European Journal of Physical and Rehabilitation Medicine,
Journal Year:
2020,
Volume and Issue:
56(5)
Published: Nov. 1, 2020
INTRODUCTION:
This
paper
is
the
first
update
of
second
edition
rapid
living
systematic
review
on
latest
scientific
literature
informing
rehabilitation
patients
with
COVID-19
and/or
describing
consequences
disease
and
its
treatment,
as
they
relate
to
limitations
in
functioning
interest.
The
aim
this
study
was
report
data
a
search
performed
papers
published
July
2020.EVIDENCE
ACQUISITION:
methodology
described
applied
eligible
included
databases
between
1,
2020
31,
SYNTHESIS:
Eight-hundred-ninety-two
were
identified
through
database
searching
(after
removal
duplicates);
these,
only
23
studies
included.
According
OCEBM
2011
Levels
Evidence
Table,
level
3
30.5%
cases
4
69.5%.
No
RCT
found.
Nineteen
studied
patients,
assessed
acute
(10
studies),
post-acute
(8
studies)
chronic
phase
(one
study).
Four
reported
impact
subjects
pre-existing
health
conditions.CONCLUSIONS:
current
production
still
focuses
more
all
possible
aspects
complications
pathology
than
interventions
or
new
organization
models
deal
it.
Albeit
evidence
handling
from
rehabilitative
point
view
improving
each
month,
further
are
mandatory
role
scenario.
Nature Reviews Rheumatology,
Journal Year:
2021,
Volume and Issue:
17(6), P. 315 - 332
Published: April 26, 2021
Immune-related
manifestations
are
increasingly
recognized
conditions
in
patients
with
COVID-19,
around
3,000
cases
reported
worldwide
comprising
more
than
70
different
systemic
and
organ-specific
disorders.
Although
the
inflammation
caused
by
SARS-CoV-2
infection
is
predominantly
centred
on
respiratory
system,
some
can
develop
an
abnormal
inflammatory
reaction
involving
extrapulmonary
tissues.
The
signs
symptoms
associated
this
excessive
immune
response
very
diverse
resemble
autoimmune
or
diseases,
clinical
phenotype
that
seemingly
influenced
epidemiological
factors
such
as
age,
sex
ethnicity.
severity
of
also
varied,
ranging
from
benign
self-limiting
features
to
life-threatening
syndromes.
Little
known
about
pathogenesis
these
manifestations,
tend
emerge
within
first
2
weeks
infection,
whereas
others
appear
a
late
post-infectious
stage
even
asymptomatic
patients.
As
body
evidence
comprises
case
series
uncontrolled
studies,
diagnostic
therapeutic
decision-making
unsurprisingly
often
based
scarcely
experience
expert
opinion.
Additional
studies
required
learn
mechanisms
involved
development
apply
knowledge
achieve
early
diagnosis
most
suitable
therapy.
European Journal of Neurology,
Journal Year:
2021,
Volume and Issue:
28(10), P. 3348 - 3359
Published: March 8, 2021
To
assess
neurological
manifestations
and
health-related
quality
of
life
(QoL)
3
months
after
COVID-19.In
this
prospective,
multicenter,
observational
cohort
study
we
systematically
evaluated
signs
diseases
by
detailed
examination
a
predefined
test
battery
assessing
smelling
disorders
(16-item
Sniffin
Sticks
test),
cognitive
deficits
(Montreal
Cognitive
Assessment),
QoL
(36-item
Short
Form),
mental
health
(Hospital
Anxiety
Depression
Scale,
Posttraumatic
Stress
Disorder
Checklist-5)
disease
onset.Of
135
consecutive
COVID-19
patients,
31
(23%)
required
intensive
care
unit
(ICU)
(severe),
72
(53%)
were
admitted
to
the
regular
ward
(moderate),
32
(24%)
underwent
outpatient
(mild)
during
acute
disease.
At
3-month
follow-up,
20
patients
(15%)
presented
with
one
or
more
syndromes
that
not
evident
before
COVID-19.
These
included
polyneuro/myopathy
(n
=
17,
13%)
patient
presenting
Guillain-Barré
syndrome,
mild
encephalopathy
2,
2%),
parkinsonism
1,
1%),
orthostatic
hypotension
ischemic
stroke
1%).
Objective
testing
revealed
hyposmia/anosmia
in
57/127
(45%)
at
follow-up.
Self-reported
was
lower
(17%)
months,
however,
improved
when
compared
phase
(44%;
p
<
0.001).
apparent
23%,
impaired
31%.
Assessment
symptoms
depression,
anxiety,
posttraumatic
stress
11%,
25%,
respectively.Despite
recovery
from
infection,
prevalent
Above
all,
persistent
large
proportion
patients.
European Journal of Neurology,
Journal Year:
2021,
Volume and Issue:
28(10), P. 3245 - 3253
Published: Feb. 12, 2021
Abstract
Background
and
purpose
Neurological
complications
of
SARS‐CoV‐2
infection
are
noticed
among
critically
ill
patients
soon
after
disease
onset.
Information
on
delayed
neurological
sequelae
is
nil.
Following
a
longitudinal
study
design,
the
occurrence
cognitive
decline
individuals
with
history
mild
symptomatic
was
assessed.
Methods
Stroke‐
seizure‐free
Atahualpa
residents
aged
≥40
years,
who
had
pre‐pandemic
assessments
as
well
normal
brain
magnetic
resonance
imaging
electroencephalogram
recordings,
underwent
repeated
evaluations
6
months
outbreak
in
Atahualpa.
Patients
requiring
oxygen
therapy,
hospitalization,
those
initial
manifestations
were
excluded.
Cognitive
defined
reduction
Montreal
Assessment
(MoCA)
score
between
post‐pandemic
that
≥4
points
greater
than
observed
two
MoCAs.
The
relationship
assessed
by
fitting
logistic
mixed
models
for
data
exposure‐effect
models.
Results
Of
93
included
(mean
age
62.6
±
11
years),
52
(56%)
infection.
Post‐pandemic
MoCA
decay
worse
seropositive
individuals.
recognized
11/52
(21%)
1/41
(2%)
seronegative
In
multivariate
analyses,
odds
developing
18.1
times
higher
(95%
confidence
interval
1.75–188;
p
=
0.015).
Exposure‐effect
confirmed
this
association
(
β
0.24;
95%
0.07–0.41;
0.006).
Conclusions
This
provides
evidence
pathogenesis
complication
remains
unknown.
International Journal of Molecular Sciences,
Journal Year:
2021,
Volume and Issue:
22(5), P. 2681 - 2681
Published: March 6, 2021
Emerging
data
indicate
that
neurological
complications
occur
as
a
consequence
of
severe
acute
respiratory
syndrome
coronavirus
2
(SARS-CoV-2)
infection.
The
blood–brain
barrier
(BBB)
is
critical
interface
regulates
entry
circulating
molecules
into
the
CNS,
and
regulated
by
signals
arise
from
brain
blood
compartments.
In
this
review,
we
discuss
mechanisms
which
SARS-CoV-2
interactions
with
BBB
may
contribute
to
dysfunction
associated
disease
2019
(COVID-19),
caused
SARS-CoV-2.
We
consider
aspects
peripheral
disease,
such
hypoxia
systemic
inflammatory
response
syndrome/cytokine
storm,
well
CNS
infection
viral
brain.
also
contribution
risk
factors
for
developing
COVID-19
could
increase
or
otherwise
damage
Journal of Medical Virology,
Journal Year:
2020,
Volume and Issue:
93(3), P. 1304 - 1313
Published: Oct. 1, 2020
Abstract
The
outbreak
of
coronavirus
disease
2019
(COVID‐19),
caused
by
severe
acute
respiratory
syndrome
coronavirus‐2
(SARS‐CoV‐2),
has
become
a
significant
and
urgent
threat
to
global
health.
This
review
provided
strong
support
for
central
nervous
system
(CNS)
infection
with
SARS‐CoV‐2
shed
light
on
the
neurological
mechanism
underlying
lethality
infection.
Among
published
data,
only
1.28%
COVID‐19
patients
who
underwent
cerebrospinal
fluid
(CSF)
tests
were
positive
in
CSF.
However,
this
does
not
mean
absence
CNS
most
because
postmortem
studies
revealed
that
some
showed
negative
results
CSF
SARS‐CoV‐2.
20
neuropathological
reported
so
far,
was
detected
brain
58
cases
nine
studies,
three
have
sufficient
details
patients.
Almost
all
vitro
vivo
experiments
neuroinvasive
potential
In
infected
animals,
found
within
neurons
different
areas
wide
spectrum
neuropathology,
consistent
clinical
symptoms
Several
lines
evidence
indicate
used
hematopoietic
route
enter
CNS.
But
more
supports
trans‐neuronal
hypothesis.
been
invade
via
olfactory,
gustatory,
trigeminal
pathways,
especially
at
early
stage
Severe
deficits
are
higher
risk
mortality,
animals
showing
became
dead,
suggesting
involvement
may
be
one
cause
death.
Annals of Neurology,
Journal Year:
2021,
Volume and Issue:
89(5), P. 1041 - 1045
Published: Feb. 8, 2021
Patients
with
coronavirus
disease
2019
(COVID-19)
can
present
distinct
neurological
manifestations.
This
study
shows
that
inflammatory
diseases
were
associated
increased
levels
of
interleukin
(IL)-2,
IL-4,
IL-6,
IL-10,
IL-12,
chemokine
(C-X-C
motif)
ligand
8
(CXCL8),
and
CXCL10
in
the
cerebrospinal
fluid.
Conversely,
encephalopathy
was
high
serum
CXCL8,
active
tumor
growth
factor
β1.
Inflammatory
syndromes
central
nervous
system
COVID-19
appear
early,
as
a
parainfectious
process
without
significant
systemic
involvement,
or
direct
evidence
severe
acute
respiratory
syndrome
2
neuroinvasion.
At
same
time,
is
mainly
influenced
by
peripheral
events,
including
cytokines.
ANN
NEUROL
2021;89:1041-1045.