3. Discussion
We present the first description of cranial polyneuropathy involvement
in a child infected with SARS-COV-2. Although COVID-19 is mainly
associated with a respiratory illness, neurological involvement shall
not be underestimated as it has been reported in more than 35% cases in
a recent study of 214 patients (6). Three types of neurological symptoms
have been described: (i) central nervous system manifestations as
dizziness, headache, impaired consciousness, acute cerebrovascular
disease, ataxia, or seizure, (ii) peripheral nervous system
manifestations as taste impairment, smell impairment, vision impairment,
and neuropathic pain, (iii) and skeletal muscular injury manifestations.
Theses neurological manifestations tended to occur early in the illness
(median time, 1-2 days), in patients with severe infection, respiratory
symptoms of COVID-19 developing secondarily as in our observation. Of
the 214 patients, only 5 had isolated peripheral nerve damage, 4 of
which progressed to severe COVID-19 as in our observation.
Our observation could be considered an atypical case of Guillain-Barré
syndrome, with exclusive craniofacial impairment. One case of
Guillain-Barré syndrome associated with SARS-CoV-2 was described in a 61
year old woman (7), recently followed by the description of five
patients with Guillain–Barré syndrome 5 to 10 days after the onset of
COVID-19, 4 of them presenting with facial weakness or diplegia (8). The
pathophysiology of this peripheral nerve damage is not yet established
and may not be unequivocally related to a per or post infectious
immunological mechanism as seen with other infectious agents (9).
Indeed, the cranial polyneuropathy we report was clinically inaugural,
in a heavily immunocompromised patient. Besides, we did not observed the
typical Guillain Barre CSF change with high protein without high
cellularity. In any case, in our observation as in the Toledano series,
the extent of the facial nerves involvement is striking. All these
particularities point to the possible involvement of SARS-Cov 2
neurotropism.
Over the years, some coronaviruses have been associated with
neurological diseases in animals. Among the five different coronaviruses
able to infect humans, at least three strains are neuroinvasive and
neurotropic (10,11). Early in 2002 and 2003, studies on the samples from
patients with SARS revealed the presence of SARS-CoV particles in the
brain, where they were located almost exclusively in the neurons (9).
Experimental studies carried out in mice infected with coronavirus have
shown that the brain stem might be strongly impacted (12,13) which
raises the hypothesis that an impairment of the central nervous system
might be involved in the respiratory failure (14). A potential tropism
for cranial nerves has also been disccused, especially with the
olfactory nerves and bulbs acting as a doorway to the cerebral nervous
system upon a primary nasal infection.
In our patient, no pathogen other than SARS-CoV 2 could be detected,
despite two lumbar punctures and extensive research. However, it remains
possible that viral co-infections (EBV and HSV) interplayed with the
coronavirus in the pathogenesis of this polyneuropathy. Moreover, the
conditioning, the resulting immunosuppression or the pre-existing
cerebral vasculopathy may also have play a role even if this type of
cranial polyneuropathy had not been reported as side effect of
conditioning nor in sickle cell disease.
In conclusion, peripheral nerve involvement is rarely described in
COVID-19 but might predict an aggressive course of the disease, and
facial or cranial nerve involvement may be suggestive. By any means,
physicians should consider SARS-CoV-2 infection in immunocompromised
patients with peripheral nerve abnormalities even without respiratory
manifestations or fever. A prompt diagnosis could prevent delayed
management and prevention of transmission of the virus.
4. Conflict of Interest: The other authors have no conflicts of
interest to disclose.