We would like to thank Finsterer et al.[1] for their interest in our short clinical vignette. Their comments and concerns give
us an opportunity to further discuss this case report.
Neurological complications in COVID-19 patients are a knowledge in progress. We agree
that our case may have several differential diagnoses. Although our patient's lesions
did not show post-contrast enhancement, they had a perivenular aspect ([Figure 1]) and disappeared after high doses of corticosteroids.
Figure 1 (A) FLAIR/T2 images in the sagittal plane showing lesions with hyperintensity with
a larger axis perpendicular to the ependymal surface of the lateral ventricles (see
arrows) and absence of restriction to diffusion, suggesting demyelinating lesions;
(B) axial SWI showing periventricular lesions with perivenular involvement (see arrows),
suggesting demyelinating lesions. (C) ADC map showing lesions with hyperintensity
(high diffusion of water molecules, see arrows).
Contrast enhancement may not occur in some demyelinating lesions, including in ADEM-like
presentations, which was the main possibility for our case. Gadolinium enhancement
in ADEM is variable and may be absent, not invalidating its demyelinating nature[2]. The DWI sequence was normal and the lesions disappeared, which did not favor the
diagnosis of ischemic injury. Our patient, in addition, had no previous cardiovascular
risk factors, and his echocardiogram and electrocardiogram were normal. Lesions were
transitory and without bleeding, which goes against the diagnosis of acute necrotizing
encephalitis.
We agree that we must include the possibility of PRES. We know that PRES syndrome
can be precipitated by the use of corticosteroids[3]. There was also no evidence of hypertensive hemodynamic changes of note in this
patient. That is why we used the term possible and not definitive worsening symptoms.
SWI and ADC did not provide any additional data ([Figure 1]). Spectroscopy and perfusion-weighted imaging sequences were not available in our
center.
We did not perform electroneuromyography, although his clinical presentation was suggestive
of critically ill patient neuropathy. Peripheral nerve complicaions have been described
in COVID-19 patients. Most reports are related to Guillain-Barré syndrome and its
variants[4]. We were unable to adequately exclude the concomitance of this manifestation in
our patient. Examination of cerebrospinal fluid is crucial. However, we were unable
to perform it because he had an extensive pressure ulcer in the lumbosacral region,
which even required antimicrobial therapy.
The main message of this case was to think about the possibility of demyelinating
autoimmune lesions occurrence after COVID-19 infection, even within a scenario in
which the patient does not present all the criteria and characteristics typical for
this disease. In this context, high doses of corticosteroids may be considered to
treat and improve clinical recovery.
