      • The combination of these two factors and SARS-CoV-2 infection caused the patient to develop PRES.

      Keywords

      Dear Editor:
      We are grateful to Doo FX et al. for their research, which greatly helped us understand clinical manifestations of posterior reversible encephalopathy syndrome (PRES), a rare neurological disease in the COVID-19 patient.
      • Doo F.X.
      • Kassim G.
      • Lefton D.R.
      • Patterson S.
      • Pham H.
      • Belani P.
      Rare presentations of COVID-19: PRES-like leukoencephalopathy and carotid thrombosis.
      However, in this letter, we want to put forward a different view on the pathogenic mechanism of PRES in the patient.
      On the one hand, previous studies have concluded that transient acute kidney injury creates an environment of cerebral hyperperfusion, which may be involved in formation of PRES. At the same time, the posterior part of the cerebral hemisphere is more susceptible to high blood perfusion to form vasogenic edema because the sympathetic nervous system of the vertebrobasilar artery is weaker than that of the internal carotid artery system. The posterior circulation is more prone to vasodilation than the anterior circulation.
      • Fischer M.
      • Schmutzhard E.
      Posterior reversible encephalopathy syndrome.
      • Tetsuka S.
      • Ogawa T.
      Posterior reversible encephalopathy syndrome: a review with emphasis on neuroimaging characteristics.
      It is consistent with the symmetrical parieto-occipital white matter hyperintensity found in the magnetic resonance imaging (MRI) of the PRES patient.
      On the other hand, immunomodulatory drugs can cause vascular endothelial dysfunction, which may trigger the occurrence of PRES.
      • Fischer M.
      • Schmutzhard E.
      Posterior reversible encephalopathy syndrome.
      The patient was given two doses of tocilizumab due to his serious illness. With the use of these drugs, the vascular endothelium was destroyed by the presence of exogenous toxins, making the presence of the vasoconstrictor substance in the vascular endothelium released, and then vasospasm occurs, which destroys the stability of the blood-brain barrier and creates conditions for the emergence of PRES.
      • Fischer M.
      • Schmutzhard E.
      Posterior reversible encephalopathy syndrome.
      • Tetsuka S.
      • Ogawa T.
      Posterior reversible encephalopathy syndrome: a review with emphasis on neuroimaging characteristics.
      It is worth noting that both acute kidney injury and the use of tocilizumab before epilepsy symptoms associated with PRES. Judging from the order of time, this seems to support the two mediation of formation of PRES. More interestingly, there are also several similar cases reported in the COVID-19 pandemic. Some patients with SARS-CoV-2 infection, who have suffered acute kidney injury or have used interleukin inhibitors such as anakinra and tocilizumab, were finally confirmed to have typical vasogenic edema by brain MRI, which is consistent with PRES.
      • Parauda S.C.
      • Gao V.
      • Gewirtz A.N.
      • et al.
      Posterior reversible encephalopathy syndrome in patients with COVID-19.
      • Llansó L.
      • Urra X.
      Posterior reversible encephalopathy syndrome in COVID-19 disease: a case-report [published online ahead of print, 2020 Aug 26].
      • Conte G.
      • Avignone S.
      • Carbonara M.
      • et al.
      COVID-19-associated PRES-like encephalopathy with perivascular gadolinium enhancement.
      This suggests that the two may be potential risk factors for the development of PRES.
      Therefore, we believe that combined effects of three factors including acute kidney injury, use of immunomodulatory drugs such as tocilizumab, and invasion of COVID-19 co-created the environment for the arrival of PRES, rather than simply caused by the direct effects of SARS-CoV-2 infection in the case.

      Declaration of competing interest

      The authors declare that they have no competing interests.

      Acknowledgements

      This study was supported by Natural Science Foundation of China ( 81571276 ).

      Statistical analysis

      No statistical analysis.

      Authors' contribution statements

      FT designed and supervised the overall research. DS wrote the first draft of manuscript. All authors contributed to manuscript revision, read and approved the submitted version.

      References

        • Doo F.X.
        • Kassim G.
        • Lefton D.R.
        • Patterson S.
        • Pham H.
        • Belani P.
        Rare presentations of COVID-19: PRES-like leukoencephalopathy and carotid thrombosis.
        Clin Imaging. 2021; 69: 94-101https://doi.org/10.1016/j.clinimag.2020.07.007
        • Fischer M.
        • Schmutzhard E.
        Posterior reversible encephalopathy syndrome.
        J Neurol. 2017; 264: 1608-1616https://doi.org/10.1007/s00415-016-8377-8
        • Tetsuka S.
        • Ogawa T.
        Posterior reversible encephalopathy syndrome: a review with emphasis on neuroimaging characteristics.
        J Neurol Sci. 2019; 404: 72-79https://doi.org/10.1016/j.jns.2019.07.018
        • Parauda S.C.
        • Gao V.
        • Gewirtz A.N.
        • et al.
        Posterior reversible encephalopathy syndrome in patients with COVID-19.
        J Neurol Sci. 2020; 416117019https://doi.org/10.1016/j.jns.2020.117019
        • Llansó L.
        • Urra X.
        Posterior reversible encephalopathy syndrome in COVID-19 disease: a case-report [published online ahead of print, 2020 Aug 26].
        SN Compr Clin Med. 2020; : 1-3https://doi.org/10.1007/s42399-020-00470-2
        • Conte G.
        • Avignone S.
        • Carbonara M.
        • et al.
        COVID-19-associated PRES-like encephalopathy with perivascular gadolinium enhancement.
        AJNR Am J Neuroradiol. 2020; 41: 2206-2208https://doi.org/10.3174/ajnr.A6762