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Quantifying cortical EEG responses to TMS in (un)consciousness.
[locked-in syndrome]
We
normally
assess
another
individual
's
level
of
consciousness
based
on
her
or
his
ability
to
interact
with
the
surrounding
environment
and
communicate
.
Usually
,
if
we
observe
purposeful
behavior
,
appropriate
responses
to
sensory
inputs
,
and
,
above
all
,
appropriate
answers
to
questions
,
we
can
be
reasonably
sure
that
the
person
is
conscious
.
However
,
we
know
that
consciousness
can
be
entirely
within
the
brain
,
even
in
the
absence
of
any
interaction
with
the
external
world
;
this
happens
almost
every
night
,
while
we
dream
.
Yet
,
to
this
day
,
we
lack
an
objective
,
dependable
measure
of
the
level
of
consciousness
that
is
independent
of
processing
sensory
inputs
and
producing
appropriate
motor
outputs
.
Theoretically
,
consciousness
is
thought
to
require
the
joint
presence
of
functional
integration
and
functional
differentiation
,
otherwise
defined
as
brain
complexity
.
Here
we
review
a
series
of
recent
studies
in
which
Transcranial
Magnetic
Stimulation
combined
with
electroencephalography
(
TMS
/
EEG
)
has
been
employed
to
quantify
brain
complexity
in
wakefulness
and
during
physiological
(
sleep
)
,
pharmacological
(
anesthesia
)
and
pathological
(
brain
injury
)
loss
of
consciousness
.
These
studies
invariably
show
that
the
complexity
of
the
cortical
response
to
TMS
collapses
when
consciousness
is
lost
during
deep
sleep
,
anesthesia
and
vegetative
state
following
severe
brain
injury
,
while
it
recovers
when
consciousness
resurges
in
wakefulness
,
during
dreaming
,
in
the
minimally
conscious
state
or
locked-
in
syndrome
.
The
present
paper
will
also
focus
on
how
this
approach
may
contribute
to
unveiling
the
pathophysiology
of
disorders
of
consciousness
affecting
brain
-injured
patients
.
Finally
,
we
will
underline
some
crucial
methodological
aspects
concerning
TMS
/
EEG
measurements
of
brain
complexity
.
Diseases
Validation
Diseases presenting
"and"
symptom
achondroplasia
adrenomyeloneuropathy
aniridia
carcinoma of the gallbladder
cutaneous mastocytosis
cystinuria
esophageal squamous cell carcinoma
harlequin ichthyosis
hodgkin lymphoma, classical
hydrocephalus with stenosis of the aqueduct of sylvius
kallmann syndrome
liposarcoma
locked-in syndrome
neonatal adrenoleukodystrophy
omenn syndrome
oral submucous fibrosis
pleomorphic liposarcoma
primary hyperoxaluria type 1
proteus syndrome
pyomyositis
pyruvate dehydrogenase deficiency
sneddon syndrome
triple a syndrome
trochlear dysplasia
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