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A.THANGAMANI RAMALINGAM
OBJECTIVES
 Basics of Central sensitization(CS)
 Neuro immunology
 Recognition of CS
 Implications for
physiotherapy/therapist(assessment/management/g
uidelines)
 What Evidences say?
PAIN
“An unpleasant sensory and emotional
experience associated with actual or potential
tissue damage, or described in terms of such
damage” ISAP (1979)
 Pain is a noxious unwanted
perception
 “Pain is subjective,
individual and modified by
degrees of attention,
emotional state and the
conditioning of past
experiences.” (Livingstone
1943)
PHYSIOLOGY OF PAIN
Receptors
A fibers – Localized and
quick type of pain C fibers
– Slow acting type of
pain(Peripheral Nervous
System)
Spinal Cord (Substantia
Gelatinosa)
Spinothalamic Tracts
(Lateral / Anterior)
Thalamus
Cerebral Cortex
(Somatosensory Cortex)
Influenced
by Limbic
system &
Reticular
formation
Nociceptive processing
Pain sensitization
 Primary hyperalgesia or peripheral pain sensitization
pain
 Secondary hyperalgesia or central sensitization
Unimodal/polymodal
nociceptors
Central sensitization
Top down mechanisms Bottom up mechanisms
 Augmentation of
responsiveness(Meyer et al
1995)
 Altered sensory processing
(Staud et al.,2007)
 Malfunctioning of descending
inhibitory system(Meeus et al.,
2008)
 Potentiation of neuronal
synapses (zuho 2007)
 Temporal summation of
secondpain or windup(Nijis
2007)
 Pro inflammatory
cytokines(samad et al)
Prostoglandin
E2/cox-2
releasestressors
Issue –tactile allodynia/punctuate
hyperalgesia/temporal summation/sensory after effects
Increased sensitivity to
various stimuli
 Light
 Touch
Cold
Heat
Pressure or punctuate
Chemical substances
Electrical stimuli
Reductionist
Rationalist
Neuro immunology
Neuro immunological response
Glial cells-neuro immunology
Dr. Watkins, at the Headache Cooperative of the Pacific’s
2009 Winter Colloquium
 Glial cell activation has been
demonstrated in every clinically
relevant animal model study to date,
including that of peripheral nerve
injury, bone cancer, multiple sclerosis
(MS), spinal cord injury, herniated
disks, low back pain, and migraine,
noted Dr. Watkins, Professor of
Psychology and Neuroscience at the
University of Colorado at Boulder.
“Targeting the glial cells and their
proinflammatory products doesn’t
make a patient analgesic, and it doesn’t
suppress all pain sensitivity. It simply
returns the pain to normal. It removes
the abnormal pain,
NMDA Vs
MSD-neuro immunology
Biomechanical injury/loading
Altered electro physiology
Change in neuro immune
response
Conditions
 Rheumatoid arthritis
 OA
 Temporo mandibular disorders
 Fibromyalgia
 Chronic neck and back pain-disc pathologies
 Headache
 Neuropathic pain
 CRPS
 Visceral pain hypersensitivity syndrome
Central sensitization syndromes
 Co morbidity of conditions
IBS/FM/CFS/CWP/headache /MSDs
Recognition of Central
sensitization
Screening
Using medical diagnosis
History taking
Clinical examination
Analyzing the treatment
responses
Using medical diagnosis
History taking
Clinical examination
Analyzing the treatment
responses
Clinical decision making
 Diagnostic criteria
 eg:
2010 PRELIMINARY DIAGNOSTIC CRITERIA (EXCERPT)
CRITERIA Diagnostic criteria for fibromyalgia if the following 3
conditions are met:
1.Widespread pain index (WPI) ≥7 and symptom severity (SS) scale score
≥5 or WPI 3 - 6 and SS scale score ≥9.
2.Symptoms have been present at a similar level for at least 3 months.
3.The patient does not have a disorder that would otherwise explain the
pain.
 Biomarkers
 Clinical testing of hyper algesia/allodynia
Physiotherapy
 Behavioral pain measures
Physiological measures
EMG – muscle tension
Heart rate
Skin temperature
EEG and brain imaging
Self-report measures
Visual Analog Scale(VAS)
Graphic Rating Scale(GRS)
Simple Descriptor Scale(SDS)
Numerical Rating Scale(NRS)
Faces Rating Scale(FRS)
McGill Pain Questionnaire
Pain Rating Scales
Pain Discomfort Scale MPQ
Sixteen Pain Behaviors-biopsychosocial
assessment Rudy et al.
Asymmetry
Slow response time
Guarded movement
Limping
Bracing
Personal contact
Position shifts
Partial movement
Absence of movement
Eye movement
Grimacing
Quality of speech
Pain statements
Limitation statements
Sounds
Pain relief devices
(under use)
Quantitative sensory testing (QST)
 compare pressure pain
threshold (PPT) values
of myotomes,
sclerotomes, and
dermatomes
corresponding to
segments - algometer
 two-point discrimination
(TPD)- aesthesiometer
 vibratory sensation
 thermal pain threshold
and tolerance
 suprathreshold heat pain
response.
 DNIC-diffuse noxious
inhibitory control
assessment
Measurement of secondary
hyperalgesia
CSI
(test-retest reliability =
0.817; Cronbach's alpha
= 0.879)
SCREENING TOOLS FOR
NEUROPATHIC PAIN.
 Leeds Assessment of Neuropathic Symptoms and
Signs (LANSS)
 Neuropathic Pain Questionnaire (NPQ)
 Douleur Neuropathique en 4 questions (DN4)
 pain DETECT
 ID-Pain
Mechanisms-based classifications
of musculoskeletal pain
 'Disproportionate, non-mechanical, unpredictable pattern
of pain provocation in response to multiple/non-specific
aggravating/easing factors', 'Pain disproportionate to the
nature and extent of injury or pathology‘
 'Strong association with maladaptive psychosocial factors
(e.g. negative emotions, poor self-efficacy, maladaptive
beliefs and pain behaviours)‘
 'Diffuse/non-anatomic areas of pain/tenderness on
palpation'. This cluster was found to have high levels of
classification accuracy (sensitivity 91.8%, 95% confidence
interval (CI): 84.5-96.4; specificity 97.7%, 95% CI: 95.6-99.0).
 Mechanisms-based classifications of musculoskeletal pain: part 1 of 3: symptoms and signs
of centralsensitisation in patients with low back (± leg) pain.Smart KM1, Blake C Staines A, Thacker
M Doody C Man Ther.2012 Aug;17(4):336-44. doi: 10.1016/j.math.2012.03.013. Epub 2012 Apr 23
Management
Guidelines
1. Assessment of pressure pain thresholds at sites
remote from the symptomatic site;
2. Assessment of sensitivity to touch during manual
palpation at sites remote from the symptomatic site;
and
3. Assessment of pressure pain thresholds during and
following exercise
 Nijs J, Van Houdenhove B, Oostendorp R a B. Recognition of central
sensitization in patients with musculoskeletal pain: Application of
pain neurophysiology in manual therapy practice. Manual therapy
[Internet]. Elsevier Ltd; 2010 Apr [cited 2014 Feb 24];15(2):135–41.
Available from: http://www.ncbi.nlm.nih.gov/pubmed/20036180
Education
Face to face session
Booklet/written –
homework
Application
Anterior cingulate cortex – responds to
physical and emotional pain -EXERCISE
Biofeedback
Gauthier et al. (1994) for headaches
Behavioral/Cognitive Approaches
• Guided Imagery
• Systematic
desensitization
• Reframing
• Meditation
• Stress management
techniques – not as
effective as other
techniques
• Thinking about the pain
and expectations –
Bandura et al. (1987)–
an increase in
endorphines with
cognitive technique
How do placebos influence pain?
Patient’s expectation about the effects
of the treatment
Airily (2008) study of differential
effectives of placebo based on perceived
cost ($.10 v. $2.50)
http://www.npr.org/templates/story/story
.php?storyId=87938032
Classical conditioning
Patient’s may change behaviors
Physiological changes which inhibit
the experience of pain
 10khz medium
frequency current
has marked
discrimination
between motor and
pain threshold
 Clinically we use
2and 4khz
equipments for
therapy
Evidences
Neck/back pain
 Weak pain days
 CS α pain intensity
 Strong pain days
 CS α no of pain areas
Post operative cases
DAY(m
ean/sd
)
20HZS
EN
2OHZ
MOT
2OHZP
AIN
50
HZSEN
50HZ
MOT
50HZP
AIN
100HZ
SEN
100HZ
MOT
100HZ
PAIN
NPRS GROC
ONE
4.800 6.733 9.533 4.97 6.933 9.733 5.133 7.066 10.233
4.73 5.0
THREE
5.300 7.033 9.600 5.40 7.100 9.933 5.433 7.2000 10.233
3.43 5.63
SEVEN
5.333 7.166 9.700 5.43 7.300 10.03 5.566 7.433 10.366
2.40 5.96
Chronic back pain cases
DAY(me
an/sd)
20HZSEN 2OHZM
OT
2OHZPAI
N
50
HZSEN
50HZMO
T
50HZPAI
N
100HZSE
N
100HZM
OT
100HZPA
IN
NPRS
one 4.4 6.25 10.8 4.75 6.6 11.2 4.75 6.6 11.5
5.05
thre
e
4.55 6.5 11.5 4.8 6.6 11.3 5.2 7.3 12.1 4.0
five 5.05 6.8 11.8 5.10 7 12 5.3 7.2 12.4 3.6
 Response to 100 hz low
frequency current on
different groups
OA
 Interventions such as cognitive-
behavioral therapy and neuroscience
education potentially target cognitive-
emotional sensitization (and descending
facilitation), and centrally acting drugs and
exercise therapy can improve endogenous
analgesia (descending inhibition) in patients
with osteoarthritis.
 Phys Ther. 2013 Jun;93(6):842-51. doi: 10.2522/ptj.20120253. Epub 2013 Feb 7.
Pain treatment for patients with osteoarthritis and central sensitization.
Lluch Girbés E1, NijsJ, Torres-Cueco R, López Cubas C
Activity dependent treatments
in neuropathic pain
Treadmill running Electrical stimulation
 ,TR induced strong agonistic
effects in relieving pain. TR
reduced the levels of pro-
nociceptive factors such as
BDNF, NGF and GDNF in
DRG.
 Combination of ES and
TR induced intermediate
levels suggesting an
optimal balancing of
treatment effects.
 ES enhanced motor and sensory
reinnervation
 ES speeded up expression of
BDNF and GDNF in DRG ., and
of BDNF and NT3 in the ventral
horn.
Exp Neurol.2013 Feb;240:157-67. doi:
10.1016/j.expneurol.2012.11.023. Epub 2012
Nov 30.Differential effects of activity
dependent treatments on axonal
regeneration and neuropathic pain
after peripheral nerve injury.Cobianchi
S1, Casals-DiazL, Jaramillo J, Navarro X
TENS
Positive study Negative study
 Frequency-dependent
antihyperalgesic and
analgesic effects in humans.
 No long-lasting analgesic
and antihyperalgesic effects
of a single TES treatment
 (TES(60Hz) > TES(100Hz))
• Anesth Analg.2010 Nov;111(5):1301-7. doi:
10.1213/ANE.0b013e3181e3697e. Epub 2010 Jun 8.The analgesic
and antihyperalgesic effects of transcranial
electrostimulation with combined direct and
alternating current in healthy volunteers.Nekhendzy
V, Lemmens HJ, Tingle M, Nekhendzy M, Angst MS.
 Tens influence on centrally
sensitized OAk patients may
be augmented to the input of
electrical stimuli.
 Adverse therapy effect of
tens.
 To increase treatment
effectiveness - identify a
subgroup of symptomatic
OAk patients, i.e., non-
sensitized patients.
 Trials.2012 Feb 21;13:21. doi: 10.1186/1745-6215-13-
21.Effect of tens on pain in relation to central
sensitization in patients with osteoarthritis of
the knee: study protocol of a randomized
controlled trial.Beckwée D1, De Hertogh
W, Lievens P, BautmansI, Vaes P.
 Acetaminophen, serotonin-reuptake inhibitor drugs,
selective and balanced serototin and norepinephrine-
reuptake inhibitor drugs, the serotonin precursor
tryptophan, opioids, N-methyl-D-aspartate (NMDA)-
receptor antagonists, calcium-channel alpha(2)delta (a2δ)
ligands, ketamine ,pragabalin,
duloxetine,transcranial magnetic stimulation.
+
 transcutaneous electric nerve stimulation
(TENS), manual therapy and stress
management each target central pain processing
mechanisms in animals that – theoretically – desensitize
the CNS in humans
Message/tips for therapist
Tips
Treat acute pains at right times
The pain tolerance –can be improved/cs is
reversible
Get the pain control first then go for exercise
therapy
Use pressures sensibly
Use appropriate therapy windows when we use
electro physical agents.
Understand pain behaviours.
Pain can be triggered from normal
tissues(secondary hyperalgesia),not necessarily
psychogenic.
Pain has a learned component and produces
physical changes in CNS and musculoskeletal
system.
Education and learning(motor and cognitive)
plays important role
(AustJPhysiotherv45i2Shacklock)
A multidisciplinary approach to care of chronic
pain conditions is an absolute necessity
ensure that whichever treatment protocol is
utilized the treatments must not induce any
pain for the patient
APPROACH to CS
block or reduction of the nociceptive input from the injured areas
specific pharmacological intervention on the cord mechanisms
pharmacologic or psychologic interventions at supraspinal level
descending modulatory system
a multimodal physical therapy program
a clinician should use caution with generically prescribing exercise to
patients experiencing chronic pain.
psychosocial characteristics, such as inappropriate beliefs about pain, pain
catastrophizing, and/or depression may contribute to the mechanisms of
central sensitization.
Why deep tissues are
more frequently
affected in chronic pain
state?
Mirror-image pain
(pain or hyperalgesia in
unaffected side or area)
stress-induced
hyperalgesia
To provide a comprehensive treatment for
‘unexplained’ chronic pain disorders
characterized by central sensitization, it is
advocated to combine the best evidence
available with treatment modalities known to
target central sensitization
References
 Woolf CJ. Central sensitization : Implications for the diagnosis and treatment of
pain. Pain [Internet]. International Association for the Study of Pain;
2011;152(3):S2–15. Available from: http://dx.doi.org/10.1016/j.pain.2010.09.030
 Winkelstein B a. Mechanisms of central sensitization, neuroimmunology &
injury biomechanics in persistent pain: implications for musculoskeletal
disorders. Journal of electromyography and kinesiology : official journal of the
International Society of Electrophysiological Kinesiology [Internet]. 2004 Feb
[cited 2014 Feb 24];14(1):87–93. Available from:
http://www.ncbi.nlm.nih.gov/pubmed/14759754
 Nijs J, Van Houdenhove B, Oostendorp R a B. Recognition of central
sensitization in patients with musculoskeletal pain: Application of pain
neurophysiology in manual therapy practice. Manual therapy [Internet]. Elsevier
Ltd; 2010 Apr [cited 2014 Feb 24];15(2):135–41. Available from:
http://www.ncbi.nlm.nih.gov/pubmed/20036180
 Nijs J, Wilgen CPV, Oosterwijck JV, Ittersum MV, Meeus M. How to explain
central sensitization to patients with “ unexplained ” chronic musculoskeletal
pain : Practice guidelines. Manual Therapy [Internet]. Elsevier Ltd;
2011;16(5):413–8. Available from: http://dx.doi.org/10.1016/j.math.2011.04.005
 Smart KM, Blake C, Staines A, Doody C. Self-reported pain severity , quality of
life , disability , anxiety and depression in patients classified with “ nociceptive ”,
“ peripheral neuropathic ” and “ central sensitisation ” pain . The discriminant
validity of mechanisms-based classifications of low back ( Æleg ) pain. Manual
Therapy [Internet]. Elsevier Ltd; 2012;17(2):119–25. Available from:
http://dx.doi.org/10.1016/j.math.2011.10.002
 Smart KM, Blake C, Staines A, Thacker M, Doody C. Mechanisms-based
classifications of musculoskeletal pain : Part 3 of 3 : Symptoms and signs of
nociceptive pain in patients with low back ( Æleg ) pain. Manual Therapy
[Internet]. Elsevier Ltd; 2012;17(4):352–7. Available from:
http://dx.doi.org/10.1016/j.math.2012.03.002
 Smart KM, Blake C, Staines A, Thacker M, Doody C. Mechanisms-based
classifications of musculoskeletal pain : Part 2 of 3 : Symptoms and signs of
peripheral neuropathic pain in patients with low back ( Æleg ) pain. Manual
Therapy [Internet]. Elsevier Ltd; 2012;17(4):345–51. Available from:
http://dx.doi.org/10.1016/j.math.2012.03.003
 18. Smart KM, Blake C, Staines A, Thacker M, Doody C. Mechanisms-
based classifications of musculoskeletal pain : Part 1 of 3 : Symptoms and signs
of central sensitisation in patients with low back ( Æleg ) pain. Manual Therapy
[Internet]. Elsevier Ltd; 2012;17(4):336–44. Available from:
http://dx.doi.org/10.1016/j.math.2012.03.013
 Kumar SP. Physical Therapy and Central Sensitization : Are We
Explaining to Patients with “ Unexplained ” Pain ? Journal de Physique (main
title). 2013;41–5.
 48. Review L. Central Sensitization In Urogynecological Chronic
Pelvic Pain: A Systematic Literature Review. Pain Physician. 2013;291–308.
 49. Mcclintic AM, Garcia JB, Gofeld M, Kliot M, Kucewicz JC, Loeser
JD, et al. Intense focused ultrasound stimulation can safely stimulate inflamed
subcutaneous tissue and assess allodynia. The Lamp. 2014;2(1):1–9.
 50. Dodick D, Silberstein S, Jefferson T. Central Sensitization Theory
of Migraine : Clinical Implications. Society. 2006;
 51. Farasyn A, Meeusen R. Effect of Roptrotherapy on Pressure-Pain
Thresholds in Patients with Subacute Nonspecific Low Back Pain. ReVision.
2007;15(1):41–54.
 52. Munglani R. Neurobiological Mechanisms Underlying Chronic
Whiplash Associated Pain : The Peripheral Maintenance of Central
Sensitization. ReVision. 8:169–79.
 53. Dickenson AH. The Pharmacology of Central Sensitization.
Imprint. 2002;10(1):35–43.
 54. Salter MW. The Neurobiology of Central Sensitization. Journal of
Musculoskeletal Pain. 10(1):23–33.
 55. Whiplash JOF, Disorders R. Central Sensitization in Chronic
Whiplash and Related Musculo- skeletal Disorders. Journal of Whiplash &
Related Disorders. 1998;64–6.
 Mayer TG, Neblett R, Cohen H, Howard KJ, Choi YH, Williams MJ, et al. The
Development and Psychometric Validation of the Central Sensitization
Inventory. Pain Practice. 2012;12(4):276–86.
 Winkelstein BA. Mechanisms of central sensitization , neuroimmunology and
injury biomechanics in persistent pain : implications for musculoskeletal
disorders. Electromyography. 2004;14(1):87–93.
 Meeus M, Nijs J. Central sensitization : a biopsychosocial
explanation for chronic widespread pain in patients with fibromyalgia and
chronic fatigue syndrome. Clinical Rheumatology. 2007;465–73.
 Staud R. Is It All Central Sensitization ? Role of Peripheral Tissue
Nociception in Chronic Musculoskeletal Pain. Arthritis & Rheumatism.
2010;448–54.
 Watkins LR, Maier SF. GLIA : A NOVEL DRUG DISCOVERY
TARGET FOR CLINICAL PAIN. Discovery. 2003;2(December).
 Predicting outcome of TENS in chronic pain_ a prospective, randomized,
placebo controlled trial.pdf.
Central sensitization for physiotherapist

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Central sensitization for physiotherapist

  • 3.  Basics of Central sensitization(CS)  Neuro immunology  Recognition of CS  Implications for physiotherapy/therapist(assessment/management/g uidelines)  What Evidences say?
  • 4. PAIN “An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage” ISAP (1979)  Pain is a noxious unwanted perception  “Pain is subjective, individual and modified by degrees of attention, emotional state and the conditioning of past experiences.” (Livingstone 1943)
  • 5. PHYSIOLOGY OF PAIN Receptors A fibers – Localized and quick type of pain C fibers – Slow acting type of pain(Peripheral Nervous System) Spinal Cord (Substantia Gelatinosa) Spinothalamic Tracts (Lateral / Anterior) Thalamus Cerebral Cortex (Somatosensory Cortex) Influenced by Limbic system & Reticular formation
  • 7.
  • 8.
  • 9. Pain sensitization  Primary hyperalgesia or peripheral pain sensitization pain  Secondary hyperalgesia or central sensitization Unimodal/polymodal nociceptors
  • 10.
  • 11.
  • 12. Central sensitization Top down mechanisms Bottom up mechanisms  Augmentation of responsiveness(Meyer et al 1995)  Altered sensory processing (Staud et al.,2007)  Malfunctioning of descending inhibitory system(Meeus et al., 2008)  Potentiation of neuronal synapses (zuho 2007)  Temporal summation of secondpain or windup(Nijis 2007)  Pro inflammatory cytokines(samad et al) Prostoglandin E2/cox-2 releasestressors
  • 13. Issue –tactile allodynia/punctuate hyperalgesia/temporal summation/sensory after effects Increased sensitivity to various stimuli  Light  Touch Cold Heat Pressure or punctuate Chemical substances Electrical stimuli
  • 17. Glial cells-neuro immunology Dr. Watkins, at the Headache Cooperative of the Pacific’s 2009 Winter Colloquium  Glial cell activation has been demonstrated in every clinically relevant animal model study to date, including that of peripheral nerve injury, bone cancer, multiple sclerosis (MS), spinal cord injury, herniated disks, low back pain, and migraine, noted Dr. Watkins, Professor of Psychology and Neuroscience at the University of Colorado at Boulder. “Targeting the glial cells and their proinflammatory products doesn’t make a patient analgesic, and it doesn’t suppress all pain sensitivity. It simply returns the pain to normal. It removes the abnormal pain,
  • 19. MSD-neuro immunology Biomechanical injury/loading Altered electro physiology Change in neuro immune response
  • 20. Conditions  Rheumatoid arthritis  OA  Temporo mandibular disorders  Fibromyalgia  Chronic neck and back pain-disc pathologies  Headache  Neuropathic pain  CRPS  Visceral pain hypersensitivity syndrome
  • 21. Central sensitization syndromes  Co morbidity of conditions IBS/FM/CFS/CWP/headache /MSDs
  • 23. Screening Using medical diagnosis History taking Clinical examination Analyzing the treatment responses
  • 27. Clinical decision making  Diagnostic criteria  eg: 2010 PRELIMINARY DIAGNOSTIC CRITERIA (EXCERPT) CRITERIA Diagnostic criteria for fibromyalgia if the following 3 conditions are met: 1.Widespread pain index (WPI) ≥7 and symptom severity (SS) scale score ≥5 or WPI 3 - 6 and SS scale score ≥9. 2.Symptoms have been present at a similar level for at least 3 months. 3.The patient does not have a disorder that would otherwise explain the pain.  Biomarkers  Clinical testing of hyper algesia/allodynia
  • 29.  Behavioral pain measures Physiological measures EMG – muscle tension Heart rate Skin temperature EEG and brain imaging Self-report measures Visual Analog Scale(VAS) Graphic Rating Scale(GRS) Simple Descriptor Scale(SDS) Numerical Rating Scale(NRS) Faces Rating Scale(FRS) McGill Pain Questionnaire
  • 30. Pain Rating Scales Pain Discomfort Scale MPQ
  • 31. Sixteen Pain Behaviors-biopsychosocial assessment Rudy et al. Asymmetry Slow response time Guarded movement Limping Bracing Personal contact Position shifts Partial movement Absence of movement Eye movement Grimacing Quality of speech Pain statements Limitation statements Sounds Pain relief devices (under use)
  • 32. Quantitative sensory testing (QST)  compare pressure pain threshold (PPT) values of myotomes, sclerotomes, and dermatomes corresponding to segments - algometer  two-point discrimination (TPD)- aesthesiometer  vibratory sensation  thermal pain threshold and tolerance  suprathreshold heat pain response.  DNIC-diffuse noxious inhibitory control assessment
  • 34. CSI (test-retest reliability = 0.817; Cronbach's alpha = 0.879)
  • 35. SCREENING TOOLS FOR NEUROPATHIC PAIN.  Leeds Assessment of Neuropathic Symptoms and Signs (LANSS)  Neuropathic Pain Questionnaire (NPQ)  Douleur Neuropathique en 4 questions (DN4)  pain DETECT  ID-Pain
  • 36. Mechanisms-based classifications of musculoskeletal pain  'Disproportionate, non-mechanical, unpredictable pattern of pain provocation in response to multiple/non-specific aggravating/easing factors', 'Pain disproportionate to the nature and extent of injury or pathology‘  'Strong association with maladaptive psychosocial factors (e.g. negative emotions, poor self-efficacy, maladaptive beliefs and pain behaviours)‘  'Diffuse/non-anatomic areas of pain/tenderness on palpation'. This cluster was found to have high levels of classification accuracy (sensitivity 91.8%, 95% confidence interval (CI): 84.5-96.4; specificity 97.7%, 95% CI: 95.6-99.0).  Mechanisms-based classifications of musculoskeletal pain: part 1 of 3: symptoms and signs of centralsensitisation in patients with low back (± leg) pain.Smart KM1, Blake C Staines A, Thacker M Doody C Man Ther.2012 Aug;17(4):336-44. doi: 10.1016/j.math.2012.03.013. Epub 2012 Apr 23
  • 38. Guidelines 1. Assessment of pressure pain thresholds at sites remote from the symptomatic site; 2. Assessment of sensitivity to touch during manual palpation at sites remote from the symptomatic site; and 3. Assessment of pressure pain thresholds during and following exercise  Nijs J, Van Houdenhove B, Oostendorp R a B. Recognition of central sensitization in patients with musculoskeletal pain: Application of pain neurophysiology in manual therapy practice. Manual therapy [Internet]. Elsevier Ltd; 2010 Apr [cited 2014 Feb 24];15(2):135–41. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20036180
  • 39. Education Face to face session Booklet/written – homework Application
  • 40. Anterior cingulate cortex – responds to physical and emotional pain -EXERCISE
  • 41. Biofeedback Gauthier et al. (1994) for headaches
  • 42. Behavioral/Cognitive Approaches • Guided Imagery • Systematic desensitization • Reframing • Meditation • Stress management techniques – not as effective as other techniques • Thinking about the pain and expectations – Bandura et al. (1987)– an increase in endorphines with cognitive technique
  • 43. How do placebos influence pain? Patient’s expectation about the effects of the treatment Airily (2008) study of differential effectives of placebo based on perceived cost ($.10 v. $2.50) http://www.npr.org/templates/story/story .php?storyId=87938032 Classical conditioning Patient’s may change behaviors Physiological changes which inhibit the experience of pain
  • 44.  10khz medium frequency current has marked discrimination between motor and pain threshold  Clinically we use 2and 4khz equipments for therapy
  • 46. Neck/back pain  Weak pain days  CS α pain intensity  Strong pain days  CS α no of pain areas
  • 47. Post operative cases DAY(m ean/sd ) 20HZS EN 2OHZ MOT 2OHZP AIN 50 HZSEN 50HZ MOT 50HZP AIN 100HZ SEN 100HZ MOT 100HZ PAIN NPRS GROC ONE 4.800 6.733 9.533 4.97 6.933 9.733 5.133 7.066 10.233 4.73 5.0 THREE 5.300 7.033 9.600 5.40 7.100 9.933 5.433 7.2000 10.233 3.43 5.63 SEVEN 5.333 7.166 9.700 5.43 7.300 10.03 5.566 7.433 10.366 2.40 5.96
  • 48. Chronic back pain cases DAY(me an/sd) 20HZSEN 2OHZM OT 2OHZPAI N 50 HZSEN 50HZMO T 50HZPAI N 100HZSE N 100HZM OT 100HZPA IN NPRS one 4.4 6.25 10.8 4.75 6.6 11.2 4.75 6.6 11.5 5.05 thre e 4.55 6.5 11.5 4.8 6.6 11.3 5.2 7.3 12.1 4.0 five 5.05 6.8 11.8 5.10 7 12 5.3 7.2 12.4 3.6
  • 49.  Response to 100 hz low frequency current on different groups
  • 50. OA  Interventions such as cognitive- behavioral therapy and neuroscience education potentially target cognitive- emotional sensitization (and descending facilitation), and centrally acting drugs and exercise therapy can improve endogenous analgesia (descending inhibition) in patients with osteoarthritis.  Phys Ther. 2013 Jun;93(6):842-51. doi: 10.2522/ptj.20120253. Epub 2013 Feb 7. Pain treatment for patients with osteoarthritis and central sensitization. Lluch Girbés E1, NijsJ, Torres-Cueco R, López Cubas C
  • 51. Activity dependent treatments in neuropathic pain Treadmill running Electrical stimulation  ,TR induced strong agonistic effects in relieving pain. TR reduced the levels of pro- nociceptive factors such as BDNF, NGF and GDNF in DRG.  Combination of ES and TR induced intermediate levels suggesting an optimal balancing of treatment effects.  ES enhanced motor and sensory reinnervation  ES speeded up expression of BDNF and GDNF in DRG ., and of BDNF and NT3 in the ventral horn. Exp Neurol.2013 Feb;240:157-67. doi: 10.1016/j.expneurol.2012.11.023. Epub 2012 Nov 30.Differential effects of activity dependent treatments on axonal regeneration and neuropathic pain after peripheral nerve injury.Cobianchi S1, Casals-DiazL, Jaramillo J, Navarro X
  • 52. TENS Positive study Negative study  Frequency-dependent antihyperalgesic and analgesic effects in humans.  No long-lasting analgesic and antihyperalgesic effects of a single TES treatment  (TES(60Hz) > TES(100Hz)) • Anesth Analg.2010 Nov;111(5):1301-7. doi: 10.1213/ANE.0b013e3181e3697e. Epub 2010 Jun 8.The analgesic and antihyperalgesic effects of transcranial electrostimulation with combined direct and alternating current in healthy volunteers.Nekhendzy V, Lemmens HJ, Tingle M, Nekhendzy M, Angst MS.  Tens influence on centrally sensitized OAk patients may be augmented to the input of electrical stimuli.  Adverse therapy effect of tens.  To increase treatment effectiveness - identify a subgroup of symptomatic OAk patients, i.e., non- sensitized patients.  Trials.2012 Feb 21;13:21. doi: 10.1186/1745-6215-13- 21.Effect of tens on pain in relation to central sensitization in patients with osteoarthritis of the knee: study protocol of a randomized controlled trial.Beckwée D1, De Hertogh W, Lievens P, BautmansI, Vaes P.
  • 53.  Acetaminophen, serotonin-reuptake inhibitor drugs, selective and balanced serototin and norepinephrine- reuptake inhibitor drugs, the serotonin precursor tryptophan, opioids, N-methyl-D-aspartate (NMDA)- receptor antagonists, calcium-channel alpha(2)delta (a2δ) ligands, ketamine ,pragabalin, duloxetine,transcranial magnetic stimulation. +  transcutaneous electric nerve stimulation (TENS), manual therapy and stress management each target central pain processing mechanisms in animals that – theoretically – desensitize the CNS in humans
  • 55. Tips Treat acute pains at right times The pain tolerance –can be improved/cs is reversible Get the pain control first then go for exercise therapy Use pressures sensibly Use appropriate therapy windows when we use electro physical agents. Understand pain behaviours.
  • 56. Pain can be triggered from normal tissues(secondary hyperalgesia),not necessarily psychogenic. Pain has a learned component and produces physical changes in CNS and musculoskeletal system. Education and learning(motor and cognitive) plays important role (AustJPhysiotherv45i2Shacklock) A multidisciplinary approach to care of chronic pain conditions is an absolute necessity ensure that whichever treatment protocol is utilized the treatments must not induce any pain for the patient
  • 57. APPROACH to CS block or reduction of the nociceptive input from the injured areas specific pharmacological intervention on the cord mechanisms pharmacologic or psychologic interventions at supraspinal level descending modulatory system a multimodal physical therapy program a clinician should use caution with generically prescribing exercise to patients experiencing chronic pain. psychosocial characteristics, such as inappropriate beliefs about pain, pain catastrophizing, and/or depression may contribute to the mechanisms of central sensitization.
  • 58. Why deep tissues are more frequently affected in chronic pain state? Mirror-image pain (pain or hyperalgesia in unaffected side or area) stress-induced hyperalgesia
  • 59. To provide a comprehensive treatment for ‘unexplained’ chronic pain disorders characterized by central sensitization, it is advocated to combine the best evidence available with treatment modalities known to target central sensitization
  • 60. References  Woolf CJ. Central sensitization : Implications for the diagnosis and treatment of pain. Pain [Internet]. International Association for the Study of Pain; 2011;152(3):S2–15. Available from: http://dx.doi.org/10.1016/j.pain.2010.09.030  Winkelstein B a. Mechanisms of central sensitization, neuroimmunology & injury biomechanics in persistent pain: implications for musculoskeletal disorders. Journal of electromyography and kinesiology : official journal of the International Society of Electrophysiological Kinesiology [Internet]. 2004 Feb [cited 2014 Feb 24];14(1):87–93. Available from: http://www.ncbi.nlm.nih.gov/pubmed/14759754  Nijs J, Van Houdenhove B, Oostendorp R a B. Recognition of central sensitization in patients with musculoskeletal pain: Application of pain neurophysiology in manual therapy practice. Manual therapy [Internet]. Elsevier Ltd; 2010 Apr [cited 2014 Feb 24];15(2):135–41. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20036180  Nijs J, Wilgen CPV, Oosterwijck JV, Ittersum MV, Meeus M. How to explain central sensitization to patients with “ unexplained ” chronic musculoskeletal pain : Practice guidelines. Manual Therapy [Internet]. Elsevier Ltd; 2011;16(5):413–8. Available from: http://dx.doi.org/10.1016/j.math.2011.04.005  Smart KM, Blake C, Staines A, Doody C. Self-reported pain severity , quality of life , disability , anxiety and depression in patients classified with “ nociceptive ”, “ peripheral neuropathic ” and “ central sensitisation ” pain . The discriminant validity of mechanisms-based classifications of low back ( Æleg ) pain. Manual Therapy [Internet]. Elsevier Ltd; 2012;17(2):119–25. Available from: http://dx.doi.org/10.1016/j.math.2011.10.002  Smart KM, Blake C, Staines A, Thacker M, Doody C. 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