This presentation is a briefing of pain pathway and it's management.

1. Pain pathway and Acute pain
management

2. PAIN(IASP definition)
Pain is defined as an unpleasant sensory and emotional
experience associated with actual or potential tissue
damage or described in terms of such damage.

3. The perception of pain as a symptom
is dependent not only on sensory
inputs but also on the individual’s
cognitive reaction to the pain, their
emotional state, their underlying
disease and their social and cultural
background.
The biopsychosocial
model of pain

4. Stimulus
• Mechanical
• Chemical
• Thermal

5. 2 types of pain
a)Nociceptive pain:Any pain caused primarily by stimulation of the
nociceptor can be said to be nociceptive pain
Visceral Somatic
b)Neuropathic pain:Caused by impulse generation within the pathway
proximal to the nociceptor (this could be in the nerve, the spinal cord
or the brain)
Central
Peripheral

6. PAIN PATHWAY
• Pain is the result of a complex interplay between signalling systems,
modulation from higher centres and the unique perception of the
individual.
• Primary afferent pain fibres-> second-order neurons (dorsal horn of
the spinal cord) Ascending spinothalamic and spinoreticular -> brain,
(pain signals processed by the thalamus and sent to the cortex) .
• Descending tracts, via the midbrain periaquaductal grey and nucleus
raphe magnus, have a role in pain modulation

7. Pain signals
nociceptors
primary afferent neuron
(spinal cord)second-order neuron,
Thalamus
cerebral cortex
.

8. • Cognitive influences derived from the frontal lobe,
coupled with sensory influences from cortex and
emotional influences from the amygdyla, affect pain
perception in the mid-brain around the
periaqueductal gray matter (PAG) and the
rostroventrolateral medulla (RVM) in the medulla

9. Pain receptors-Nociceptors
• Nociceptors are free nerve endings of nerve fibers
• 2 types:
i)High-threshold mechanoreceptors(HTM)
ii)Polymodal nociceptors(PMN)

10. Inflammatory mediators
• activates and sensitize nociceptor.
• 5-HT,Cytokines,bradykinin,histamine,PGs,leucotrienes

11. Primary afferent neuron
• 2 main fibre types:
i)Aδ(finely myeinated) –fast pain(lamina I & V)
ii)C fibers(unmyelinated)-slow pain(lamina II,sustantia
gelatinosa)
• Cell bodies in dorsal root ganglion or trigeminal ganglion.
• Terminate in dorsal horn(lamina I-VI).
• These fibres travel just lateral to myelinated Aβ fibres(vibration &
light touch).

12. Spinal cord
• Primary afferent fibres synapse with second-order neurons.
• Complex interactions occurs between excitatory and inhibitory
interneurons.
• Descending inhibitory tract from higher center acts here.

13. • 3 types of second order neurons
i)Nociceptive specific(NS)-high threshold noxious stimuli;found in
lamina II & III
ii)Wide dynamic range(WDR)-range of sensory stimuli;ffoun in lamina
V & VI
iii)Low-threshold(LR)-Offfensive stimuli

14. Gate-control theory –Melzack and Wall 1965
• Mechanisms that modulate pain signals:
i)Inhibitory control by higher centres close the
ii)activity in Aβ collaterals gate
iii)spinal modulation by variety of mechanisms-endogenous opiods and
cannabinoid systems,inhibitory AAs (GABA,NO,galanin,cholecystokinin)
• Lamina II inhibitory interneurons can be activated directly or indirectly by
stimulation of large sensory afferents from skin(Aβ fibres)which then
suppress transmission in small unmyelinated C fibre afferents and therefore
blocks the pain.

15. Ascending tracts
• Spinothalamic –contains axons of neurones in lamina I &
V;projects medial & lateral nucleus of thalamus
• spinoreticular tract-arises from cells deeper in grey
matter;projects to thalamus & hypothalamus

16. Brain
• Thalamus-key area of processing somatosensory information.
• From thalamus to primary & secondary somatosensory
cortices,insula,anterior cingulate cortex & prefrontal
cortex;perception of pain

17. Descending tracts
• Modulation of pain.
• 5 HT,noradrenaline-neurotransmiter in descending inhibition.
• Periaquaductal grey(PAG) &nucleus raphe magnus(NRM) are areas of
brainstem involved in reducing pain

18. Mechanism in neuropathic pain
• Damage to either peripheral or central nervous system.
• Neuronal plasticity-adaptive process exhibited by nervous system to
pain.
• μ-opioid receptors are down regulated in neuropathic pain and hence
limited opioid resonsiveness

19. Assessment of severity of pain
• Unidimentional
1)Verbal rating scales
2)Binary scale
3)Numerical
4)Faces rating scale
5)Visual analog scale
•Multidimensional
1)Mc Gill pain questionnaire
2)Brief pain inventory
3)West Haven-Yale pain
inventory

20. • VRS-mild,moderate,severe
• Binary scale-yes/no
• NRS-rate pain from 0 to 10
• Face rating scale(Wong-baker)-point to various facial expressions

21. Assessment of nature of pain
• Nociceptive or neuropathic or mixed type
1)Neuropathic pain Questionnaire(NPQ)
2)Douleur neuropathique en 4((DN 4)

22. Challenges in pain assessment in particular
patient population s

23. Acute pain management
• A/C pain-normal,predicted,physiological response to an adverse
chemical,thermal,or mechanical stimulus.
• Elements of pain:
TRANSDUCTION:chemical/thermal/mechanical stimuli-action potential.
TRANSMISSION:AP conduction to NS via 1st,2nd,3rd order neurons
MODULATION:inhiition or augmentation of pain signals.
PERCEPTION:final common pathway as a result of painful input to
somatsensory and limbic cortices

24. Pain management
Evaluation
Medical
psychological
Management
Post-op pain
Chronic pain

25. Medical evaluation:Clinical history
i)The site of pain-gives a possible clue for the source of pain.
ii)The onset of pain- whether abrupt or slow gives a clue about the
severity of pain and possible etiology.
iii)The duration of pain tells whether it is acute or chronic.
iv)Character of pain.(the neuralgic pains- either shooting or stabbing.
Deafferentation pains- burning type. The malignancy pains- dull &
boring type)

26. Psychological evaluation
• The goal is to determine the contribution of affective,cognitive &
behavioral factors to the perception & report of pain.
• Various objective psychological test measures are used to evaluate
pain patients.
• i) Minnesota Multiphasic Personality Inventory (MMPI)
• Ii) Symptom checklist 90
• Iii) Million Behavioral Health Inventory

27. Past history –
• patients with systemic illness like DM, APD, IHD etc need to be
managed differently.
Personal history
• details regarding occupation ( job satisfaction, work compensation
and others.)
• Habits like tobacco chewing, smoking,alcohol etc
• Marital life, children, menstrual history, family disputes

28. Physical examination
• This part of evaluation should be like continuation of clinical history.
• include the general physical examination and systemic examination

29. Non opioid analgesics
1.PARACETAMOL
• Mild- moderate pain
• MOA:weak inhibit of COX 1 &2 enzymes, weak anti-inflammatory
properties
• Activates descending inhibitory spinal pathways(5 HT mechanism)
• Dosage-10-15mg/kg/dose
• Toxic dose:>150mg/kg
• Hepatotoxicity

30. 2) NSAIDS
• Treatment of inflammatory pain & osteoarthritis.
• MOA:inhibition of PG production, by inhibiting COX 1 & 2
• Anti inflammatory, analgesic, antipyretic
Non selective COX inhibitors:Aspirin,Ibuprofen,Naproxen, Ketoprofen,
Flurbiprofen,Mephenamic acid,Piroxicam,Indomethacin
Preferential COX2 inhibitors: Nimesulide, Diclofenac, Aceclofenac
Selective COX-2 inhibitors:Celecoxib, Etoricoxib, Parecoxib
• Nephrotoxicity

31. • Ibuprofen:400mg Orally Q6H
• Diclofenac:oral/rectal/IM route;50mg/100mg tablets available
• Ketorolac:oral(10-20mg Q6H) /IM/IV;

32. Opioids
• Strong opioids-Morphine, Fentanyl
Morphine:
• MOA:Inhibits release of excitatory transmiters
• 5-10 mg Q4H
Fentanyl:
• MOA:Inhibits ascending pathway
• 0.5-1 mcg/kg
• Weak opioids:Codeine, Pethidine, tramadol

33. Adjuvant analgesic
• Adjuvants are drugs with primary indication other than analgesia
Antidepressants:Amitryptylin, Desipramine,
Anticonvulsant analgesics:Gabapentin, Pregabalin, Carbamazepine
Antihistamine:Hyoscine
Corticosteroids:Prednisolone, Dexamethasone
NMDA receptor agonist:Ketamine, Dextromethorphan

34. WHO analgesic ladder

35. Non pharmacological methods of analgesia
1) CBT
2) TENS(transcutaneous electrical nerve stimulation)
3) Hot and cold fomentation

36. Whatever drug or combination of drugs is chosen, the key to
successful pharmacological management is careful assessment
and review, aiming for an acceptable balance between the
benefits of treatment in providing pain relief, maximising function,
and improving quality of life and adverse effects.

37. Reference
• Davidson principles and practice of medicine 23rd edition
• Guyton And Hall Textbook of Medical Physiology
• Surgery journal- anatomy and physiology of pain, Charlotte E
Steeds;Published on January 28,2016
•
• anatomy and physiology of pain
• Charlotte Eanatomy and physiology of pain
• Charlotte E. Steeds

38. Thank you…