Science,
Journal Year:
2016,
Volume and Issue:
354(6312), P. 578 - 584
Published: Nov. 3, 2016
The
mammalian
nervous
system
encodes
many
different
forms
of
pain,
from
those
that
arise
as
a
result
short-term
low-grade
interactions
with
noxious
thermal,
chemical,
or
mechanical
sources
to
more
serious
pain
induced
by
trauma
and
disease.
In
this
Review,
we
highlight
recent
advances
in
our
understanding
the
neural
circuits
encode
these
types
pain.
Promising
therapeutic
strategies
based
on
are
also
highlighted.
Pharmacological Reviews,
Journal Year:
2018,
Volume and Issue:
70(2), P. 315 - 347
Published: March 2, 2018
Injury
to
or
disease
of
the
nervous
system
can
invoke
chronic
and
sometimes
intractable
neuropathic
pain.
Many
parallel,
interdependent,
time-dependent
processes,
including
neuroimmune
interactions
at
peripheral,
supraspinal,
spinal
levels,
contribute
etiology
this
"disease
pain."
Recent
work
emphasizes
roles
colony-stimulating
factor
1,
ATP,
brain-derived
neurotrophic
factor.
Excitatory
processes
are
enhanced,
inhibitory
attenuated
in
dorsal
horn
throughout
somatosensory
system.
This
leads
central
sensitization
aberrant
processing
such
that
tactile
innocuous
thermal
information
is
perceived
as
pain
(allodynia).
Processes
involved
onset
differ
from
those
its
long-term
maintenance.
Opioids
display
limited
effectiveness,
less
than
35%
patients
derive
meaningful
benefit
other
therapeutic
approaches.
We
thus
review
promising
targets
have
emerged
over
last
20
years,
Na+,
K+,
Ca2+,
hyperpolarization-activated
cyclic
nucleotide–gated
channels,
transient
receptor
potential
channel
type
V1
adenosine
A3
receptors.
Despite
progress,
gabapentinoids
retain
their
status
first-line
treatments,
yet
mechanism
action
poorly
understood.
outline
recent
progress
understanding
show
how
has
provided
insights
into
cellular
actions
pregabalin
gabapentin.
Interactions
with
α2δ-1
subunit
voltage-gated
Ca2+
channels
produce
multiple
neuron
type-specific
cord
higher
centers.
suggest
drugs
affect
rather
a
single
specific
target,
greatest
promise
for
future
development.
Clinical Journal of Pain,
Journal Year:
2018,
Volume and Issue:
34(9), P. 858 - 877
Published: Feb. 27, 2018
This
review
aims
to
provide
a
framework
for
evaluating
the
utility
of
virtual
reality
(VR)
as
distraction
intervention
alleviate
pain
and
distress
during
medical
procedures.
We
first
describe
theoretical
bases
underlying
VR
analgesic
anxiolytic
effects
define
main
factors
contributing
its
efficacy,
which
largely
emerged
from
studies
on
healthy
volunteers.
Then,
we
comprehensive
overview
clinical
trials
using
different
procedures,
such
burn
injury
treatments,
chemotherapy,
surgery,
dental
treatment,
other
diagnostic
therapeutic
procedures.A
broad
literature
search
was
performed
terms
"virtual
reality,"
"distraction,"
"pain."
No
date
limit
applied
all
retrieved
immersive
procedures
were
selected.VR
has
proven
be
effective
in
reducing
procedural
pain,
almost
invariably
observed
even
patients
subjected
extremely
painful
with
injuries
undergoing
wound
care,
physical
therapy.
Moreover,
seemed
decrease
cancer-related
symptoms
settings,
including
chemotherapy.
Only
mild
infrequent
side
observed.Despite
these
promising
results,
future
long-term
randomized
controlled
larger
sample
sizes
not
only
self-report
measures
but
also
physiological
variables
are
needed.
Further
required
both
establish
predictive
select
who
can
benefit
design
hardware/software
systems
tailored
specific
needs
able
greatest
at
lowest
cost.
Pain Practice,
Journal Year:
2018,
Volume and Issue:
18(8), P. 1048 - 1067
Published: March 11, 2018
Spinal
cord
stimulation
(SCS)
is
a
minimally
invasive
therapy
used
for
the
treatment
of
chronic
neuropathic
pain.
SCS
safe
and
effective
alternative
to
medications
such
as
opioids,
multiple
randomized
controlled
studies
have
demonstrated
efficacy
difficult-to-treat
conditions
failed
back
surgery
syndrome.
Conventional
believed
mediate
pain
relief
via
activation
dorsal
column
Aβ
fibers,
resulting
in
variable
effects
on
sensory
thresholds,
measurable
alterations
higher
order
cortical
processing.
Although
potentiation
inhibition,
suggested
by
Wall
Melzack's
gate
control
theory,
continues
be
leading
explanatory
model,
other
segmental
supraspinal
mechanisms
been
described.
Novel,
non-standard,
waveforms
high-frequency
burst
shown
some
clinically
superior
conventional
SCS,
however
their
action
remain
determined.
Additional
are
needed,
both
mechanistic
clinical,
better
understand
optimal
strategies
different
conditions,
improve
patient
selection
optimize
efficacy.
British Journal of Anaesthesia,
Journal Year:
2019,
Volume and Issue:
123(5), P. 637 - 654
Published: Sept. 21, 2019
The
relationship
between
gut
microbiota
and
neurological
diseases,
including
chronic
pain,
has
received
increasing
attention.
microbiome
is
a
crucial
modulator
of
visceral
whereas
recent
evidence
suggests
that
may
also
play
critical
role
in
many
other
types
inflammatory
headache,
neuropathic
opioid
tolerance.
We
present
narrative
review
the
current
understanding
on
pain
regulation
discuss
possibility
targeting
for
management
pain.
Numerous
signalling
molecules
derived
from
microbiota,
such
as
by-products
metabolites,
neurotransmitters,
neuromodulators,
act
their
receptors
remarkably
regulate
peripheral
central
sensitisation,
which
turn
mediate
development
Gut
microbiota-derived
mediators
serve
modulators
induction
directly
or
indirectly
regulating
excitability
primary
nociceptive
neurones.
In
nervous
system,
neuroinflammation,
involves
activation
cells
blood-brain
barrier,
microglia,
infiltrating
immune
cells,
to
modulate
maintenance
sensitisation.
Thus,
we
propose
regulates
by
diet
pharmabiotic
intervention
represent
new
therapeutic
strategy
Cell Reports,
Journal Year:
2015,
Volume and Issue:
13(6), P. 1246 - 1257
Published: Nov. 1, 2015
Neuropathic
pain
is
a
chronic
debilitating
disease
that
results
from
nerve
damage,
persists
long
after
the
injury
has
subsided,
and
characterized
by
spontaneous
mechanical
hypersensitivity.
Although
loss
of
inhibitory
tone
in
dorsal
horn
spinal
cord
major
contributor
to
neuropathic
pain,
molecular
cellular
mechanisms
underlying
this
disinhibition
are
unclear.
Here,
we
combined
pharmacogenetic
activation
selective
ablation
approaches
mice
define
contribution
parvalbumin
(PV)-expressing
interneurons
naive
conditions.
Ablating
PV
neurons
produce
pain-like
allodynia
via
PKCγ
excitatory
interneurons.
Conversely,
activating
nerve-injured
alleviates
These
findings
indicate
modality-specific
filters
gate
but
not
thermal
inputs
increasing
interneuron
activity
can
ameliorate
hypersensitivity
develops
following
injury.