This document discusses central sensitization (CS), including its recognition and implications for physiotherapy. It defines CS and reviews evidence that CS can be assessed using questionnaires, quantitative sensory testing, and factors like temporal summation. Management of CS may include education, cognitive approaches, TENS, exercise and medications targeting central pain processing. The document provides tips for physiotherapists in managing patients with CS, such as using appropriate pressures and treatment windows, addressing pain behaviors and beliefs, and taking a multidisciplinary approach.

1. A.THANGAMANI RAMALINGAM

2. OBJECTIVES

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

6. Nociceptive processing

9. Pain sensitization
 Primary hyperalgesia or peripheral pain sensitization
pain
 Secondary hyperalgesia or central sensitization
Unimodal/polymodal
nociceptors

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

14. Reductionist
Rationalist

15. Neuro immunology

16. Neuro immunological response

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,

18. NMDA Vs

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

22. Recognition of Central
sensitization

23. Screening
Using medical diagnosis
History taking
Clinical examination
Analyzing the treatment
responses

24. Using medical diagnosis
History taking

25. Clinical examination

26. 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

28. Physiotherapy

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

33. Measurement of secondary
hyperalgesia

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

37. Management

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

45. Evidences

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

54. Message/tips for therapist

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
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