Lancaster Physician Spring 2020 - 24

L A N C A S T E R M E D I C A L S O C I E T Y.O R G

Healthy Communities

COVID-19
AND NEUROLOGY

VENKATACHALAM MANGESHKUMAR, MD, FRCP, FAAN
AND TATYANA BOZHKO, CNRP
Neurology & Stroke Associates, PC

T

he first human coronavirus was discovered in the 1960s. Corona means
"crown" or "halo," reminiscent of the
solar corona. Coronavirus is frequently linked to the common cold. Previous
major breakouts were SARS-1 (severe acute
respiratory syndrome) and MERS (Middle
East respiratory syndrome). According to
taxonomy of the virus, COVID-19 (SARS-2)
is the seventh member of the corona family.
COVID-19 virus is a single-strand positive-sense genome with four specific proteins.
The spikes (which contain "S" protein) on the
surface of COVID-19 are club-shaped and
bind to the ACE2 receptors that are widely
expressed in many human cells. You might
think of the spikes as keys and the ACE2
receptors as the keyholes to visualize how
they interact. COVID-19 internalizes into
human cells through the ACE2 receptor to
undergo translation, transcription, and replication. Multiple viral genomes are formed
to exit the cell and infect other ACE2 receptor cells. Expression of ACE2 receptors are
found copiously in the lungs. They are also
expressed in kidney, mouth, GI system, and
heart. ACE2 receptors are also found in the
nasal mucosa, eyes, and brain.
Often, COVID-19 patients are asymptomatic
("shedders" of the virus) or have only mild
symptoms. Some may have serious multi-organ involvement. The lungs are particularly
vulnerable because of copious representation
of ACE2 receptors in the lower lungs. This
can lead to acute respiratory distress, systemic
shock, and death in some cases from the
so-called "cytokine storm."
There are increasing reports from around
the world and in the United States about
neurological manifestations with COVID19 infection. Both central and peripheral
nervous systems may be involved. Various

presentations may include mental status
change, confusion, listlessness, concentration
difficulty, staring spells, impaired consciousness, seizures, headaches, dizziness, nausea,
and vomiting. Others may include hyposmia
(reduced smell), hypogeusia (reduced taste),
lack of appetite, coma, stroke-like syndromes,
neuralgia, axonal neuropathies, GBS-like
(Guillain-Barre) syndrome, and severe
muscle pains. If a patient has a stroke with
co-infection of COVID-19, it may result in
worsening of stroke symptoms.
Meningoencephalitis and acute necrotizing
encephalopathy have been reported. There is
one case report (by Neo Poyiadji and others)
of hemorrhagic necrotizing encephalopathy
that was published in a medical journal in
March 2020. Thought leaders in neurology
postulate that CNS (central nervous system)
access of COVID-19 may be due to retrograde
spread from neural plexus of the olfactory
nerves, trigeminal nerve, pharyngeal nerve,
and other nerves in the head and neck region.
It is also hypothesized that autonomic and
synaptic neural spread of the virus occurs in a
retrograde fashion affecting cardiorespiratory
centers of the brain stem that can further
compromise the cardiorespiratory system.
The affinity of "P" protein of COVID-19 to
ACE2 receptors is thought to happen where
sufficient expression of ACE2 receptors is in
the brain cells-particularly in the circumventricular region, the third ventricle (next to the
thalamus), brain stem, and other areas of the
brain, including the blood-brain barrier. It is
possible there is a "brain cytokine storm," just
like the "systemic cytokine storm." It is also
known that the ACE receptors cross talk to
other receptors like dopamine, bradykinin,
NMDA, and others; therefore, leading to
mental status changes and confusion. It is
believed that ACE2 receptors are supposed
to be neuroprotective. If the hypothalamus
is involved, there may not be a fever. In fact,

LANCASTER

24

PHYSICIAN

some patients have no fever or respiratory
symptoms, surprisingly. We have ventilation
treatment for acute respiratory distress syndrome, but there is no luxury of ventilator
rescue for the brain.
The other issue we face as neurologists during
the pandemic is how we manage patients
with neuro-immunological disorders such as
multiple sclerosis, myasthenia gravis, CIDP
(chronic inflammatory demyelinating polyneuropathy), auto immune encephalitis, and
others. These high-risk patients will have to be
dealt with on a case-by-case basis, but with an
overwhelming patient load, it is not humanly
possible to interrogate every one. There are
many vulnerable patients, particularly the
elderly, with pre-existing conditions such
as Parkinson's disease, dementia, ALS, and
numerous other disorders. These patients are
at risk for COVID-19 infection but may not
mount a fever as one would expect. Therefore,
they may not meet the criteria for testing.
These are the patients that physicians may
consider retrospectively testing for IgG and
IgM antibodies if that testing becomes more
widely available.
Another foreseeable issue after the COVID-19
pandemic is neurological manifestation like
GBS syndrome, transverse myelitis, and other
conditions that have not been reported yet
to our knowledge. Several viruses have been
implicated as a causative link for multiple sclerosis including coronavirus in the past. Lastly,
if a vaccination is identified, is there going to
be past vaccinal neurological manifestation?
We have many questions with inadequate
answers. Over time, we may have more
clarity. However, for now, we may have to
think outside the box to the best of our
ability by applying medical prudence as
we help our patients.



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