pain pathway ,physiology

1. Pathway , physiology ,
perception Of Pain
Pathway , physiology ,
perception Of Pain
Presented by – Dr.Zareesh.S.Akhtar
1 Year M.D.S
In dept of ODMR

2. Contents
 Introduction
 Significance
 History
 Definition
 Characteristics Of Pain
 Classification of pain
 Components Of Pain
 Pain receptors
 Neural pain Pathway
 Sensory Neuron
 Peripheral mechanism
of injury induced pain

3.  Visual Analogue Scale
 Applied Physiology
 Applied Clinical
Aspect
 Conclusion
 Reference
 Pathways of pain
 Theories Of Pain
 Visceral Pain
 Referred Pain
 Tooth Pain

4. Introduction
 Pain is defined as unpleasant and emotional experience
associated with or without actual tissue damage.
 Pain sensation is described in many ways like sharp
,pricking ,electrical dull aching, shooting , cutting
,stabbing , trobbing etc.
 As such pain is typically associated with noxious
stimuli ,events that are potentially or actually damaging
to tissue.

5. Tumor-
swelling
Calor-heat
Dolor-pain
Rubor-
redness
Functio
laesa-loss
of function

6. Significance Of Pain
 Pain gives us warning signal about the problem /Injury.
 Pain prevents further damage by causing reflex
withdrawal of the body from source of the injury.
 Pain urges the person to take proper treatment to prevent
major damage.

7. History
 Derived from Latin Word ‘Poena’- Punishment from God
 Derived from Greek word –’poin’
 Bible –Reference to pain not only in relationship to injury or
illness but also anguish of soul
 Aristotle - considered pain to be the ‘passion of the soul’
 Plato –contented pain and pleasure arose from within the body

8. Definition
“An unpleasant sensory and emotional experience associated
with actual or potential tissue damage or described in term of
such damage”
-IASP
“ An unpleasant emotional experience usually initiated by a
noxious stimulus and transmitted over a specialized neural
network to the central nervous system where it is interpreted as
such ”
-Monheim.

9. Characteristics Of Pain
1.Threshold and Intensity
- If the intensity of the stimuli is below the threshold (Sub-
Threshold) Pain is not felt.
- As the intensity increases more and more ,pan is felt more and
more according to Webers-frecher’s Law
(This law ensures that while our body can perceive pain due to
low intensity stimulus ,a severe crushing injury will not cause
death due to pain sensation ,yet as stimulus increases ,sense of
perception also increases .)

10. 2.Adaptation
- Pain receptors show no adaption and so the pain continues as long
a receptors continue to be stimulated.
3.Localization of Pain
- Pain sensation is somewhat poorly localized .However superficial
pain is comparatively better localized than deep pain.
4.Influence of the rate of damage on intensity of pain
- If the rate of tissue injury is high ,intensity of pain is also high

11. Classification Of Pain
Basis Type of Pain
Duration Acute
Chronic
Mechanism Nociceptive(physiological)
Neuropathic(pathological)

12.  Acute Pain
 Pain that is caused by noxious stimulation due to
injury ,a disease process , or the abnormal function of
muscle or viscera
 Two types of
1- acute [nociceptive]pain
2- somatic and visceral

13. [somasthetic] [From viscera]
Superficial [from skin and
subcutaneous tissue]
eg.superficial cuts/burns etc.
Deep [from muscle
/bone/fascia/periosteum ]
eg.fracture
/arthritis/fibrositis,rupture of
muscle belly.

14.  Chronic Pain
 Pain that extend 3to 6 month beyond onset beyond the
expected period of healing
 It may be nociceptive ,inflammatory ,neuropathic or
functional in origin
 A distinguishing feature is that psychological
mechanisms or environmental factors frequently play a
major role.

15. Neuropathic Pain
Definition –Pain that is caused by a lesion or disease of the somatosensory
system [PNS or CNS]
Pain is not well localized , pathologic pain
Peripheral Nerves
-Traumatic brachial plexus injury
-Diabetes mellitus
-Carpel tunnel syndrome
-Post herpetic neuralgia
Central Nervous System
-Central post stroke pain
-Neuropathic association with spinal cord injury

16. Nociceptor
 Nociceptor are free nerve endings that sense heat
,mechanical and chemical tissue damage
 Nociceptive pain is well localized
 Sharp
 There is obvious tissue injury or illness ant site
 Inflamation present
 Its an physiological pain

17. Orofacial Pain classification ( OKESON )
Axis 1 (physical conditions)
1 Somatic Pain
A.Superficial Somatic Pain
a.Cutaneous pain
b.Mucogingival
B.Deep Somatic Pain
a.Muscle pain
b.TMJ pain
c.Osseous pain
d.Periodontal pain
2 Visceral pain
a.Pulpal pain
b.Vascularpain
c. Neurovascular pain
d.Visceral mucosal pain
e.Glandular ocular auricular pain
 Axis 2 (psychologic condition)
1.mood disorder
2. Anxiety disorder
3.Somatoform disorder
4.Other Condition – psychologic
factor affecting a medical condition

22. Components Of Pain
FIBRE TYPE FUNCTION CONDUCTION
VELOCITY
(mts/sec)
SPIKE
DURATION
(mili sec)
Aα (Myelinated fibers) Proprioception ,somatic motor 30-120 0.4-0.5
Aβ (Myelinated fibers) Touch ,pressure and motor
function
30-120
Aγ (Myelinated fibers) Motor to muscle spindle 15-35
Aδ (Myelinated fibers) Pain ,temperature , touch 5-25
B (Myelinated fibers) Preganglionic autonomic fibers 3-15 1.2
C(Unmyelinated
fibers)
Pain ,temperature , touch and
conducts impulses generated by
cutaneous receptor
0.7-1.3 2

23.  Gilron, Ian. (2000). Neural Blockade in the Evaluation and Management of Chronic Pain: An Overview. Pain Research and Management. 5. 93-100. 10.1155/2000/546792.

24. FAST PAIN
 Felt witin 0.1 sec
 Sharp
,priciking,acute,electric
pain
 When needle is struck
into the skin /electric
shock /cuts
 Not felt in most deeper
tissue of the body
 Transmitted through A
pain Fibers
SLOW PAIN
 Felt after a sec or more
/maybe minute
 Burning ,aching
,Throbbing ,Chronic Pain
 Associated with tissue
destruction
 Can occur in skin and in
any deep tissue or organ
 Result from primitive
Type C pain Fibers

25. SENSORY
COMPONE
NT
Sensory
receptor
Afferent
neuron
Ascending
Track
Somatosen
sory
Cortex
Motor
Component
Efferent
Neuron
Descending
Track

26. Pain Receptors
Sensory Receptor
 At the distal terminals are the afferent [sensory] nerve specialized
sensory receptor that respond to physical or chemical stimuli
 Once these receptor are adequately stimulated ,an impulse is generated
in the primary afferent neuron that is carried centrally into the CNS
 Classified in 3 Group
1. Exteroreceptors
2. Proprioceptors
3. Interorecepters

27. EXTERORECEPTORS
 Stimulated by immediate external environment
 Provide information from the skin and mucosa
 Eg-
1. Merkel’s corpuscles [tactile receptors in the submucosa of tongue]
2. Meissner’s corpuscles tactile receptors in skin
3. Free nerve ending perceive superficial pain and touch

28. PROPRIOCEPTORS
 Provide information from the musculoskeletal structure concerning the
position and movement of the body
 Automatic Functioning
 Eg-
 Muscle spindle mechanoreceptors found between skeletal muscle fibers
 Golgi tendon organ mechanoreceptors in the tendon of muscles signal
muscle tension
 Periodontal mechanoreceptors respond to biomechanical stimuli.

29. INTEROCEPTORS
 Located in and transmit impulse from viscera of the body
 Eg-
 Pacinian Corpuscles concerned with perception of pressure
 Free nerve ending perceive visceral pain and other sensation

30. Neural Pain Pathway
 Sensory input from various stimuli [either external or
internal ] is received by specific peripheral receptor
called as nociceptors
 Nocicepters respond as transducers and transmit
impulse
 Perception of pain
 Found in all parts of body

31.  External Nociceptors- skin ,cornea and mucosa
 Internal Nociceptors-Muscles ,joint ,bladder,gut and
continuing along GIT
 Cell bodies of these neuron are located in either the
dorsal root ganglia or the trigeminal ganglia
 Trigeminal Ganglia are specialized nerves for the
face ,whereas the dorsal root ganglia associate with
the rest of the body.

32. Sensory Neuron
FIRST ORDER NEURON
[POSTERIOR NERVE ROOT GANGLIA]
SECOND ORDER NEURON
[SUBSTANTIA GELATINOSA]
THIRD ORDER NEURON
[THALAMIC NUCLEUS,
RETICULAR FORMATION ,
TECTUM ,GREY MATTER,SOMATOSENSORY]

33. First Order Neuron
 Each sensory receptor is attached to a first
order primary afferent neuron that carries the
impulse to the CNS
 The axon of these first order neuron are found
to have varying thickness
 Larger fibers conduct impulse more rapidly than
smaller fibers

34. Second Order Neuron
 The primary afferent neuron carries impulse into the CNS
and synapse with the second order neuron
 This second order neuron is sometimes called transmission
neuron since it transfers the impulse on to the higher centers.
 The synapse of the primary afferent and the second order
neuron occurs in the dorsal horn of the spinal cord

35. Third Order Neuron
 Cell Bodies of third order neuron of the nociception
relaying pathway are housed in the ventro- posterior
lateral ,the ventro –posterior inferior and intralaminar
thalamic nuclei
 Third order neuron fibers from the thalamus relay
thermal sensory information to the somesthetic cortex.

36. Peripheral mechanism of injury induced
pain[NEUROPHYSIOLOGY OF PAIN ]
TRANSDUCTON
TRANSMISSION
PERCEPTION
MODULATION

37. TRANSDUCTION
1-Activation of nociceptor
 Intense thermal and mechanical stimuli ,noxious chemicals ,
noxious cold
2-Stimulation of inflammatory mediators
 Damaged tissue release bradykinin ,potassium, histamine ,serotonin
and arachidonic acid
 Arachidonic acid produce prostaglandins and leukotrienes.

38. Bradykinin +Leukotriene +Prostaglandins [PG stimulates nociceptors directly]
Increases plasma extravasation
Edema
Leukotriene stimulates nociceptors indirectly by PMNs
Release Chemical mediators
Stimulates nociceptor

39.  BK causes sympathetic nerves terminal to release PG thus
stimulates nociceptor.
 Sympathetic nerve terminal release another PG in response to its
own Neurotransmitter norepinephrine
 Such ongoing inflammatory state cause physiologic sensitization
of nociceptors thus generating a response even to a non –painful
stimuli and exaggerated response to noxious stimuli

40. TRANSMISSION
 Process by which peripheral nociceptive information is relayed to CNS
 First order neuron synapses with the secondary order neuron from where
impulse is csrried to higher center of brain
 Repeated or intense C fibers activation brings specific changes on N-
methyl-d aspartate receptors resulting in central sensitization ,thus ,response
of second order neuron increases as well as size of the receptive field also
increases.

41. PERCEPTION
 It is the subjective experience of pain
 It is the sum of complex activities in CNS that may shape the character
and intensity of pain perceived and ascribe meaning to pain.

42. MODULATION
 It is the mechanism by which transmission of impulse to brain is
reduced
a) Descending inhibitory system that originates supraspinally
b) Periaqueductal gray
c) Anucleus raphe magnus
d) Nucleus tractus solitarius
e) Locus ceruleus /subceruleus
f) Endogenous opioid peptide

43. Pain Pathway
Pain
[Receptor]
Free nerve ending
Posterior nerve root Ganglion [First order neuron ]
Fibers from lateral spinothalamic tract [Second order neuron ]
Ventral posterolateral nucleus of thalamus ,reticular formation and midbrain [Third
order neuron]
Sensory Cortex [Center]

44. Theories Of Pain
1. Convergence theory
2. Facilitation Theory
3. Gate Control Theory

45. Convergence theory
 Both somatic and visceral afferent fibers converge upon second order
neuron
 Somatic fibers conduct impulses more frequent.
 Visceral pain felt as somatic pain because brain is familiar with somatic
regions.

46. Facilitation Theory
 Visceral and somatic fibers join at adjoining spinothalamic
neuron i.e second order neuron
 Activation of spinothalamic neuron occurs due to strong
impulses resulting in impulses passing through spinothalamic
pathway
 This results in misinterpretation in location of pain

47. Gate Control Theory
 Proposed by Ronald Melzack and Pat-rick wall
 The pain stimuli transmitted by afferent fibers are blocked by Gate
mechanism located in posterior gray horn of spinal cord .If gate is
OPENED ,pain is felt .If gate is CLOSED pain is suppressed.
 Due to this ,there is relief of pain through rubbing ,massaging or
application of ice pack ,acupuncture and electrical analgesia.

48. 1. When pain stimulus is applied on any part of body ,beside pain
receptor,then the receptors of other sensation are also stimulated
2. When all these impulses reach the spinal cord through posterior
nerve root,then the fibers of touch sensation send collaterals t
the neuron of pain pathway
3. Impulses of touch sensation to passing to these collaterals
inhibit the release of glutamate and substance –P from pain
fibers
4. This closes the gate and pain sensation get blocked.

49. Visceral Pain
 They are dull and diffuse ,poorly
localized and associated with
symptoms like nausea and reffered to
other area
 Stimuli for visceral pain –Ischemia
,Obstruction ,Spasm ,Chemical
Stimuli.

50. Referred Pain
 Pain felt in a part of the body
other than its actual source
 Pain at diaphragm felt at tip and
over shoulder
 Pain in maxillary sinus felt at
nearby teeth
 A tooth abscess can cause jaw
bone pain.

51. Tooth Pulp Pain

52. 1 -Exposure of dentinal tubules causes toothache and other
non noxious sensation.
2 -Both Aδ And C fibers response to stimuli in dentine
3 -Transmission of stimuli across dentine ,mediated by
movement of fluid in dentinal tubules.

53. 4 -Fibers terminate at medullary dorsal horn and synapse and
also at trigeminal sensory nucleus
5 -From Trigeminal nucleus send to thalamus and then to
sensory cortex
6 -Pulpal innervation are capable of regenerating and
reinnervating

54. Determinants of painful experience during
dental treatment
 Pain occurs due to invasive procedures like extraction and
surgeries or non invasive procedures .With regards to children
,studies have shown that dentists do not believe in pain referred by
child and tend not to use available method to control pain
 Anxiety is determinant for pain during dental care and pain is
related to LA procedures .There are evidence that dentist attitude
are determinants for pain.

55. Visual Analogue Scale

56. Applied Physiology

57. The sensory functions are affected by lesion in
sensory pathway or other nervous disorders
 Anesthesia – loss of sensation .
 Hyperesthesia –increase sensitivity to sensory
stimuli.
 Hypoesthesia –decrease sensitivity to sensory
stimuli.
 Hemiesthesia - loss of sensation to one part of body.
 Paresthesia – abnormal sensation.

58.  Dissociated anesthesia- loss of some sensation with
loss of consciousness produced by anesthetic agents
 General Anesthesia –loss of all sensation with loss
of consciousness produced by anesthetic agents
 Local anesthesia –loss of sensation in restricted
area of body
 Tactile Anesthesia – loss of tactile sensation

59.  Hyperalgesia –increase in sensitivity to pain
 Paralgesia – abnormal pain sensation
 Thermic anesthesia –loss of thermal sensation
 Analgesia – loss of pain sensation .

60. Applied Clinical
Aspect
Applied Clinical
Aspect

61. HERPES ZOSTER
 Herpes zoster is a viral infection affecting dorsal root
ganglion .Results in severe pain towards the ganglion.
 Pain can be mild to extreme in the affected dermatome ,with
sensation that are often described as stinging ,tingling
,aching , numbing or throbbing.
 Symptoms-
1. Burning pain
2. Itching
3. Hyperesthesia
4. Paresthesia
Bader MS. Herpes zoster: diagnostic, therapeutic, and preventive approaches. Postgrad Med. 2013 Sep;125(5):78-91. doi: 10.3810/pgm.2013.09.2703. PMID:
24113666.

62. Treatment
 Analgesics
-Mild to moderate –Topical Lotion containg CALAMINE
-Severe Pain –Opiod medication such as morphine
-Once the lesion have crusted over,Capsaicin cream can be used
-Topical Lidocaine and Nerve Block may also reduce pain
-Administrating Gabapentine along with Antiviral May offer Relif of post
Herpetic Neuralgia (PHN)

63.  Antiviral
-These drug reduce the severity and duration but do not prevent
Post herpetic Neuralgia
-Acylovir Has been Standard Treatment ,Can be replaced by new
drug Valaciclovir and Famciclovir.

64. TRIGEMINAL NEURALGIA
• Trigeminal Neuralgia is a Chronic Pain disorder that affects
the 5th C.N
• Trigeminal neuralgia (TN) is characterised by unilateral,
intense, touch-evoked, stabbing paroxysmal pain. It
typically affects the second and third trigeminal branch.
• Trigeminal neuralgia can be either idiopathic or secondary
to multiple sclerosis or a space-occupying lesion.
• Types
• -Typical
• -Atypical
Maarbjerg S, Di Stefano G, Bendtsen L, Cruccu G. Trigeminal neuralgia - diagnosis and treatment. Cephalalgia. 2017 Jun;37(7):648-657. doi: 10.1177/0333102416687280. Epub 2017
Jan 11. PMID: 28076964.

65. Treatment
 Anticonvulsant carbamazepine is first line drug
 Baclofen ,lamotrigine,oxcarbazepine ,phenytoin,
gabapentin and pregabalin is second line of drug
 Antidepressant medication such as Amitriptyline
have shown good efficacy ,especially with
pregabalin

66.  Non destructive Surgery
Microvascular decompression this involves a small incision behind the ear and
some bone is removed from that area and incision through meninges are made to
expose the nerve .Any vascular compressions of the nerve are carefully moved and
a sponge –like pad placed between the compression and the nerve

67.  Destructive Surgery
• Glycerol Injection deposition of glycerol at this point
cause damage to the nerve to hinder pain signals
• Radiofrequency –application of a heated needle to
damage the nerve
• Sterotactic Radiosurgery [Gamma knife surgery] – is a
form of radiation therapy that focuses high power
energy on a small area of body

68. Conclusion
 Pain can induce physiological and anatomical changes
within the nervous system .The complexity of pain
transmission means there are many pharmologica targets
and multimodel theraphy is required to optimize pain
control.

69. References
Article
 Maarbjerg S, Di Stefano G, Bendtsen L, Cruccu G. Trigeminal neuralgia - diagnosis and treatment.
Cephalalgia. 2017 Jun;37(7):648-657. doi: 10.1177/0333102416687280. Epub 2017 Jan 11. PMID:
28076964.
 Bader MS. Herpes zoster: diagnostic, therapeutic, and preventive approaches. Postgrad Med. 2013
Sep;125(5):78-91. doi: 10.3810/pgm.2013.09.2703. PMID: 24113666.
 Costa, Ruth & Ribeiro, Suelen & Cabral, Etenildo. (2012). Determinants of painful experience during
dental treatment. Revista Dor. 13. 365-370. 10.1590/S1806-00132012000400011.
 Ryan Moffat, Colin P. Rae,Anatomy, physiology and pharmacology of pain, Anaesthesia & Intensive Care
Medicine,Volume 12, Issue 1,2011,Pages 12-15,ISSN 1472-0299
 Case report study on Brown Sequard syndrome –Ponachi et al Neurology Asia 2007;12;65-67.
 Gilron, Ian. (2000). Neural Blockade in the Evaluation and Management of Chronic Pain: An Overview.
Pain Research and Management. 5. 93-100. 10.1155/2000/546792.
 Consice MEDICAL PHYSIOLOGY –Chaudhuri
 Monheim’s Local Anesthesia and pain control in dental practice
 Essential Of medical physiology –K.Sembulingam and Prema Sembulingam.

70. THANK YOU