Transcript Or Central Sensitization

Central
Sensitization
Denise Jagroo
London 2016
WHY?
 Why
do all my pelvic pain patients seem
just like….
ME?
Why???....
Why do my
patients have
so many comorbidities?
Are the
conditions
systemic?
Why do I have
so many
conditions?
Are these
conditions
related?
Are they
treatable?
???
Why are all
the conditions
so similar from
patient to
patient
Why does this
“Profile” keep
popping up in
the literature?
Why???
Why are we
(my pain
patients and
I) “wired”
different?
Is this
genetic?
Its like playing whack-a-mole
About Denise..
New York University: Undergraduate and
Graduate
 Doctorate in Physical Therapy 2002
 Manual

Therapy Certification
University of St. Augustine
About Denise…
 Certificate
of Achievement in Pelvic
Physical Therapy

American Physical Therapy Association
Women’s Health Section
 Board
Health

Certified Specialist in Women’s
American Physical Therapy Association
Women’s Health Section
About Denise….
 Established
a Pelvic Rehab Clinic at the
Manhattan Veteran’s Hospital 2009
 Owner


of Private Practice In New York
Staten Island
Denise Jagroo Physical Therapy
About Denise
Lecture nationally and internationally to
health clinicians regarding
Pelvic Health and Rehabilitation
About Denise…
 Author:

“Your Best Pregnancy”
 Host
Webseries on YouTube
 Exercise equipment
 Blogger
Sensitization
 Before
we talk about central sensitization,
what is sensitization?
 Sensitization
- an increase in the
excitability of neurons, so they are more
sensitive to stimuli or sensory inputs
 Natural physiological response to help us
avoid pain
What?
What is Central
Sensitization?
 Type
of neuronal plasticity (woolf , 2007)
 Activity-dependent synaptic plasticity in the spinal
cord that generates post-injury pain hypersensitivity
HUH?
 The
connection between neurons can
CHANGE in strength!
 Either
due to using it too much or using it
too little
Abnormal
Changes in
the CNS
Peripheral
Input
Hypersensitive
painful and
prolonged
response
(fibromyalgia)
Central Sensitization
 Benign
inputs begin to produce painful
responses.
 Or worse, no input, such as phantom limb
pain.
What is Central Sensitization?
Simply put:
An amplification of neural signaling within the CNS
that elicits pain hypersensitivity
- (Woolf 2007)
Diffuse
noxious
inhibitory
controls
Endorphins
Enkephalins
Inhibitory
Controls
TENS
Acupuncture
 It’s
not as simple as a telephone wire
Ok, so far…
 Not
as simple as we thought
 There
are changes that can happen in
the CNS
 Can
change the effect of a stimulus
 Remember
to think of our patients…
Sensitization: the 70’s
Injury
Nociceptor
peripheral
terminals could
become
“sensitized”
Threshold reduced
(mainly to heat stimuli)
and ONLY within the
site of injury where the
terminal was exposed
to inflammatory
modulators, the zone
of primary
hyperalgesia (Perl,
1976)
?
 Injury
 Afterwards
it doesn’t take as much to
make someone say ‘ouch!’
 Something
seems more painful than it
should be…
By the 1980s..
 Realization
that synapses were subject to
a form of use-dependent plasticity that
could increase their strength or efficacy
Woolf 1983
E-stim
(~10–20 second), low frequency (1–10Hz) burst
of action potentials into the CNS
increased synaptic efficacy in nociceptive
neurons in the dorsal horn of the spinal cord 
lasted for tens of minutes AFTER the end of the
conditioning stimulus
?
 Stim
 Then
 But
NO STIM!
still feeling the effects!! Even after stim
taken away!
Neural windup?
 NO!
 This
phenomenon (central sensitization)
differed from windup, which represented
a progressively increasing output during
the course of a train of identical stimuli
Central Sensitization
central sensitization was concerned instead with the
facilitation that manifested AFTER the end of the
conditioning stimuli
•once triggered it remained autonomous for some time, or only required
a very low level of nociceptor input to sustain it
represented a condition where input in one set of
nociceptor sensory fibers (the conditioning input)
amplified subsequent responses to other non stimulated
non-nociceptor or nociceptor fibers
Changes in
Astrocytes
Changes in
Microglia
Maintenance
of Central
Sensitization
Changes in
gene
transcription
and
membrane
excitability
Changes in
gap junctions
Central Manifestation
This central
facilitation
manifested
as :
• ↓in threshold (allodynia)
• ↑in responsiveness and
prolonged aftereffects to
noxious stimuli (hyperalgesia)
• and a receptive field expansion
that enabled input from noninjured tissue to produce pain
(secondary hyperalgesia)
In simple terms…
Central sensitization:

Pain that’s more intense = (Hyperalgesia)

Pain where there shouldn’t be pain =
(Seconday Hyperalgesia)

Pain from something that shouldn’t be
painful = (Allodynia)
Central Sensitization
LaMotte 1991 & 1992
-1% Intradermal Capsaicin injections in
humans
- in receptive field of peroneal nerve
(below knee) studied via subcutaneous
microelectrode
-TRPV1 (detection/regulation of body
temp, sensation of scalding heat/pain)
Central Sensitization
 Injection




Site:
Intense pain lasting minutes (at injection
site)
3 zones: heat hyperalgesia 1-2 hours
Dynamic tactile allodynia: several hours &
beyond heat area
Largest zone to pinprick—WAY OUTSIDE—24
HOURS
Biomarkers
 FMRI:
Functional magnetic resonance
imaging or functional MRI (fMRI) is an MRI
procedure that measures brain activity by
detecting associated changes in blood
flow
Biomarkers
 Increased
excitability of neurons in
somatosensory cortex evoked by low
threshold aB stim within secondary
hyperalgesia
 Brainstem changes
 Cerebral processing
Visceral Effects
Brock 2010
 GI Tract: esophageal stim thermal &
mechanical pain hypersensitivity in
RECTUM
Conditioning
nociceptive
stimuli originating
in viscera (lower
esophagus to
acid)
Induces
Central
Sensitizationvi
scerovisceral
pain
pain
hypersensitivity in
upper esophagus
& viscerosomatic
(pain in CHEST
WALL)!!
Again…
Central sensitization:

Pain that’s more intense = (Hyperalgesia)

Pain where there shouldn’t be pain =
(Seconday Hyperalgesia)

Pain from something that shouldn’t be
painful = (Allodynia)
Cross Talk
Cross-Talkin’
: Close neural connections in the
sacral spinal cord are ESSENTIAL complex
coordinated visceral functions in the pelvis

: Intimate connections also allow
neuroinflammation to spread from involved to
uninvolved neurons via dorsal horn
Viscero-somatic reflexes
 Visceral
somatic reflexes: afferent stim
from a visceral source can affect somatic
structures
 Nerve
cell bodies in dorsal horn of spinal
cord and other CNS regions receive
convergent input from both somatic and
visceral structures
Viscerovisceral &
Viscerosomatic Convergence
(Di Saia 2012)
 Afferent signals converge —aberrant
interactions that can result In painful
sensations from organs that are not
directly inflamed or stimulated (cross-talk)
and from nearby somatic structures
(cross-sensitization)
Viscerovisceral &
Viscerosomatic Convergence
The concept of viscerovisceral &
viscerosomatic convergent helps explain
why there is so much overlap in the
presence of conditions such as
 endometriosis
 Interstitial Cystitis (PBS)
 IBS
 Vulvodynia
Cross –Talkin’
 End
terminal stimulatedsubstance
Pretrogade traveling down C andA
delta fibersincreased expression of
sodium channels & sensitization distally at
the terminal nociceptors PAIN organ
system to organ system & spread of
pathologies
 Central
connection
Cross Talkin’
 Noxious
Prodromic
 (PeripheralCentral) noxious afferent stim
from an irritated pelvic organ leads to
Cross-Talkin’
 Andromic
(CentralPeripheral)
 Afferent stim & co-sensitization of another
non-irritated pelvic organ
Cross-Talkin’
 Reflexive



pathways may occur:
Locally via axon collaterals (dichotomizing
afferents)
Spinal cord (DRG)
CNS
Cross Talkin’
 SOOooooo…

Neuroinflammation via andromic
pathwaysfunctional changes in the
organ with little or no evidence
of an organic etiology
Who??
 are
there individuals with a higher
inherited propensity for developing
central sensitization than others?
 Does this convey an increased risk both of
developing conditions with pain
hypersensitivity, and their chronification
 Some theories….
Neuromatrix
 Pain

Center…
Is it just the sensory thalamus and cortex?

-Melzack 2001
Neuromatrix
“Body Self”
thalamus
Somatosensory
projections
Limbic system
Neurons
cortex
Vestibular
Visual
Projected to
areas of the
brain
Sentient neural
hub
Produce
‘experience of
movement’
Produce muscle
patterns for
complex actions
Continuous
changing
stream of
awareness
Neuromatrix
 Brain
processes can be activated and
modulated by inputs from the body or in
the absence of any inputs
 Origins lie in neural networks; stimuli may
trigger the patterns but do not produce
them
Neuromatrix
 What
about if I pinched you?
Neuromatrix
 The
body = perceived as a unity,
identified as ‘the self’

This ‘experience’ is produced by central
neural processes and cannot derive from
the peripheral nervous system or spinal cord
 The
self
brain processes that underlie body-
 Built
in by genetic specification
 Modified by experience
Neurosignature
 Triggered
or modulated by input
 Input is only the trigger, does not produce
neurosignature
Neuromatrix
 Multidimensional
experience produced
by multiple influences
 Determined by genetic and sensory
factors
 Modulated by sensory inputs and by
cognitive events/psycholgical stress
Cortisol: GOOD!
 Pain
& Injury= disrupts brain’s homeostatic
regulation system

Produces ‘stress’ and initiates programs to
reinstate homeostasis

After injury Cortisol
 Produces
and maintains high levels of glucose
for rapid response after injury, threat or other
emergency
Cortisol!
 However,
potentially highly destructive
substance because to ensure high levels
of glucose

Breaks down protein in muscle and inhibits
the ongoing replacement of calcium in
bone
Cortisol: BAD!

Sustained cortisol release
 Produces
myopathy
 Weakness
 Fatigue
 Decalcification of bone
 Accelerate neural degeneration of the
hippocampus during aging
 Suppresses immune system
Ok, so far….how did we
start talking about this?
 INJURY
 Central



sensitization:
Pain that’s more intense
Pain where there shouldn’t be pain
Pain from something that shouldn’t be
painful
Also, don’t forget cross talkin’
 Organs
‘talk’ to eachother
 Could be good…but could be bad!
And…
 So



what is ‘pain’?
Neuromatrix
Neurosignature
Stress
What does this lead to?
A
Hot Mess
 A ‘Drama Queen’
 Someone who is experiencing discomfort
in their pelvis and guarding/tensing their
PFM muscles as a reaction
So what does this mean to us?
 “Pain”



in the pelvis:
Complex (central, hormonal, emotional
factors…)
Need a dynamic approach
Need to address central issues,
musculoskeletal issues and stress issues, etc
Overactive pelvic floor
Dysfunction
Pelvic Floor Disorders
 Overactive



pelvic floor muscles:
PFM do not relax, or may even contract
when relaxation is functionally needed
(micturition, defecation)
Based on symptoms such as voiding
problems, obstructed defecation, or
dyspareunia
Absence of voluntary pelvic floor muscle
relaxation
Overactive Pelvic Floor
Dysfunction
Symptoms:
 constipation.
 Pain is often chronic
 aggravated by micturition, sexual intercourse,
orgasm, defecation and sitting on hard surfaces,
and reduces the ability to work and quality of life in
general. (Rognlid, 2010)
A Headache in the pelvis
By David Wise
“Now imagine you maintain this clenched
fist for a day. Now imagine you maintain this
fist for a week. Now imagine a month of
tightening your fist constantly twenty-four
hours a day. Now imagine doing it for a
year. Now imagine doing it for several years.
This is one way to understand the state of
the pelvic floor in people with pelvic pain.”
Some causes…
 Some
of the conditions that our patients
come in with that may cause overactive
pelvic floor syndrome…
Pelvic Pain
 Vestibulitis
 Dyspareunia
 Vulvodynia
 Fibroids
 Endometriosis
 Coccydynia
 Pudendal
 Prostatitis
Neuralgia
 Interstitial
Cystitis/Painful
Bladder Syndrome
Treatment
Respiratory Sinus Arrhythmia
Breathing
A
Descriptioin of the relationship between
heart rate and breathing and refers to the
heart rate varying in response to
respiration
 When
you breathe in, the heart rate
 When you breathe out, heart rate
RSA breathing (Wise 2008)
 Under
circumstances of mental or
physical disease, the relationship b/w HR
and breathing is interrupted
6
deep abdominal breaths per minute is
considered an optimal resp rate
 Breathing
rates that accomplish
preliminary quieting of the body can vary
from 2 – 9 breaths
RSA Breathing
 Divide
 Then
heart rate by 6
divide that number by 2 represents
the number heartbeats allocated for a
single inhalation or exhalation
Physical Therapy Treatment for
Overactive Pelvic Floor
Dysfunction
Downtraining: program to relax the pelvic floor
muscles
 As presence of painful PFM spasm and /or
overactivity are frequently identified in patients
presenting with CPP, most reported PFM exercise
regimens have used a de-training focus (Shelly et al
2002) based on the principle that:
Downtraining
 An
over activated muscle should not be
further loaded with active exercise until
normal, pain-free range and contractile
activity have been restored.
 Relaxation exercises are often
combined with a cognitive-behavioral
approach involving imagery and desensitization
 Stretching
Pelvic Floor Stretches
Hamstring Stretch
Hip flexor/Gluteus Stretch
Piriformis Stretch
Stretches: Adductors
Treatment: Diaphragmatic
Breathing
 Diaphragmatic
Breathing: Relaxation and
breathing techniques utilize awareness of
breathing rate, rhythm, and volume. Most
often breathing techniques are used to
minimize physiologic responses to stress,
possibly by increasing parasympathetic
response. (Wahbeh, 2008)
-Breathe in through your nose, out through
your mouth
Diaphragmatic Breathing
 Quiets
Autonomic Arousal
 Mind-Body
calming technique
Treatment: Diaphragmatic
Breathing
 ”Place
your tongue gently on the roof of your
mouth, place your lips together and part your
teeth”
 Place
your hand on your abdomen and feel it rise
as you inhale

Most people breathe short and shallow using postural
muscles
Treatment: Breathing
 Count
during your inhales/exhales
 Count
your breaths during each minute
Treatment: Diaphragmatic
Breathing


You breathe properly when you sleep
Watch a baby breathe
 Pursed
Lip Breathing: Breathe like you are
breathing out through a straw
Diaphragmatic Breathing
Treatment
 Visualization:
Imagine your breathe is like a sphere
that is moving down through your body and
relaxing your muscles as it travels

Relax the muscles from top to bottom: “Relax your jaw
muscles, let go of the tension in your neck…”
 Relaxation
Techniques
 Stress Management
Treatment
 Referral



to other professional services
Medications
Surgical techniques
Psychosocial Interventions
Treatment
 Meditation
 Yoga
 Create


a warm, relaxing environment:
Lighting
Music
 Trigger
Point Release
Dynamic Approach
 Addressing
the problem through a
dynamic approach
Using:
 Biofeedback
 Manual Techniques
 Exercise
 Breathing
Dynamic Approach
Using:
Relaxation techniques
Advice on diet
Referrals to other professional services
Medications/Surgical techniques if
necessary
Thank You!
Denise Jagroo
 [email protected]
 www.drjagroo.com