You better hope doctors figure this out by the time you get COVID-19. I however will be demanding massive anti-coagulation therapies because of the clotting seen in autopsies. I'm not medically trained so don't listen to me.
Magnetic Resonance Imaging Alteration of the Brain in a Patient With Coronavirus Disease 2019 (COVID-19) and Anosmia
The neurotropism of human
coronaviruses has already been demonstrated in small animals, and in
autoptic studies the severe acute respiratory syndrome coronavirus
(SARS-CoV), which was responsible for the SARS outbreak during 2002 to
2003, was found in the brains of patients with infection.1
It has been proposed that the neuroinvasive potential of the novel
SARS-CoV-2, responsible for coronavirus disease 2019 (COVID-19), may be
at least partially responsible for the respiratory failure of patients
with COVID-19.2
In this article, we share the magnetic resonance imaging (MRI) evidence
of in vivo brain alteration presumably due to SARS-CoV-2 and
demonstrate that anosmia can represent the predominant symptom in
COVID-19.
A 25-year-old female radiographer with no significant
medical history who had been working in a COVID-19 ward presented with a
mild dry cough that lasted for 1 day, followed by persistent severe
anosmia and dysgeusia. She did not have a fever. She had no trauma,
seizure, or hypoglycemic event. Three days later, nasal fibroscopic
evaluation results were unremarkable, and noncontrast chest and
maxillofacial computed tomography results were negative. On the same
day, a brain MRI was also performed. On 3-dimensional and 2-dimensional
fluid-attenuated inversion recovery images, a cortical hyperintensity
was evident in the right gyrus rectus (Figure 1) and a subtle hyperintensity was present in the olfactory bulbs (Figure 1). Because many patients in Italy are experiencing anosmia3
and the cortical signal alteration was suggestive of viral infection, a
swab test was performed and reverse transcription–polymerase chain
reaction analysis yielded positive results for SARS-CoV-2. During a
follow-up MRI performed 28 days later, the signal alteration in the
cortex completely disappeared and the olfactory bulbs were thinner and
slightly less hyperintense (Figure 24).
The patient recovered from anosmia. No brain abnormalities were seen in
2 other patients with COVID-19 presenting anosmia who underwent brain
MRI 12 and 25 days from symptom onset.
Figure
1. Brain Magnetic Resonance Imaging Alterations in a Patient With
Coronavirus Disease 2019 (COVID-19) Presenting With Anosmia 4 Days From
Symptom Onset
Coronal
(A) and axial (B) reformatted 3-dimensional fluid-attenuated inversion
recovery (FLAIR) images showing cortical hyperintensity in the right
gyrus rectus (yellow arrowheads in A and B). In the inset in A, a
coronal 2-dimensional FLAIR image shows subtle hyperintensity in the
bilateral olfactory bulbs (white arrowheads). The cortical
hyperintensity is present only in the posterior portion of the right
gyrus rectus (B). Accordingly, the cortical hyperintensity of the right
gyrus rectus is evident in the more posterior coronal image (A) and not
in the anterior coronal one (inset).
Figure 2. Follow-up Magnetic Resonance Imaging Study in the Same Patient 28 Days From Symptom Onset
Coronal
(A) and axial (B) reformatted 3-dimensional fluid-attenuated inversion
recover (FLAIR) images showing complete resolution of the previously
seen signal alteration within the cortex of the right gyrus rectus. In
the inset, a coronal 2-dimensional FLAIR image shows a slight reduction
of the hyperintensity and the thickness of the olfactory bulbs,
suggesting a postinfection olfactory loss.4
To our knowledge, this is the first report of in vivo
human brain involvement in a patient with COVID-19 showing a signal
alteration compatible with viral brain invasion in a cortical region
(ie, posterior gyrus rectus) that is associated with olfaction.
Alternative diagnoses (eg, status epilepticus, posterior reversible
encephalopathy syndrome–like alterations, other viral infections, and
anti–N-methyl-d-aspartate
receptor encephalitis) are unlikely given the clinical context. Based
on the MRI findings, including the slight olfactory bulb changes, we can
speculate that SARS-CoV-2 might invade the brain through the olfactory
pathway and cause an olfactory dysfunction of sensorineural origin;
cerebrospinal fluid and pathology studies are required to confirm this
hypothesis. Ours and others’ observations of normal brain imaging in
other patients with COVID-19–associated olfactory dysfunctions4
and the disappearance of the cortical MRI abnormalities in the
follow-up study of this patient suggest that imaging changes are not
always present in COVID-19 or might be limited to the very early phase
of the infection. Further, anosmia can be the predominant COVID-19
manifestation, and this should be considered for the identification and
isolation of patients with infection to avoid disease spread.
Published Online: May 29, 2020. doi:10.1001/jamaneurol.2020.2125
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