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PAIN PATHWAY
Presented By
Dr.PAYAL DASH
1st year P.G. TRAINEE
DEPT. OF PUBLIC HEALTH DENTISTRY
1
CONTENTS
• Introduction
• Background
• Pain physiology
• Dual Pain Pathway
• Classification/Types of pain
• Theories of pain
• Assessment of pain
• Sequalae of pain
2
• Applied Aspect
• Management of pain
• Conclusion
• References
3
INTRODUCTION
What is Pain?
4
• According to Task Force on Taxonomy of the
International Association for the Study of Pain (IASP)
pain is “An unpleasant sensory and emotional experience
associated with actual or potential tissue damage ,or
described in terms of such damage.”
• Sherrington defined pain as “psychical adjunct of an
imperative protective reflex” i.e. pain is a sensation which
draws attention of the individual as a whole.
5
• Nociceptors: Receptors sensitive to painful stimulus
responsible for initiating the generation of pain
• Nociception: defined as noxious stimulus
• Allodynia: pain that is produced by a stimulus not
normally painful
• Hyperalgesia:increased sensitivity to painful stimuli
• Hypothesia: reduced sensation in response to stimulus
• Anesthesia:absence of sensation in response to a
stimulus
6
• Causalgia: persistent burning pain caused by
deaffertation of sensory innervation
• Neuralgia: pain experienced in the tissues along the
distribution of the nerve
7
Pain Receptors,stimuli and chemical mediators of
pain
• Nociceptors -A delta myelinated nerve fibres
• C unmyelinated nerve fibres
Types of nociceptors-
Somatic nociceptors
Visceral nociceptors
8
• Pain stimuli
Activated by 3 stimuli: Mechanical
Thermal
Chemical
Chemical mediators of pain include:
k+, ATP, ADP released following cell death
Bradykinin -dying cells
Leukotrienes-mast cells
Serotonin-platelets 9
• Histamine-mast cells
• Substance P and calcitonin gene-related peptide
• QUALITATIVE TYPES OF PAIN-
Fast pain -A delta fibres
0.1ms
Slow pain-C fibres
1sec
10
BACKGROUND
11
• STRUCTURE & FUNCTION
A.Nerve cell body/Soma
Principal costitutents are similar to a
cell.Cytoplasm reveals
1.Nissl Granules/Bodies- Basophilic
granules
-parallely arranged ,membrane bounded
cisternae/cavitites
-covered by particles of ribose
nucleoproteins
12
2.Neurofibrillae- Fine
Threads 6-10nm in diameter
-traverse the cytoplasmic matrix
forming loose framework of fibrils in
the cytoplasm
Function
-maintains the functional and
anatomical integrity of the axon
-Neurotrophins transported down the
axon -Anterograde transport ( upto
400mm/day).
-Retrograde transport
(200mm/day)from the nerve endings
to the cell body.
13
B.Dendrites
-5-7processes extending out from the
cell body and extend extensively after
they leave the cell
-contain Nissl Granules,mitochondria
and neurofibrillae
-receptive processes of the neuron
Function
-transmit the impulses towards the cell
body
-non conducted local potential
changes generated by synaptic
connections are integrated.
14
C.Axon
-originates from Axon hillock, in which
there are no Nissl Granules.
-cytoplasmic fluid known as Axoplasm
-cell membrane enveloping the
cytoplasm -Axolemma
Function-
Initial segment of axon -a site where
propagated action potentials are
generated
-An axonal process-transmits propagated
impulses away from the cell body to the
nerve endings.(All or none transmission)
15
-Myelin sheath
protein lipid complex envelopes the
axon except at its endings and at
periodic constrictions about 1mm
apart called Nodes of Ranvier.
Functions-
1.Prevents cross stimulation of
adjacent axons because of its high
insulating property it confines the
nerve impulse to individual fibers.
2.Facilitates conduction of nerve
impulse
16
Types of axons:-
Afferent : nerve fibres which
carry impulses to CNS
Efferent : nerve fibres which
convey impulses from CNS to
periphery
D.Synaptic knobs(Terminal
buttons)
-Axons divides into terminal branches
each ending in number of synaptic
knobs
-contain granules or vesicles in which
synaptic transmitter secreted by the
nerve is stored.
Function-
Nerve endings where action potentials
cause the release of synaptic
transmitter
17
18
Neurotransmitters
Acetylcholine
Monoamines
Catecholamines
(Noradrenaline,
Adrenaline,Dopamine)
Serotonin,Histamine
Amino acids
GABA,Glutamate,
Aspartate,Glycine
Nitric oxide
Neuropeptides
Substance P
VIP
Myelinated Nerves Unmyelinated Nerves
1.Schwann cell membrane is coiled
many times round the axon forming
the multiple layers of membrane
that make up the myelin.
2.Example
All preganglionic fibers of ANS
3.Conduction of nerve impulse is
faster (50-100 times) because of
Saltatory Conduction i.e. leaping of
impulse from node to node over
inter segmental region.
1.Axons are simply surrounded in the
Schwann cell without wrapping of
myelin.
2.Example-
All post ganglionic fibres of ANS
3.Conduction is slower because it isa
continuous process.
19
• NEUROGLIA(Glial cells)
1.Microglia-phagocytic cells that enter
the CNS from meninges and blood
vessels.
2.Astrocytes-
Foundthroughout the brain joining to
blood vessels and investing synaptic
structures,neuronal bodies and
neuronal processes.
20
MACROGLIA MICROGLIA
MICROGLIA
Functions- Transport mechanisms
inflammtory and reparative reactions
maintain optimal concentration of ions and
neurotransmitters (glutamine) in brain
neurons.
3.Oligodendroglia
Cells that form myelin around axon within
CNS
21
ASTROCYTE
PHYSIOLOGY OF PAIN
22
PAIN PHYSIOLOGY
• The main electrical properties of the nerve fibres are
-Excitability , i.e. the capability of generating electrical
impulses (action potential).
-Conductivity , i.e. the ability of propagating the electrical
impulses generated along the entire length of nerve fibres.
23
• Resting membrane potential
• potential difference across cell
membrane at rest
• Value- -70mV
24
• Action potential
• Defined as the brief sequence of changes
which occur in the resting membrane
potential when stimulated by a threshold
stimulus.
• Phases:-
1.Depolarization phase
When the nerve is stimulated,polarized state
(-70mv) is altered ,i.e. the RMP is abolished
and the interior of the nerve becomes positive
(+35mV)
2.Repolarization phase
Within no time reverse occurs to the nearly
original potential known as repolarization
phase.
25
• Action Potential Curve
1.Resting membrane potential
2.Stimulus artefact
3.Latent period
4.Firing level
5.Overshoot
6.Spike potential
7.After depolarisation
8.After hyperpolarisation
26
• Characteristics of nerve
excitability
1.Strength-Duration Curve
Rheobase - minimum intensity of
stimulus
Chronaxie- minimum duration for
which double the rheobase intensity
must be applied to produce a
response.
27
• 2.All or none response
• When stimulus of subthreshold
intensity is applied no action
potential is observed.
• Threshold intensity-Spike of
action potential
• Suprathreshold intensity-no
increase in magnitude of action
potential
28
3.Accomodation
When the stimulus strength is increased slowly to the firing level (during
constant application ),no action potential is produced.
Due to slow opening of Na+ channels and delayed closing of K+ channels.
4.Infatiguability
A nerve fibre cant be fatigued even if it is stimulated for a long time.This is due
to that during action potential neither a fresh impulse can be generated nor
conducted through the fibre.
29
• Inhibition of excitability
1.High extracellular calcium concentration- A high extracellular Ca2+
concentration decreases membrane permeability to Na+ ions
2.Local anaesthetics- Procaine ,Tetracaine , lidocaine block Na+ channels
30
• CONDUCTIVITY
Refers to the propagation of nerve impulse in the form of a wave of
depolarization through the nerve fibre.
31
• Propagation of action
potential in myelinated
axon
-Saltatory conduction
32
• Classification of nerve fibres
Letter classification of Erlanger and Gasser
33
FIBRE TYPE MYELINATED
/NON-
MYELINATED
CONDUCTION
VELOCITY(M/S
)
A α Myelinated 70-120
βMyelinated 30-70
γMyelinated 15-30
ẟMyelinated 12-30
B Myelinated 3-15
C Non-
myelinated
0.5-2
NEUROMUSCULAR
JUNCTION
1.Terminal button
2.Presynaptic membrane
3.Synaptic cleft
4.Post synaptic
membrane
34
NEUROMUSCULAR TRANSMISSION
• Sequence of events
are
• Release of acetylcholine by
the nerve terminals
• effect of acetylcholine on
postsynaptic membrane
35
• development of end plate
potential
• miniature end plate potential
• removal of acetylcholine by
cholinesterase
• initiation of action potential in
muscle fibre
36
PAIN PATHWAY
37
38
DUAL PAIN PATHWAY IN SPINAL CORD AND
BRAIN STEM
• pain receptors use two
separate pathways for
trasmitting pain signals
into the CNS.
• NEOSPINOTHALAMIC
TRACT (for fast pain )
• PALEOSPINOTHALAM
IC TRACT (for slow
pain)
39
40
41
THEORIES OF PAIN
• Specifity theory
• 4 types of sensory receptors-heat,cold,touch,pain
• a nerve responded to only one type
• Pattern theory
• A single nerve responded to each type of sensation by
creating a code
• Gate control theory
• Melzack and Wall 1965
• Non painful stimulus can block transmission of painful
stimulus 42
43
TYPES OF PAIN
• Superficial pain
Bright,stimulating quality
lasts as long as the stimulus
no referred pain
• Deep pain
Dull,depressing quality
may cause reffered pain,secondary
hyperalgesia
• Cutaneous pain
Felt as a fast ,sharp pricking pain
followed by less sharp,precisely
localised,burning pain
44
• Visceral pain
relates to adequate local cause suchas prior injury,sustained hyperaemia
or inflammation
Causes-
45
Ischemia
Chemical
stimuli
Spasm of
hollow viscus
Overdistension
of a hollow
viscus
Insensitive
Viscera
• Acute pain
• Sudden onset is self limiting
servebiological purpose as either a protective mechanism
or as a danger sign can be localised by a patient
46
• Chronic pain
• pain persists for more than 6
months
• not self limiting and is of longer
duration
• Referred pain
• pain sensation produced in some
part of the body felt in other
structures away from the place of
origin
• Phantom pain
a perception that an individual
experieneces relative to a limb or an
organ that is not physically part of the
body. 47
CLASSIFICATION
OF
ORO FACIAL PAIN
48
49
1.Dental pain
2.Mucogingival
3.Bone and periosteum
4.Disorders of eye and
ear
5.Enlargement of salivary
glands
EXTRACRANIAL PAIN
FROM TEETH
a.Myofacial pain
b. Trotter's syndrome
c.Eagle's syndrome
MUSCULOSKELETAL
SYSTEM
Neoplasms,
aneurysm,
haematoma,
oedema
PAIN FROM
INTRACRANIAL STRUCTURES
50
Migraine headache
Cluster headache
Chronic
paraxyosmal
hemicranias
VASCULAR
STRUCTURES
Trigeminal neuralgia
Glossopharyngeal
Neuralgia
Geniculate
neuralgia
NEUROLOGICAL
STRUCTURES
Atypical odontalgia
Neuritis
DEAFFERATION PAIN
SYNDROME
51
1.Anxiety
2.Depression
3.Hysterical pain
PSYCHOGENIC
CAUSES
• Trotters Syndrome
• caused by tumor of nasopharynx
involving pharyngeal wall and
eustachian tube
• May be associated with middle ear
deafness ,defective mobility of soft
palate and trismus of jaws
52
Cluster headache-
-episodes of severe unilateral headpain occuring around the eye
-multiple headaches per day -4 to 6 weeks
Etiology-
1.originates in hypothalamus which stimulates trigeminal and vascular systems
in brain
53
Clinical Manifestations
-80 percent males affected
-sudden ,unilateral and stabbing attacks
-lasts from 15 minutes to 2 hours and recurs several times daily
-Sweating of the face,ptosis, increased salivation and edema of the eyelid
Treatment
-Aborted by 100% oxygen
-Inj of sumatriptan/sublingual/ inhaled ergotamine
-Lithium
54
Chronic paroxysmal hemicranias
- Form of clusterheadache
-occurs in women between 30-40ages
-rapid onset,shorter pain
-5-20minutes' duration
-differs from cluster in its high frequency and shorter duration of attacks
Site of pain- temporal and orbital regions
55
• Atypical Odontalgia
• Tooth pain persistent for more than 4 months
• normal radiographs
• No clinically observable cause
• Pain is dull,aching,throbbing or burning
• Neuritis
• caused by infammation of peripheral branches of trigeminal or facial nerves
• accompanied by paraesthesia
• Pain is burning,bright and stimulating character
56
• Hysterical Pain
• Pain in head and orofacial conditions in which no pathophysiological factor is
present.
• Treatment-
• Aspirin 650 mg TID
• Nsaids -Ibuprofen 200-4--mg TID
• Anticonvulsants- Phenytoin,carbamazepin
57
• According to American Academy of Orofacial Pain
58
Intracranial structures
extracranial structures
musculoskeletal disorders
Neurovascular disorders
• Bell (1989) classified orofacial pain as
• AXIS I (physical condition)
1.Somatic pain
2.Neuropathic pain
AXIS II (Psychologic conditions)
1.Mood disorders
2.Anxiety disorders
3.Somatoform disorders
4.others 59
• IASP CLASSIFICATION
• published in 1986 revised in 1994
• Scheme for coding Chronic Pain Diagnoses
60
AXIS DEFINITION
1 Regions (eg head ,face,mouth)
2 Systems (eg nervous system)
3 Temporal Characteristics of pain (eg,continuous , recurring irregularly,
paroxysmal)
4 Patient's statement of intensity:time since onset of pain (eg mild ,medium
severe ; 1 mo or less;more than 6 months)
5 Etiology (eg ,genetic,infective, psychological)
Adapted from Merskey H and Bogduk N.
ASSESSMENT OF PAIN
• VISUAL ANALOGUE
SCALE( VAS )
• consists of 10cm line
• 0cm is “no pain” and 10cm is “pain
as bad as it could be”
• score is measured from the “no
pain” end of the scale
• Numeric scales -1 to 10
• Descriptive rating scales- no
pain,mild,moderate,severe pain
• sensitive to treatment effects
61
-can be incorporated into pain
diaries
-can be used with children
McGill Pain Questionnaire(MPQ)
• Measures the motivational-affective
and cognitive-evaluative qualities of
pain and sensory experience
• patients choose from 78 adjectives
(arranged in 20 groups)
• assesses sensory (groups 1 to 10)
affective (groups 11 to 15)
evaluative( group 16)
dimensions of pain
62
SEQUALAE OF PAIN
63
Psychological
sequelae
Muscular sequelae
Autonomic nervous
system sequelae
APPLIED ASPECT
• HYPERALGESIA- Hypersensitivity of pain
• Causes-
• excessive sensitivity of pain receptors - Primary
hyperalgesia
• facilitation of secondary transmission- Secondary
hyperalgesia
64
• HERPES ZOSTER
(Shingles)
• infects dorsal root ganglion
• severe pain in dermatomal segment
subserved by the ganglion
• elicits segmental type of pain that
circles halfway around the body
65
• Tic Douloureux
• Lancinating pain over one side of
the face in the sensory distribution
area of the fifth or ninth nerves
• pain-sudden electric shocks
• Clinical features-
• Sudden,excruciating recurring pain
in lips ,gingiva, cheeks
• Affects middle aged (women)
• Right side more involved
66
Treatment-
Carbamazepine 100mg single
dose daily
Phenytoin-300-400mg daily
Baclofen-5-10mg TID
• Glossopharyngeal
Neuralgia
• Occurs in areas innervated by
glossopharyngeal nerve
• Affects both men and women
• unilateral pain
• may be sharp,excruciating
• Treatment-
Carbamezapine,baclofen
• Geniculate Neuralgia
• Rare paroxysmal neuralgia
involving the nervus
intermedius,sensory component of
facial nerve
• More common in females
• Treatment-Acyclovir 800 mg 5
times daily a day for 10-14 days
67
68
MANAGEMENT OF PAIN
• NON-PHARMACOLOGICAL MANAGEMENT
• Physiotherapy
• Psychological techniques
• PHARMACOLOGICAL MANAGEMENT
• NSAIDs,Opiods,Adjuvant drugs,Topical Medications
69
• METHODS OF PAIN CONTROL
• Removing the cause
• Blocking the pathway of painful impulses
• Raising the pain threshold
70
71
REFERENCE
• Guyton and Hall-Textbook of physiology
• Gray's anatomy
• Burkit's oral medicine
• Indu khurana-Textbook of human physiology
• Monheim's-Local Anesthesia and pain control in dental
practice
72

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pain pathway

  • 1. PAIN PATHWAY Presented By Dr.PAYAL DASH 1st year P.G. TRAINEE DEPT. OF PUBLIC HEALTH DENTISTRY 1
  • 2. CONTENTS • Introduction • Background • Pain physiology • Dual Pain Pathway • Classification/Types of pain • Theories of pain • Assessment of pain • Sequalae of pain 2
  • 3. • Applied Aspect • Management of pain • Conclusion • References 3
  • 5. • According to Task Force on Taxonomy of the International Association for the Study of Pain (IASP) pain is “An unpleasant sensory and emotional experience associated with actual or potential tissue damage ,or described in terms of such damage.” • Sherrington defined pain as “psychical adjunct of an imperative protective reflex” i.e. pain is a sensation which draws attention of the individual as a whole. 5
  • 6. • Nociceptors: Receptors sensitive to painful stimulus responsible for initiating the generation of pain • Nociception: defined as noxious stimulus • Allodynia: pain that is produced by a stimulus not normally painful • Hyperalgesia:increased sensitivity to painful stimuli • Hypothesia: reduced sensation in response to stimulus • Anesthesia:absence of sensation in response to a stimulus 6
  • 7. • Causalgia: persistent burning pain caused by deaffertation of sensory innervation • Neuralgia: pain experienced in the tissues along the distribution of the nerve 7
  • 8. Pain Receptors,stimuli and chemical mediators of pain • Nociceptors -A delta myelinated nerve fibres • C unmyelinated nerve fibres Types of nociceptors- Somatic nociceptors Visceral nociceptors 8
  • 9. • Pain stimuli Activated by 3 stimuli: Mechanical Thermal Chemical Chemical mediators of pain include: k+, ATP, ADP released following cell death Bradykinin -dying cells Leukotrienes-mast cells Serotonin-platelets 9
  • 10. • Histamine-mast cells • Substance P and calcitonin gene-related peptide • QUALITATIVE TYPES OF PAIN- Fast pain -A delta fibres 0.1ms Slow pain-C fibres 1sec 10
  • 12. • STRUCTURE & FUNCTION A.Nerve cell body/Soma Principal costitutents are similar to a cell.Cytoplasm reveals 1.Nissl Granules/Bodies- Basophilic granules -parallely arranged ,membrane bounded cisternae/cavitites -covered by particles of ribose nucleoproteins 12
  • 13. 2.Neurofibrillae- Fine Threads 6-10nm in diameter -traverse the cytoplasmic matrix forming loose framework of fibrils in the cytoplasm Function -maintains the functional and anatomical integrity of the axon -Neurotrophins transported down the axon -Anterograde transport ( upto 400mm/day). -Retrograde transport (200mm/day)from the nerve endings to the cell body. 13
  • 14. B.Dendrites -5-7processes extending out from the cell body and extend extensively after they leave the cell -contain Nissl Granules,mitochondria and neurofibrillae -receptive processes of the neuron Function -transmit the impulses towards the cell body -non conducted local potential changes generated by synaptic connections are integrated. 14
  • 15. C.Axon -originates from Axon hillock, in which there are no Nissl Granules. -cytoplasmic fluid known as Axoplasm -cell membrane enveloping the cytoplasm -Axolemma Function- Initial segment of axon -a site where propagated action potentials are generated -An axonal process-transmits propagated impulses away from the cell body to the nerve endings.(All or none transmission) 15
  • 16. -Myelin sheath protein lipid complex envelopes the axon except at its endings and at periodic constrictions about 1mm apart called Nodes of Ranvier. Functions- 1.Prevents cross stimulation of adjacent axons because of its high insulating property it confines the nerve impulse to individual fibers. 2.Facilitates conduction of nerve impulse 16 Types of axons:- Afferent : nerve fibres which carry impulses to CNS Efferent : nerve fibres which convey impulses from CNS to periphery
  • 17. D.Synaptic knobs(Terminal buttons) -Axons divides into terminal branches each ending in number of synaptic knobs -contain granules or vesicles in which synaptic transmitter secreted by the nerve is stored. Function- Nerve endings where action potentials cause the release of synaptic transmitter 17
  • 19. Myelinated Nerves Unmyelinated Nerves 1.Schwann cell membrane is coiled many times round the axon forming the multiple layers of membrane that make up the myelin. 2.Example All preganglionic fibers of ANS 3.Conduction of nerve impulse is faster (50-100 times) because of Saltatory Conduction i.e. leaping of impulse from node to node over inter segmental region. 1.Axons are simply surrounded in the Schwann cell without wrapping of myelin. 2.Example- All post ganglionic fibres of ANS 3.Conduction is slower because it isa continuous process. 19
  • 20. • NEUROGLIA(Glial cells) 1.Microglia-phagocytic cells that enter the CNS from meninges and blood vessels. 2.Astrocytes- Foundthroughout the brain joining to blood vessels and investing synaptic structures,neuronal bodies and neuronal processes. 20 MACROGLIA MICROGLIA MICROGLIA
  • 21. Functions- Transport mechanisms inflammtory and reparative reactions maintain optimal concentration of ions and neurotransmitters (glutamine) in brain neurons. 3.Oligodendroglia Cells that form myelin around axon within CNS 21 ASTROCYTE
  • 23. PAIN PHYSIOLOGY • The main electrical properties of the nerve fibres are -Excitability , i.e. the capability of generating electrical impulses (action potential). -Conductivity , i.e. the ability of propagating the electrical impulses generated along the entire length of nerve fibres. 23
  • 24. • Resting membrane potential • potential difference across cell membrane at rest • Value- -70mV 24
  • 25. • Action potential • Defined as the brief sequence of changes which occur in the resting membrane potential when stimulated by a threshold stimulus. • Phases:- 1.Depolarization phase When the nerve is stimulated,polarized state (-70mv) is altered ,i.e. the RMP is abolished and the interior of the nerve becomes positive (+35mV) 2.Repolarization phase Within no time reverse occurs to the nearly original potential known as repolarization phase. 25
  • 26. • Action Potential Curve 1.Resting membrane potential 2.Stimulus artefact 3.Latent period 4.Firing level 5.Overshoot 6.Spike potential 7.After depolarisation 8.After hyperpolarisation 26
  • 27. • Characteristics of nerve excitability 1.Strength-Duration Curve Rheobase - minimum intensity of stimulus Chronaxie- minimum duration for which double the rheobase intensity must be applied to produce a response. 27
  • 28. • 2.All or none response • When stimulus of subthreshold intensity is applied no action potential is observed. • Threshold intensity-Spike of action potential • Suprathreshold intensity-no increase in magnitude of action potential 28
  • 29. 3.Accomodation When the stimulus strength is increased slowly to the firing level (during constant application ),no action potential is produced. Due to slow opening of Na+ channels and delayed closing of K+ channels. 4.Infatiguability A nerve fibre cant be fatigued even if it is stimulated for a long time.This is due to that during action potential neither a fresh impulse can be generated nor conducted through the fibre. 29
  • 30. • Inhibition of excitability 1.High extracellular calcium concentration- A high extracellular Ca2+ concentration decreases membrane permeability to Na+ ions 2.Local anaesthetics- Procaine ,Tetracaine , lidocaine block Na+ channels 30
  • 31. • CONDUCTIVITY Refers to the propagation of nerve impulse in the form of a wave of depolarization through the nerve fibre. 31
  • 32. • Propagation of action potential in myelinated axon -Saltatory conduction 32
  • 33. • Classification of nerve fibres Letter classification of Erlanger and Gasser 33 FIBRE TYPE MYELINATED /NON- MYELINATED CONDUCTION VELOCITY(M/S ) A α Myelinated 70-120 βMyelinated 30-70 γMyelinated 15-30 ẟMyelinated 12-30 B Myelinated 3-15 C Non- myelinated 0.5-2
  • 35. NEUROMUSCULAR TRANSMISSION • Sequence of events are • Release of acetylcholine by the nerve terminals • effect of acetylcholine on postsynaptic membrane 35
  • 36. • development of end plate potential • miniature end plate potential • removal of acetylcholine by cholinesterase • initiation of action potential in muscle fibre 36
  • 38. 38
  • 39. DUAL PAIN PATHWAY IN SPINAL CORD AND BRAIN STEM • pain receptors use two separate pathways for trasmitting pain signals into the CNS. • NEOSPINOTHALAMIC TRACT (for fast pain ) • PALEOSPINOTHALAM IC TRACT (for slow pain) 39
  • 40. 40
  • 41. 41
  • 42. THEORIES OF PAIN • Specifity theory • 4 types of sensory receptors-heat,cold,touch,pain • a nerve responded to only one type • Pattern theory • A single nerve responded to each type of sensation by creating a code • Gate control theory • Melzack and Wall 1965 • Non painful stimulus can block transmission of painful stimulus 42
  • 43. 43
  • 44. TYPES OF PAIN • Superficial pain Bright,stimulating quality lasts as long as the stimulus no referred pain • Deep pain Dull,depressing quality may cause reffered pain,secondary hyperalgesia • Cutaneous pain Felt as a fast ,sharp pricking pain followed by less sharp,precisely localised,burning pain 44
  • 45. • Visceral pain relates to adequate local cause suchas prior injury,sustained hyperaemia or inflammation Causes- 45 Ischemia Chemical stimuli Spasm of hollow viscus Overdistension of a hollow viscus Insensitive Viscera
  • 46. • Acute pain • Sudden onset is self limiting servebiological purpose as either a protective mechanism or as a danger sign can be localised by a patient 46
  • 47. • Chronic pain • pain persists for more than 6 months • not self limiting and is of longer duration • Referred pain • pain sensation produced in some part of the body felt in other structures away from the place of origin • Phantom pain a perception that an individual experieneces relative to a limb or an organ that is not physically part of the body. 47
  • 49. 49 1.Dental pain 2.Mucogingival 3.Bone and periosteum 4.Disorders of eye and ear 5.Enlargement of salivary glands EXTRACRANIAL PAIN FROM TEETH a.Myofacial pain b. Trotter's syndrome c.Eagle's syndrome MUSCULOSKELETAL SYSTEM Neoplasms, aneurysm, haematoma, oedema PAIN FROM INTRACRANIAL STRUCTURES
  • 50. 50 Migraine headache Cluster headache Chronic paraxyosmal hemicranias VASCULAR STRUCTURES Trigeminal neuralgia Glossopharyngeal Neuralgia Geniculate neuralgia NEUROLOGICAL STRUCTURES Atypical odontalgia Neuritis DEAFFERATION PAIN SYNDROME
  • 52. • Trotters Syndrome • caused by tumor of nasopharynx involving pharyngeal wall and eustachian tube • May be associated with middle ear deafness ,defective mobility of soft palate and trismus of jaws 52
  • 53. Cluster headache- -episodes of severe unilateral headpain occuring around the eye -multiple headaches per day -4 to 6 weeks Etiology- 1.originates in hypothalamus which stimulates trigeminal and vascular systems in brain 53
  • 54. Clinical Manifestations -80 percent males affected -sudden ,unilateral and stabbing attacks -lasts from 15 minutes to 2 hours and recurs several times daily -Sweating of the face,ptosis, increased salivation and edema of the eyelid Treatment -Aborted by 100% oxygen -Inj of sumatriptan/sublingual/ inhaled ergotamine -Lithium 54
  • 55. Chronic paroxysmal hemicranias - Form of clusterheadache -occurs in women between 30-40ages -rapid onset,shorter pain -5-20minutes' duration -differs from cluster in its high frequency and shorter duration of attacks Site of pain- temporal and orbital regions 55
  • 56. • Atypical Odontalgia • Tooth pain persistent for more than 4 months • normal radiographs • No clinically observable cause • Pain is dull,aching,throbbing or burning • Neuritis • caused by infammation of peripheral branches of trigeminal or facial nerves • accompanied by paraesthesia • Pain is burning,bright and stimulating character 56
  • 57. • Hysterical Pain • Pain in head and orofacial conditions in which no pathophysiological factor is present. • Treatment- • Aspirin 650 mg TID • Nsaids -Ibuprofen 200-4--mg TID • Anticonvulsants- Phenytoin,carbamazepin 57
  • 58. • According to American Academy of Orofacial Pain 58 Intracranial structures extracranial structures musculoskeletal disorders Neurovascular disorders
  • 59. • Bell (1989) classified orofacial pain as • AXIS I (physical condition) 1.Somatic pain 2.Neuropathic pain AXIS II (Psychologic conditions) 1.Mood disorders 2.Anxiety disorders 3.Somatoform disorders 4.others 59
  • 60. • IASP CLASSIFICATION • published in 1986 revised in 1994 • Scheme for coding Chronic Pain Diagnoses 60 AXIS DEFINITION 1 Regions (eg head ,face,mouth) 2 Systems (eg nervous system) 3 Temporal Characteristics of pain (eg,continuous , recurring irregularly, paroxysmal) 4 Patient's statement of intensity:time since onset of pain (eg mild ,medium severe ; 1 mo or less;more than 6 months) 5 Etiology (eg ,genetic,infective, psychological) Adapted from Merskey H and Bogduk N.
  • 61. ASSESSMENT OF PAIN • VISUAL ANALOGUE SCALE( VAS ) • consists of 10cm line • 0cm is “no pain” and 10cm is “pain as bad as it could be” • score is measured from the “no pain” end of the scale • Numeric scales -1 to 10 • Descriptive rating scales- no pain,mild,moderate,severe pain • sensitive to treatment effects 61 -can be incorporated into pain diaries -can be used with children
  • 62. McGill Pain Questionnaire(MPQ) • Measures the motivational-affective and cognitive-evaluative qualities of pain and sensory experience • patients choose from 78 adjectives (arranged in 20 groups) • assesses sensory (groups 1 to 10) affective (groups 11 to 15) evaluative( group 16) dimensions of pain 62
  • 63. SEQUALAE OF PAIN 63 Psychological sequelae Muscular sequelae Autonomic nervous system sequelae
  • 64. APPLIED ASPECT • HYPERALGESIA- Hypersensitivity of pain • Causes- • excessive sensitivity of pain receptors - Primary hyperalgesia • facilitation of secondary transmission- Secondary hyperalgesia 64
  • 65. • HERPES ZOSTER (Shingles) • infects dorsal root ganglion • severe pain in dermatomal segment subserved by the ganglion • elicits segmental type of pain that circles halfway around the body 65
  • 66. • Tic Douloureux • Lancinating pain over one side of the face in the sensory distribution area of the fifth or ninth nerves • pain-sudden electric shocks • Clinical features- • Sudden,excruciating recurring pain in lips ,gingiva, cheeks • Affects middle aged (women) • Right side more involved 66 Treatment- Carbamazepine 100mg single dose daily Phenytoin-300-400mg daily Baclofen-5-10mg TID
  • 67. • Glossopharyngeal Neuralgia • Occurs in areas innervated by glossopharyngeal nerve • Affects both men and women • unilateral pain • may be sharp,excruciating • Treatment- Carbamezapine,baclofen • Geniculate Neuralgia • Rare paroxysmal neuralgia involving the nervus intermedius,sensory component of facial nerve • More common in females • Treatment-Acyclovir 800 mg 5 times daily a day for 10-14 days 67
  • 68. 68
  • 69. MANAGEMENT OF PAIN • NON-PHARMACOLOGICAL MANAGEMENT • Physiotherapy • Psychological techniques • PHARMACOLOGICAL MANAGEMENT • NSAIDs,Opiods,Adjuvant drugs,Topical Medications 69
  • 70. • METHODS OF PAIN CONTROL • Removing the cause • Blocking the pathway of painful impulses • Raising the pain threshold 70
  • 71. 71
  • 72. REFERENCE • Guyton and Hall-Textbook of physiology • Gray's anatomy • Burkit's oral medicine • Indu khurana-Textbook of human physiology • Monheim's-Local Anesthesia and pain control in dental practice 72