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Interoception relates to sleep and sleep disorders

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Abstract

The central nervous system senses and responds to afferent signals arising from the body. These interoceptive afferents are essential to physiological homeostatic control and are known to influence an individual’s momentary affect, cognition, motivation, and conscious experiences. Both sleep and interoception are tightly connected to physical and mental well-being. This review outlines the current knowledge about the interactions between interoception and sleep. It is demonstrated that there are complex, dynamic relations between sleep and sensory processes within each modality of interoception, including thermoception, nociception, visceral sensations, and subjective feelings about these sensations. A better understanding and appreciation of the intricate interrelations may facilitate management of functional somatic symptoms, chronic pain, insomnia, and other sleep and mental disorders.
Interoception
relates
to
sleep
and
sleep
disorders
Yishul
Wei
1
and
Eus
JW
Van
Someren
1,2,3
The
central
nervous
system
senses
and
responds
to
afferent
signals
arising
from
the
body.
These
interoceptive
afferents
are
essential
to
physiological
homeostatic
control
and
are
known
to
influence
an
individual’s
momentary
affect,
cognition,
motivation,
and
conscious
experiences.
Both
sleep
and
interoception
are
tightly
connected
to
physical
and
mental
well-
being.
This
review
outlines
the
current
knowledge
about
the
interactions
between
interoception
and
sleep.
It
is
demonstrated
that
there
are
complex,
dynamic
relations
between
sleep
and
sensory
processes
within
each
modality
of
interoception,
including
thermoception,
nociception,
visceral
sensations,
and
subjective
feelings
about
these
sensations.
A
better
understanding
and
appreciation
of
the
intricate
interrelations
may
facilitate
management
of
functional
somatic
symptoms,
chronic
pain,
insomnia,
and
other
sleep
and
mental
disorders.
Addresses
1
Department
of
Sleep
and
Cognition,
Netherlands
Institute
for
Neuroscience
(NIN),
an
Institute
of
the
Royal
Netherlands
Academy
of
Arts
and
Sciences,
Amsterdam,
The
Netherlands
2
Department
of
Integrative
Neurophysiology,
Center
for
Neurogenomics
and
Cognitive
Research
(CNCR),
Amsterdam
Neuroscience,
VU
University
Amsterdam,
Amsterdam,
The
Netherlands
3
Amsterdam
UMC,
Vrije
Universiteit,
Psychiatry,
Amsterdam
Neuroscience,
Amsterdam,
The
Netherlands
Corresponding
author:
Van
Someren,
Eus
JW
(e.j.w.someren@vu.nl)
Current
Opinion
in
Behavioral
Sciences
2020,
33:1–7
This
review
comes
from
a
themed
issue
on
Cognition
and
Perception
-
*Sleep
and
cognition*
Edited
by
Michael
WL
Chee
and
Philippe
Peigneux
For
a
complete
overview
see
the
Issue
and
the
Editorial
Available
online
13th
December
2019
https://doi.org/10.1016/j.cobeha.2019.11.008
2352-1546/ã
2019
The
Authors.
Published
by
Elsevier
Ltd.
This
is
an
open
access
article
under
the
CC
BY-NC-ND
license
(http://creative-
commons.org/licenses/by-nc-nd/4.0/).
Introduction
Central
nervous
system
(CNS)
processing
of
bodily
sig-
nals,
broadly
known
as
interoception,
has
become
an
integral
topic
in
the
current
discourse
of
affective,
cogni-
tive,
behavioral,
social,
and
clinical
neurosciences
[1

,2,3].
The
notion
of
interoception
was
traditionally
confined
to
visceral
sensations
but
has
expanded
to
encompass
other
sensory
modalities
that
inform
the
CNS
about
the
physiological
states
across
the
body,
most
notably
thermoception
and
nociception
[1

,2].
Intero-
ceptive
information
arising
from
body
tissues
is
conveyed
to
the
CNS
via
neural
and
humoral
pathways
as
well
as
through
indirect
signaling
involving
immune
cells
and
neurovascular
coupling
[4,5].
Ascending
neural
pathways
interface
with
the
central
autonomic
network
at
multiple
spinal
and
subcortical
levels
and
ultimately
deliver
inter-
oceptive
information
to
the
‘neuromatrix’
within
the
cerebral
cortex
[5,6].
Neuronal
signaling
along
the
path-
ways
is
subject
to
descending
facilitation
and
inhibition
from
the
brain
and
modulated
by
assorted
hormonal
and
inflammatory
factors
[7].
Interoceptive
sensitivity
is
thus
determined
by
not
only
the
neuro-endocrino-immuno-
logical
condition
but
also
the
affective,
cognitive,
moti-
vational,
and
arousal
state
of
the
individual.
The
aim
of
this
review
is
to
provide
a
synopsis
of
the
current
knowledge
about
the
interactions
between
sleep—which
has
prominent
bidirectional
relationship
with
all
of
the
mentioned
factors
[8,9]—and
the
intero-
ceptive
systems.
Both
sleep
and
interoception
are
mul-
tidimensional
constructs.
For
instance,
subjective
sleep
quality
and
interoceptive
feelings
4
are
often
uncorre-
lated
with
objective
measures
of
sleep
and
interoception.
Thus
far
the
relationship
between
each
dimension
of
sleep
and
each
dimension
of
interoception
has
not
been
equally
investigated.
The
present
review
discusses
the
most
representative
themes
in
the
current
literature,
including:
impacts
of
interoception
on
sleep
initiation,
the
roles
of
interoception
during
sleep,
impacts
of
sleep
deprivation
on
interoception,
associations
between
inter-
oception
and
habitual
sleep,
and
altered
interoception
in
sleep
disorders
(notably
insomnia
disorder).
Interoception
affects
sleep
initiation
Noxious
or
stressful
stimuli
naturally
increase
arousal
and
hinder
sleep.
In
contrast,
certain
types
of
interoceptive
stimuli
appear
somnogenic.
For
example,
gastrointestinal
stimulation
has
been
shown
to
reduce
sleep
onset
latency,
mirroring
the
familiar
phenomenon
of
postprandial
sleep-
iness
[2,10].
It
has
also
been
observed
in
both
animals
and
anesthetized
humans
that
carotid
sinus
stimulation
4
Following
the
nomenclature
recently
proposed
by
the
Human
Affectome
Project,
we
use
the
term
interoceptive
feelings
to
refer
to
subjective
experiences
regarding
body
parts
(or
the
body
as
a
whole)
that
may
derive
from
interoceptive
afferents
but
may
also
integrate
other
sensory
(e.g.
tactile
[69])
information
and
may
even
originate
within
the
CNS
itself
[1

].
Interoceptive
feelings
can
manifest
as
symptoms
or
complaints
in
clinical
settings.
Available
online
at
www.sciencedirect.com
ScienceDirect
www.sciencedirect.com
Current
Opinion
in
Behavioral
Sciences
2020,
33:1–7
triggers
EEG
activity
resembling
slow
waves
that
are
characteristic
of
sleep
[2,11].
The
link
between
thermoception
and
the
sleep–wake
behavior
has
attracted
particularly
widespread
attention
[12,13
,14].
Mild
skin
warming
within
the
thermoneutral
zone
during
wakefulness
reduces
vigilance
and
promotes
sleep
onset
[13
],
although
the
effect
appears
compro-
mised
in
the
elderly,
likely
due
to
the
age-related
decline
in
thermosensitivity
[15].
More
intense
heat
as
well
as
cold
exposure
at
bedtime
impedes
sleep.
However,
body
heating
a
few
hours
before
bedtime
reduces
sleep
onset
latency
and
increases
slow-wave
sleep
(SWS),
colloquially
known
as
the
‘warm
bath
effect’
and
likely
to
involve
a
cascade
of
thermoregulatory
processes
[14].
This
shows
that
sleep
propensity
depends
on
both
magnitudes
and
timing
of
the
thermal
stimuli.
Based
on
these
findings,
an
extension
of
the
traditional
two-process
model
of
sleep
has
been
proposed
[14].
In
the
extended
model,
sleep
propensity
is
not
only
determined
by
homeostatic
sleep
pressure
and
the
circadian
phase
but
also
dependent
on
sensory
gating
signals.
An
interesting
hypothesis
is
that
sleep
homeostasis
may
itself
involve
interoceptive
mechanisms.
For
instance,
sleep
depriva-
tion
is
known
to
elevate
blood
pressure
and
distal
skin
temperature
[11,13
].
These
changes
could
in
turn
be
picked
up
by
carotid
baroreceptors
and
skin
thermore-
ceptors,
generating
feedback
input
that
promotes
sleepi-
ness.
Likewise,
the
circadian
component
may
itself
also
involve
interoceptive
mechanisms,
for
example,
through
the
thermoregulatory
effects
of
melatonin
[13
].
Interoception
during
sleep
Stable
sleep
is
marked
by
profound
suppression
of
various
behavioral
defense
responses
(e.g.
hypoxic/hypercapnic
ventilatory
responses,
coughing,
swallowing,
shivering,
and
withdrawal
reflexes)
against
adverse
conditions
or
stimuli,
and
occurrences
of
such
responses
typically
involve
arousals
or
awakenings
[8,10,12,16].
In
addition
to
sleep-induced
muscle
hypotonia,
changes
associated
with
sleep
within
the
sensory
systems
are
believed
to
contribute
to
suppression
of
these
responses
[8,12,16].
The
changes
in
interoceptive
sensitivity
prevent
arousals
and
protect
sleep.
Unfortunately,
such
mechanisms
nec-
essarily
render
body
tissues
vulnerable
to
adverse
physi-
ological
conditions
or
events
(e.g.
gastroesophageal
reflux
[10]),
which
could
lead
to
severe
clinical
complications
should
those
events
become
frequent
during
sleep.
It
has
been
shown
that
manipulation
of
ambient
temper-
ature
during
sleep
is
able
to
alter
the
core
body
tempera-
ture
rhythm
as
well
as
sleep
architecture.
As
a
result
of
the
use
of
insulating
clothing
and
bedding,
sleep
is
more
easily
disturbed
by
heat
than
by
cold
exposure
[12].
At
present
it
is
unclear
whether
alterations
in
skin
tempera-
ture
or
in
core
body
temperature
exert
more
influences
on
sleep.
However,
it
has
been
demonstrated
that
subtle
skin
warming
during
sleep
can
promote
SWS
without
chang-
ing
core
body
temperature
[17],
thus
supporting
direct
impacts
of
skin
temperature
on
SWS
expression.
Studies
on
the
nociceptive
laser-evoked
potential
(LEP)
and
the
heartbeat-evoked
potential
(HEP)
during
sleep
have
shown
that
cortical
processing
of
interoceptive
information
is
present
but
attenuated
as
compared
to
wakefulness
[18,19].
Interestingly,
the
presence
of
a
late
positive
component
of
the
LEP
predicts
a
subsequent
arousal,
indicating
that
nociceptive
input
can
elicit
higher
order
cognitive
evaluation
even
during
sleep
[18].
The
roles
of
interoception
in
dreams
and
rapid
eye
movement
(REM)
sleep
are
particularly
elusive.
Intero-
ceptive
feelings
in
dreams
are
rare
[1

,18].
REM
sleep
is
characterized
by
apparently
CNS-initiated
autonomic
swings
with
minimal
interoceptive
feedback
control,
giv-
ing
rise
to
erratic
heart
rate,
blood
pressure,
and
breathing
patterns
[8,11,12,16].
The
HEP
however
indicates
increased
cortical
processing
of
cardiovascular
input
dur-
ing
REM
sleep
relative
to
non-REM
sleep
[19].
This
processing
during
REM
sleep
has
been
found
to
be
elevated
in
people
with
nightmare
disorder—regardless
of
whether
a
nightmare
during
the
assessment
night
actually
occurred
[20].
Interoception,
interoceptive
feel-
ings,
and
autonomic
output
thus
seem
dissociated
during
dreams
and
REM
sleep.
Sleep
deprivation
Acute
or
chronic
sleep
deprivation
results
in
alterations
in
interoceptive
feelings.
This
is
most
clearly
demonstrated
in
the
pain
literature,
where
various
sleep
deprivation
paradigms
(e.g.
total
sleep
deprivation,
sleep
restriction,
SWS
disruption,
and
sleep
fragmentation)
have
been
shown
to
increase
sensitivity
to
painful
stimuli
as
well
as
spontaneous
pain
[21].
An
increase
in
somatic
com-
plaints
besides
pain
following
sleep
deprivation
has
also
been
reported
[22].
More
generally,
the
‘feeling
of
sleep
deprivation’
that
many
readers
are
familiar
with
can
be
characterized
by
fatigue,
negative
mood,
and
an
overall
perception
of
unwellness
[23],
resembling
in
several
respects
the
feeling
state
of
sickness
[1

,4,9].
Interest-
ingly,
a
sleep-deprived
person
is
indeed
likely
to
be
judged
as
being
sick
by
others
[24].
A
recent
study
evaluated
the
effects
of
chronic
sleep
restriction
with
intermittent
weekend
recovery
sleep
for
up
to
three
weeks.
Multiple
measures
tapping
differ-
ent
pain-related
processes
were
assessed.
It
was
found
that
the
heat
pain
threshold
is
lowered
by
sleep
restriction
during
the
first
week
but
normalizes
afterwards.
In
con-
trast,
increased
CNS
cold
pain
facilitation
and
reduced
cold
pain
habituation
could
only
be
observed
in
the
later
weeks
of
sleep
restriction
[25
].
The
study
highlights
that
the
observed
effects
of
acute
sleep
deprivation
may
not
2
Cognition
and
perception
-
*sleep
and
cognition*
Current
Opinion
in
Behavioral
Sciences
2020,
33:1–7
www.sciencedirect.com
generalize
to
chronic
sleep
deprivation,
as
each
type
of
sleep
deprivation
may
differentially
affect
the
multiple
processes
involved
in
pain
perception.
Sleep
deprivation
may
induce
hyperalgesia
through
sev-
eral
neurochemical
pathways
including
the
opioid,
mono-
amine,
orexin,
and
endocannabinoid
systems
as
well
as
endocrine
and
immune
mechanisms
[26

].
Neuroimag-
ing
studies
probing
the
brain
substrates
of
sleep
depriva-
tion-induced
changes
in
pain
processing
have
just
begun
to
emerge.
One
recent
study
found
amplified
reactivity
of
the
primary
somatosensory
cortex
and
blunted
reactivity
of
the
nucleus
accumbens
(NAcc),
thalamus,
and
insula
in
response
to
heat
pain
stimulation
following
a
night
of
total
sleep
deprivation.
Moreover,
the
sleep
deprivation-
induced
changes
in
reactivity
of
the
primary
somatosen-
sory
cortex
and
thalamus
predict
corresponding
lowering
of
the
heat
pain
threshold
[27].
Another
study
reported
that
a
night
of
fragmented
sleep
attenuates
and
delays
NAcc
responses
to
heat
pain
stimulation
[28].
Involve-
ment
of
the
NAcc
as
implicated
by
both
studies
suggests
that
processes
related
to
affective
valuation
and
cognitive
control
are
likely
to
be
engaged
in
the
relationship
between
sleep
and
pain.
Interoception
covaries
with
habitual
sleep
It
is
not
uncommon
to
find
sleep
disturbances
to
accom-
pany
somatic
complaints.
The
experimental
evidence
summarized
above
would
imply
bidirectional
relations
between
somatic
discomfort
and
poor
sleep.
Longitudinal
studies
have
repeatedly
shown
that
self-reported
sleep
disturbances
predict
new-onset
pain
conditions
and
vice
versa
[29].
Conversely,
good
sleep
quality
has
been
shown
to
predict
(partial)
resolution
of
pain
[30].
Pain
however
does
not
seem
to
predict
persistence
versus
remission
of
insomnia
[31].
Longitudinal
data
for
the
bidirectional
relationship
between
poor
sleep
and
somatic
complaints
besides
pain
are
lacking,
but
cross-sectional
data
have
demonstrated
robust
associations
between
them
across
different
populations
[32–34,35
].
A
recent
population-based
study
conducted
in
Japan
indicated
that
pain
symptoms
are
more
reliably
associated
with
self-reported
sleep
insufficiency
than
with
self-
reported
sleep
duration
per
se
[36].
This
result
is
interest-
ing
in
light
of
a
recent
interventional
study
showing
that
sleep
extension
benefits
(cold)
pain
tolerance,
more
so
in
people
who
report
to
habitually
sleep
less
than
needed
[37].
In
a
neuroimaging
study,
reporting
to
habitually
sleep
more
than
needed
(termed
‘sleep
credit’)
was
found
to
be
associated
with
increased
gray
matter
volume
in
part
of
the
medial
orbitofrontal
cortex,
which
is
in
turn
associated
with
less
somatic
complaints,
depression,
and
paranoia
[38].
These
converging
findings
suggest
that
subjective
sleep
insufficiency
is
an
especially
impor-
tant
factor
involved
in
somatic
complaints,
with
the
medial
orbitofrontal
cortex
being
the
common
neural
substrate.
Investigating
the
intra-individual
relationship
between
fluctuations
in
sleep
and
somatic
complaints
could
pro-
vide
more
mechanistic
insights
into
their
interactions.
Several
studies
in
the
pain
literature,
mostly
carried
out
in
patients
with
assorted
somatic
pain
conditions,
have
consistently
pointed
to
sleep
(assessed
with
daily
self-
reports
and
sometimes
with
actigraphy)
as
a
more
reliable
predictor
of
subsequent
pain
than
vice
versa
[39].
The
same
‘microlongitudinal’
paradigm
has
also
been
applied
to
the
study
of
irritable
bowel
syndrome,
a
functional
gastrointestinal
disorder
characterized
by
hypersensitivity
[7].
It
was
found
that
poor
self-reported
sleep
quality
is
associated
with
next-day
abdominal
pain
but
not
with
non-pain
gastrointestinal
symptoms
[40].
Therefore,
across
heterogeneous
conditions,
it
seems
that
the
asso-
ciation
between
poor
self-reported
sleep
and
next-day
pain
is
especially
robust.
A
recent
community-based
study
assessed
how
people
themselves
perceive
daytime
pain
to
associate
with
sub-
sequent
sleep
and
vice
versa.
Interestingly,
the
perceived
sleep–pain
associations
are
asymmetric:
Sleep
worsens
more
after
a
day
with
more-than-usual
pain
than
it
improves
after
a
day
with
less-than-usual
pain.
Also,
pain
worsens
more
after
a
night
of
worse-than-usual
sleep
than
it
improves
after
a
night
of
better-than-usual
sleep.
This
asymmetry
becomes
stronger
in
people
with
more
severe
habitual
insomnia
(Figure
1)
or
pain
[35
].
The
study
highlights
the
possibility
that
the
effects
of
better
and
worse
nights
of
sleep
on
pain
are
not
of
equal
magnitudes,
which
could
potentially
explain
why
treatments
targeting
insomnia
only
marginally
alleviate
pain
in
patients
with
comorbid
insomnia
and
chronic
pain
[41].
Studies
have
also
linked
habitual
sleep
to
laboratory
test
results
on
interoceptive
feelings.
One
seminal
popula-
tion-based
study
found
reduced
cold
pain
tolerance
in
people
reporting
longer
sleep
onset
latency,
lower
sleep
efficiency,
and
more
severe
and
frequent
insomnia
[42].
In
another
study,
healthy
volunteers
reporting
more
sleep
difficulties
were
shown
to
perform
worse
on
the
intero-
ceptive
cardiac
discrimination
task.
Surprisingly,
the
asso-
ciation
is
reversed
in
people
with
affective
disorders
[43].
Sleep
disorders
Diagnosed
sleep
disorders
are
common
among
patients
with
chronic
pain.
The
most
prevalent
comorbid
sleep
disorder
is
insomnia
disorder
(ID).
A
recent
meta-analysis
estimated
that
the
prevalence
of
comorbid
ID
among
patients
with
chronic
pain
is
72%,
much
higher
than
the
prevalence
of
comorbid
restless
legs
syndrome
(RLS,
32%)
or
obstructive
sleep
apnea
(OSA,
32%)
[44
].
Nota-
bly,
laboratory
quantitative
sensory
testing
has
confirmed
increased
pain
sensitivity
and
implicated
altered
CNS
Sleep
and
interoception
Wei
and
Van
Someren
3
www.sciencedirect.com
Current
Opinion
in
Behavioral
Sciences
2020,
33:1–7
pain
facilitation
and/or
inhibition
in
ID,
RLS,
and
OSA
[29].
Chronic
pain
is
also
highly
prevalent
among
patients
with
narcolepsy
[45].
Etiological
theories
of
ID
hypothesize
that
attention
to
selective
interoceptive
or
exteroceptive
stimuli
together
with
other
cognitive
activities
could
lead
to
a
hyperarousal
state
at
bedtime
that
interferes
with
sleep
initiation
or
maintenance
[46,47].
Somatic
discomfort
around
bedtime
can
be
assessed
with
the
Pre-Sleep
Arousal
Scale—
Somatic
subscale
[48],
which
has
indeed
been
found
to
distinguish
between
people
with
ID,
subclinical
poor
sleepers,
and
normal
sleepers
and
to
independently
con-
tribute
to
self-reported
nocturnal
wake
time
and
poor
sleep
quality
[49].
Some
studies,
however,
suggested
that
insomnia
symptoms
are
more
closely
related
to
pre-sleep
cognitive
activities
than
to
pre-sleep
somatic
discomfort
[48,50].
It
has
been
proposed
instead
that
perhaps
arousal-
promoting
interoceptive
input
at
bedtime
is
not
maxi-
mally
consciously
recognized
by
people
with
ID
[51].
Altered
interoceptive
feelings
in
ID
beyond
the
pre-sleep
period
have
also
been
demonstrated.
During
wakeful
rest,
people
with
ID
report
aberrant
spontaneous
mental
con-
tent
along
several
dimensions
assessed
by
the
Amsterdam
Resting-State
Questionnaire
(ARSQ)
[52]
including
reduced
comfort,
heightened
health
concern,
height-
ented
subjective
sleepiness,
and
heightened
somatic
awareness
as
compared
to
healthy
controls
[53].
Reduced
comfort
in
people
with
ID
is
further
corroborated
by
their
deficient
‘liking’
feelings
throughout
the
day
[54].
A
detailed
analysis
of
many
dimensions
of
subjective
ther-
moception
also
revealed
a
very
different
profile
between
people
with
probable
ID
and
people
without
sleep
com-
plaints
[55].
Strong
differences
between
people
with
ID
and
people
without
sleep
complaints
are
also
reflected
in
an
objective
measure
of
interoception.
The
later
part
of
the
frontal
HEP
is
enhanced
in
people
with
ID
during
wakeful
rest
in
the
evening,
suggesting
increased
processing
of
cardiac
signals
[56]
(Figure
2a).
In
a
follow-up
study,
it
was
found
that
mean
EEG
microstate
duration
specifically
for
micro-
state
class
C
is
shortened
in
people
with
ID
[57]
(Figure
2b).
As
duration
of
class
C
microstates
has
been
shown
to
negatively
correlate
with
the
somatic
awareness
dimension
of
the
ARSQ
[52],
this
microstate
alteration
could
be
a
marker
of
heightened
somatic
awareness
in
ID.
4
Cognition
and
perception
-
*sleep
and
cognition*
Figure
1
Sleep Pain Sleep
Pain
More Pain Better Sleep
Sleep
As Usual
Pain
As Usual
Less Pain Worse Sleep
Insomnia Severity Index Insomnia Severity Index
After Worse Sleep
After Better Sleep
After More Pain
After Less Pain
1
0.5
0
–0.5
–1 0–7
8–14 15–21 22–28 0–7
8–14 15–21 22–28
1
0.5
0
–0.5
–1
Current Opinion in Behavioral Sciences
Average
perceived
pain
after
a
better
night
and
worse
night
of
sleep
than
usual
(left),
and
average
perceived
sleep
quality
after
a
day
with
more
pain
and
less
pain
than
usual
(right),
within
subgroups
of
individuals
defined
by
clinical
cutoffs
of
the
Insomnia
Severity
Index.
Error
bars
indicate
95%
confidence
intervals.
Reprinted
from
Ref.
[35
].
Current
Opinion
in
Behavioral
Sciences
2020,
33:1–7
www.sciencedirect.com
In
sum,
it
is
important
to
note
an
unfortunate
disbalance.
While
people
with
ID
show
increased
interoceptive
awareness
across
modalities,
they
are
actually
less
likely
to
either
sense
comfort
or
to
label
experiences
as
com-
fortable
or
pleasant
[51,53–55].
Neuroimaging
studies
have
commenced
to
find
neural
correlates
of
this
disba-
lance
and
suggested
that
increased
reactivity
may
relate
to
hyperconnectivity
of
the
angular
gyrus
while
deficient
comfort
sensing
likely
involves
suboptimal
orbitofrontal
processing
[58,59].
The
disbalance
toward
negative
experiences
may
have
long-standing
consequences,
as
recent
studies
have
found
that
the
affective
signatures
of
negative
emotional
experiences
could
persist
through
extinction
learning,
across
the
night,
and
over
the
long
term
in
people
with
ID
[60–63].
With
respect
to
sleep
disorders
other
than
ID,
accumu-
lating
evidence
suggests
that
OSA
is
associated
with
impaired
mechano-
and
thermosensitivity
of
the
upper
airway
resulting
from
local
neuropathy
[64,65].
A
recent
study
systematically
examined
the
functional
integrity
of
afferent
neural
pathways
from
the
palate
by
means
of
electrical
stimulation
with
alternating
currents
at
differ-
ent
frequencies
and
found
in
patients
with
OSA
impaired
perception
specifically
of
large
fiber-mediated
afferents
at
the
soft
palate
[66].
In
comparison,
others
applying
the
same
method
to
the
toes
showed
reduced
current
per-
ception
thresholds
in
people
with
RLS
for
both
large
fiber-mediated
and
small
fiber-mediated
afferents
during
the
symptomatic
period
[67].
Because
participants
with
abnormal
test
results
indicative
of
peripheral
neuropathy
were
excluded,
the
authors
concluded
that
CNS
mecha-
nisms
are
likely
to
underlie
hyperesthesia
in
RLS,
a
conclusion
also
corroborated
by
earlier
studies
using
other
methodologies
[68].
Conclusion
To
our
knowledge,
this
is
the
first
review
that
attempts
to
synthesize
the
vast
literature
on
the
links
between
sleep
and
sensory
processing
across
a
wide
range
of
interocep-
tive
modalities.
The
state
of
science
has
really
only
scratched
the
surface
of
their
complex,
dynamic
interac-
tions.
We
hope
that
our
synopsis
has
presented
a
coherent
account
of
their
intricate
relationship
and
will
inspire
innovative
future
research
on
this
important
topic.
Conflict
of
interest
statement
Nothing
declared.
Sleep
and
interoception
Wei
and
Van
Someren
5
Figure
2
(a)
(b)
0.3
0.2
0.1
0
-0.1
-0.2
-0.3
-300 -200
-100
0100
200 300 400 500 600
Time (ms)
120
100
80
60
40
20 ABC
D
E
Microstate Class
ID
CTRL
ID
CTRL
Mean Microstate Duration (ms)
HEP Amplitude (µV)
Current Opinion in Behavioral Sciences
(a)
Frontal
heartbeat-evoked
potential
(HEP)
waveforms
in
32
people
with
insomnia
disorder
(ID)
and
32
healthy
controls
(CTRL)
during
wakeful
rest
in
the
evening
with
eyes
closed.
The
average
time
courses
over
the
frontal
and
prefrontal
electrodes
(large
black
dots)
time-locked
to
the
R-
wave
peak
(0
ms)
are
depicted.
Shaded
areas
indicate
one
standard
error
of
the
mean
(SEM).
Adapted
from
Ref.
[56].
(b)
Boxplots
of
mean
EEG
microstate
duration
for
each
microstate
class
in
the
same
groups
of
people
with
ID
and
CTRL
during
wakeful
rest
in
the
evening
with
eyes
closed.
Data
are
obtained
from
Ref.
[57].
Asterisks
indicate
significant
group
differences
(
p
<
0.05).
www.sciencedirect.com
Current
Opinion
in
Behavioral
Sciences
2020,
33:1–7
Acknowledgements
This
work
is
supported
by
the
European
Research
Council
Advanced
Grant
671084
INSOMNIA
and
the
Bial
Foundation
grant
190/16.
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... visceral) signals during phasic and tonic REM microstates. Indeed, a rich source of information for the sleeping brain is arising from the body through a stream of afferent signals whose neural processing is known under the term interoception [23,24]. For instance, the processing of nociceptive stimuli is somewhat attenuated after falling asleep, but do persist to some extent in all sleep stages, including REM sleep [25]. ...
... Moreover, our findings are in line with the gradual attenuation of the HEP as we move from wakefulness to Stage 1 sleep, REM sleep, and finally deeper sleep stages (Stage 2 and SWS), indicating that HEP amplitudes are sensitive to changes in alertness and arousability during sleep [35]. Regarding spontaneous oscillatory activity, tonic periods exhibit a relative increase within the high alpha (10-14 Hz) and beta (15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28) frequency bands compared to phasic periods as observed in scalp EEG [41,61,75,76] and intracerebral recordings [13]. Although the neural correlates of increased high alpha and beta frequency power during REM sleep remain to be explored, such oscillations are also predominant and index alertness in wakefulness [77,78], during which they were associated with the activity of a cingulo-opercular network maintaining arousal and vigilance [79,80]. ...
... The processing of internal signals, including thermoception, nociception, and visceroception is an integral aspect of the sleeping brain [24]. Similarly to acoustic processing (the most studied domain in the field), sensory thresholds for interoceptive inputs (e.g. ...
Article
Full-text available
Sleep is a fundamental physiological state that facilitates neural recovery during periods of attenuated sensory processing. On the other hand, mammalian sleep is also characterized by the interplay between periods of increased sleep depth and environmental alertness. Whereas the heterogeneity of microstates during non-rapid-eye-movement (NREM) sleep was extensively studied in the last decades, transient microstates during REM sleep received less attention. REM sleep features two distinct microstates: phasic and tonic. Previous studies indicate that sensory processing is largely diminished during phasic REM periods, whereas environmental alertness is partially reinstated when the brain switches into tonic REM sleep. Here, we investigated interoceptive processing as quantified by the heartbeat evoked potential (HEP) during REM microstates. We contrasted the HEPs of phasic and tonic REM periods using two separate databases that included the nighttime polysomnographic recordings of healthy young individuals (N = 20 and N = 19). We find a differential HEP modulation of a late HEP component (after 500 ms post-R-peak) between tonic and phasic REM. Moreover, the late tonic HEP component resembled the HEP found in resting wakefulness. Our results indicate that interoception with respect to cardiac signals is not uniform across REM microstates, and suggest that interoceptive processing is partially reinstated during tonic REM periods. The analyses of the HEP during REM sleep may shed new light on the organization and putative function of REM microstates.
... It generally refers to the subjective experience of internal states and changes in the body resulting from both visceral and somatic afference (Ceunen et al., 2016). Due to its role in sensing and integrating body signals and needs, interoception is thought to contribute to biological homeostasis (Strigo & Craig, 2016), regulation of circadian rhythms, and sleep (Ewing et al., 2017;Wei & Van Someren, 2020). Interoception is also believed to aid perception of the self as a separate entity from the environment and others, thus contributing to social cognition (Fotopoulou & Tsakiris, 2017;Ondobaka et al., 2017;Palmer & Tsakiris, 2018). ...
... Notably, the association between anxiety and PLEs is well established in the literature (Cowan & Mittal, 2020). Current understanding of interoception emphasizes its role in contributing to a sense of selfhood (Quadt et al., 2018), and in regulating social cognition (Crucianelli & Filippetti, 2020;Tsakiris & Critchley, 2016) as well as sleep (Wei & Van Someren, 2020). Dysfunctions in self-perception, social cognition, and sleep characterize individuals across the psychosis spectrum. ...
Article
Aim: Interoception is the ability to sense internal bodily changes and research indicates that it may play a role in the development of mental illness. In recent years, preliminary evidence has shown that interoception is impaired in people with psychosis. Interoceptive sensibility, a meta-cognitive aspect of interoception, has never been studied across the psychosis continuum. The present study aimed at assessing interoceptive sensibility in youth with psychotic-like experiences. Method: We invited a sample of young adults (N=609; age 19-21 years) to complete an online survey that included a measure of interoceptive sensibility (the Multidimensional Assessment of Interoceptive Awareness-2) and the Community Assessment of Psychotic Experiences-Positive Scale -15 (CAPE-P15). Using the recommended cutoff for the CAPE-P15, the overall sample was divided into two groups (high/low risk for psychosis). Results: Significant group differences were observed in several dimensions of interoceptive sensibility. A logistic regression analysis indicated that scores in the subscales of Not-Distracting, Not-Worrying, Attention-Regulation, Emotional Awareness, Body Listening and Trusting significantly predicted increased risk for psychosis. Conclusion: Abnormal interoceptive sensibility may be a vulnerability marker for psychosis. These results, however, await further validation from additional comprehensive, longitudinal studies. Enhanced interoceptive sensibility has been reported following contemplative training, thus creating opportunities for future interventions to delay or prevent psychotic illness.
... Likely, part of this involvement is also seen as the negative association between the occurrence of microstate C and the Comfort (measured with questions like 'I felt comfortable', 'I felt relaxed', 'I felt happy') in our study. The ability to relax and feel comfortable is related to interoceptive aspects through the urge to restore balance in physical and emotional context [56,57]. The domain of Comfort was previously related with the ability to switch between tasks [58], correlated with character traits of self-directedness (associated with individual ability to govern behavior according to situational demand) [13] and mental and physical well-being [12]. ...