pain pathway

1. Pain pathway
Presented by
SAMITH MOHANAN

2. CONTENTS
•Introduction
•Characteristics of pain
•Types of pain sensation
•Gate control Hypothesis
•Difference b/w sometic & visceral sensory function
•Visceral pain & referred pain
•Receptors & Sensations

3. •Pathway of sensory impulses
•Tooth pulp pain
•Applied physiology
•Management
•Conclusion
•References

4. INTRODUCTION
Unpleasant sensory & emotional experience associated with actual or
potential tissue damage.
Its imp: , symptoms of many diseases & when pt experiences pain
he/she consults a physician.

5. Characteristics
• specific with specific receptors & afferent fibers.
•Less adaptation & continues as long as pain causing agent persists.
•Chronic pain- psychological effects.
•Tolerance level varies from individuals.
•Cerebral cortex – localization, discrimination & interpretation.

6. Types of pain sensation
1) Fast pain- short & sharp
conducted by Aδ fibers
localization of pain is better
2) Slow pain- more prolonged & severe
conducted by C fibers
dull, diffused & localization is poor
3) Deep pain- contraction of skeletal muscles
when pain is severe, causes sweating, nausea &
vomiting, fall in B.P

7. Aδ – fast, sensitive to mechanical noxious stimuli.
small, myelinated. High conductance speed
C – slow, sensitive to many noxious stimuli (chemical,
etc.) – small, unmyelinated. Slow conductance speed

8. Receptors
They are specialized afferent nerve endings designed to respond
appropriate & adequate stimulus.
Function
Converts various forms of energy into action potential in nerve fibers
Act as transducers
Situated at various parts of body- skin, eye, ear, nose, muscle etc

9. Properties
Excitability – specificity
receptive response
Adaptation
Effect of extend of stimulus
Localization & projection
Effect of strength of stimulus
Quality or modality of sensation
Intensity of sensation
Fatigue

10. Classification
•Exteroreceptors- responds to change in external enviornment
a) cutaneous receptors- touch, pain, temp:
b) chemical receptors- taste & smell
c) teleceptors- vision & hearing

11. •Interoceptors – exited by stimuli within the body
a) Stretch receptors- alvoeli of lungs
b) Chemoreceptors- aortic & carotid bodies
c) baroreceptors- carotid sinus & aortic arch
d) Osmoreceptors- hypothalamus
e) Volumereceptors- right atrium
f) Proprioreceptors- muscle spindle, tendon
g) Visceroreceptors- present in visera

12. Nociceptors
are special receptors that respond only to noxious stimuli
and generate nerve impulses which the brain interprets as
“pain”.

13. 1. Prevents serious damage.
2. Teaches one what to avoid
3. If pain is in joints, pain limits the activity, so no
permanent damage can occur.
but pain can become the problem, and cause people to
want to die.
Purpose of pain

14. Differences btw Somatic & Visceral sensory function.
Somatic :- seen on skin & subcutaneous tissues
subserve sensory function of touch, temp,sensation,
pressure & pain
Visceral:- have no proprioreceptors & sparesly distributed
subserve osmorecptors, barorecptors

15. PAIN STIMULI
3 types- thermal, mechanical & chemical.
Nociceptive stimuli- stimuli which threatens the welfare of tissues &
causes pain.
Chemical substances that can induce pain
intrinsic- bradykinin, histamine, prostaglandins
extrinsic- irritant acid, alkali, plant & animal stings & venoms

16. 1. gray matter
2. white matter
3. gray commissure
4. central canal
Dorsal and ventral nerve
roots
Internal Anatomy

17. Tracts of the Spinal Cord

18. Cross section of spinal cord , showing
ascending tracts & descending tracts

19. Three major pathways carry sensory information
Posterior column pathway (gracile & cuneate fasciculi)
Anterolateral pathway (spinothalamic)
Spinocerebellar pathway

20. THREE neurons from the
receptor to the cerebral
cortex
First order neuron:
Cell body located in the
dorsal root ganglion. The
Axon passes to the spinal
cord through the dorsal root
of spinal nerve, runs
ipsilaterally and synapses
with second-order neurons
in the cord and medulla
oblongata

21. Second order neuron:
Has cell body in the
spinal cord or medulla
oblongata &
Terminate on 3rd order
neuron
Third order neuron:
Has cell body in
thalamus
Axon terminates on
cerebral cortex
ipsilaterally

23. PAIN IMPULSE PATHWAY

24. PAIN IMPULSE PATHWAY
Ventral
spinocerebellar
Dorsal
spinocerebellar
(1st order neuron)
(2nd order neuron)
(3rd order neuron)
Lateral corticospinal

25. Pain
Free nerve
ending
Posterior nerve
root ganglion
Fibers from lateral
spinothalamic tract
Ventral posterolateral nucleus of thalamus,
reticular formation & midbrain.
Sensory cortex
Receptor
First order neuron
Second order neuron
Third order neuron
center

26. Tissue ischemia
Blood flow is blocked for few min- pain
Results in anaerobic metabolism & release of bradykinin &
proteolytic enzymes- cell damage

27. Muscle spasm
Indirect effect muscle spasm to compress the blood vessels & cause
ischemia
Results – release of chemicals and increase in metabolism in muscle
tissue.

28. Visceral pain
They are dull & diffuse, poorly localized, and associated with
symptoms like nausea & referred to other areas
Stimuli for visceral pain
ischemia, obstruction, spasm, chemical stimuli.

29. REFERRED PAIN FROM VISCERAL ORGANS
Referred pain
Pain felt in a part of the body that is
fairly remote from tissue causing pain.
Pain at diaphragm is felt over tip of
shoulder
Pain at maxillary sinus felt at nearby
teeth.
A tooth abscess can cause jaw bone
pain.

30. Convergence theory
 both somatic & visceral
afferent fibers converge upon 2nd
order neuron
Somatic fibers conduct
impulses more frequent.
Visceral pain is felt as somatic
pain because brain is familiar
with somatic regions.

31. Facilitation theory
Visceral & somatic fiber join at adjoining spinothalamic neurons( 2nd
order neurons)
When strong impulses conduct, activation of spinothalamic neurons,
resulting in impulses passing through spinothalamic pathway
This results in misinterpretation in location of pain.

32. Melzack & Waller- 1965
Pain impulses in spinal cord can
be modified by other afferent
impulses entering the spinal cord
with posterior horn acting as gate
Gate control hypothesis/ gate theory of pain

33. Gate open Gate closed
Physiological Aδ and C fibers
active, Overuse,
Fatigue , improper
mechanics, tired
Aδ or Aα active,
Relaxation, exercise,
strengthening/
conditioning
Medical Extent of
injury/pathological
condition
Medication,
cooling/heating
Congenitive Focusing on pain,
anxiety , fear,
depression, stress
Distraction,
relaxation,
happiness, positive
attitude

34. Tooth pulp pain
1) Exposure of dentinal tubules elicit
toothache & other non noxious
sensation.
2) Both Aδ & C fibers respond to
stimuli in dentine
3) Transmission of stimuli across
dentin, mediated by movement of
fluid through odontoblast tubules.

35. 4) Fibers terminate at medullary dorsal horn & synapse and also at
trigeminal sensory nucleus
5) From trigeminal nucleus send inf: thalamus & sensory cortex
6) Pulpal innervation are capable of regenerating & reinnervating

36. Determinants of painful experience during dental treatment
Pain occurs due to invasive procedures like extractions & surgeries or
non invasive procedures. With regard to children, studies have shown
that dentists do not believe in pain referred by children & tend not to
use available methods to control pain.
Conclusion: anxiety is determinant for pain during dental care & pain
is related to local anesthetic procedures. There are evidences that
dentists attitude are determinants for pain.
Ruth et al Rev.dor; 2012; 13(4)

37. Pain assessment visual analogue scale

39. The sensory functions are affected by lesions in sensory pathways or
other nervous disorders.
1) Anesthesia – loss of sensation
2) Hyperesthesia- increase sensitivity to sensory stimuli
3) Hypoesthesia- decrease sensitivity to sensory stimuli
4) Hemiesthesia – loss of sensation to one part of body
5) Paresthesia- abnormal sensation

40. 6) Dissociated anesthesia- loss of some sensation with loss of
consciousness produced by anesthetic agents
7) General anesthesia- loss of all sensation with loss of conciousness
produced by anesthetic agents
8) Local anesthesia- loss of sensation restricted area of body
9) Tactile anesthesia- loss of tactile sensation

41. 10) Hyperaglasia-increase in sensitivity to pain
11) Paraglesia- abnormal pain sensation
12) Thermic anesthesia- loss of thermal sensation
13) Pallanesthesia- loss of sensation of vibration
14) Analgesia- loss of pain sensation

42. Herpes zoster- viral infection affecting dorsal root ganglion. Results
in severe pain which facilitates the pain towards the ganglion.

43. Tic Doulourex
Pain felt at one side of the face
Felt like sudden electric shock, may last for secs or may be continous
Corrected by surgery at hypersensitive area

44. Brown-Sequard syndrome
All sensations are blocked at one side
Sensations like pain, heat & cold,
vibrations are blocked

45. In a study by Pornachi et al- A case reported on a 63yr old woman with
Brown-Sequard Syndrome due to spontaneous C5-C6 cervical disc
herniation. Anterior discectomy was performed with favorable
outcome.
Neurology Asia .2007;12;65-67

46. Management
NSAIDs – paracetamol, capsacin
L.A- reduces pain
Opoids-
Anticonvulsants- interferes with Na & Ca channel function

47. Conclusion
Pain can induce physiological & anatomical changes within the
nervous system. The complexity of pain transmission means there
are many pharmological targets & multimodel therapy is required to
optimize pain control.

48. References
Essential of oral physiology- Robert M Bradley
Textbook of medical physiology- Guyton & Hall
Essential of medical physiology- K.Sembulingam & Prema
Sembulingam
Textbook of human physiology- S Chand
Articles
•Determinants of painful experience during dental treatment- Ruth
Suzanne et al Rev.Dor 2012;13(4)
•Case report study on Brown sequard syndrome- Ponachi et al
Neurology Asia 2007;12;65-67
•Anatomy, physiology & pharmacology of pain- Ryan Moffat, Colin
P.Rae anesthesia & intensive care medicine; 2010;12(1)