Presented by:

Dr.Ayesha Taha

JR I

Department of Pedodontics and

Preventive Dentistry

SPPGIDMS, Lucknow

INTRODUCTION

DEFINITIONS OF PAIN

TAXONOMY

CHARACTERISTIC OF PAIN

CLASSIFICATION

OROFACIAL PAIN

PAIN OF DENTAL ORIGIN.

ASSESSMENT OF PAIN

PAIN RECEPTORS

NEURAL PATHWAYS OF PAIN.

THEORIES OF PAIN

NEURAL PATHWAYS OF PAIN.◦ Neospinothalamic tract.◦ Paleospinothalamic tract.

DIAGNOSIS OF PAIN MANAGEMENT OF PAIN CONCLUSION

Pain is a sensory experience of special significance.

It is considered to be the fifth vital sign.

Pain is the commonest symptom which physicians

are called upon to treat.

It is a cardinal sign of inflammation.

Pain is an intensely subjective experience.

• But it has two features which are nearly universal.

First it is an unpleasant experience; and

Secondly it is evoked by a stimulus which is

actually or potentially damaging to living tissues.

• That is why, although it is unpleasant, pain serves a

protective function by making us aware of actual or

impending damage to the body.

The International Association for the Study of PainPain is "an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage”

[1979 by Harold Merskey]

“An unpleasant emotional experience usually initiated by noxious stimulus and transmitted over a specialized neural network to the CNS where it is interpreted as such.”

[C. Richard Bennett: Monheim’s Local Anesthesia and Pain control in dental practice, 7th edition, CBS Publishers & distributors, 1990]

Allodynia: Pain that occurs without noxious stimulus at the site

of pain.

Analgesia: Absence of sensibility to pain

Anesthesia: Absence of all sensation

Anesthesia dolorosa: Pain In an area that is anesthetic as a

result of differentiation

Arthralgia: Pain that is felt in the joint structures

Causalgia: A syndrome of unremitting burning pain as a result

of differentiation

Dyesthesia: An unpleasant abnormal sensation

Heterotopic pain: A general term to designate pain that is felt

in an area other than its true site of origin

Hypalgesia: Diminished sensitivity to stimulation-evoked pain

Hyperalgesia: Increased sensitivity to stimulation evoked pain

Hyperesthesia: Increased sensitivity to stimulation

Hypoesthesia: Diminished sensitivity to stimulation

1) Threshold and Intensity

• If the intensity of the stimulus is below the threshold (sub-

threshold) pain is not felt. As the intensity increases more

and more, pain is felt more and more according to the

Weber-Fechner’s law.

2) Adaptation – Pain receptors show no adaptation and so the

pain continues as long as 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 (extent of damage per unit time)

is high, intensity of pain is also high.

(A)Based on speed of onset, quality & duration

(1)

Experimental

(2)

Transient

(3)

Acute

(4)

Chronic

Arthur C. Guyton, John E. Hall: Textbook of medical physiology, 11th edition, Elsevier, 2006.

1. Experimental:

noxious stimuli causes a mild uncomfortable or painful sensation .

2. Transient pain:

Short duration

Severe

Self limiting

3. Acute pathological pain :

Sharp, fast, pricking

Occurs very rapidly

Carried by large diameter myelinated Aδ fibers

Usually alleviated with the help of professional

4. Chronological pathological pain :

Burning, aching.

Gradually increases.

Carried by small diameter non-myelinated C fibers.

Experience of persistent pain that lasts many months to years.

pain often increases over time & is aggravated by many factors.

(B)Based on level of stimulation

SOMATIC PAIN

Associated with skin

and musculo-skeletal

region.

Superficial Deep

VISCERAL PAIN

Associate with viscera

and

internal organs.

Carried by

unmyelinated type

C fibers.

(C)Based on special consideration

Referred pain Phantom pain

Pain occurring in a visceral structure is usually not felt in the

viscus itself but on the surface of the body or in some other

somatic structure that may be located quite some distance

away. Such type of pain is said to be Referred pain.

It is commonly observed visceral and somatic pain

e.g. the pain of angina pectoris is often felt in the left arm or

the jaw

diaphragmatic pain is often felt in the shoulder or neck.

Arthur C. Guyton, John E. Hall: Textbook of medical physiology, 11th edition, Elsevier, 2006.

It is not accentuated by provocation of the site where the

pain is felt, it is accentuated only by manipulation of the

primary pain source.

It is dependent on continuance of the primary initiating

pain, it ceases immediately if the primary pain is arrested or

interrupted.

Anesthesia of the structure where the referred pain is felt does not arrest the pain.

Individuals who have had a limb amputated may

experience pain or tingling sensations that feel as if they

were coming from the amputated limb, just as if that limb

were still present.

Although the mechanism of phantom limb pain is not

understood, the following possible explanations are

offered.

Arthur C. Guyton, John E. Hall: Textbook of medical physiology, 11th edition, Elsevier, 2006.

If a sensory pathway is

activated anywhere along its

course, nerve impulses are

generated that travel to the

CNS where they initiate

neural activity.

This neural activity

ultimately “creates”

sensations that feel as

though they originated in

the nonexistent limb.

CLASSIFICATION OF ORO FACIAL PAIN

A. PHYSICAL CONDITIONS

SOMATIC PAIN

NEUROPATHIC

PAIN

B. PSYCHOLOGIC CONDITIONS

1.MOOD DISORDERS

2. ANXIETY DISORDERS

3. SOMATOFORM DISORDERS

4. OTHER CONDITIONS

Type of pain

SLOW

Synonyms: burning pain, aching pain, throbbing pain, nauseous pain, and chronic pain.

Onset: >1 sec.

Tissues involved: Superficial + deep tissues

Cause: Tissue destruction

Results: Unbearable Suffering.

Nerve fibre: C fibre 0.5 – 1 µm, 0.5 – 2 m/s

FAST

Synonyms:sharp pain, pricking pain, acute pain, and electric pain.

Onset: Within 0.1 second.

Tissues involved: All superficial, and not in most of the deeper tissues.

Cause: Tissue damage.

Results: Protective reflex

Nerve fibre: Aδ: 1 – 5 µm, 5 – 15 m/s

ODONTOGENIC PAIN

Pain of Dental Origin

*Most common of all Oro facial pain

*Property to mimic nearly any pain

PULPAL PAIN

PERIODONTAL PAIN

FOOD IMPACTION

DENTINAL HYPERSINSITIVITY

CRACKED TOOTH

SYNDROME

BARODONTALGIA

› Can be acute /chronic› Difficult to localize› Presence of pathology-obvious› Increased by any thermal/

chemical stimuli› Nature varies over time

› Reversible pulpitis pain is of brief duration but soon subsides as soon as the stimulus is withdrawn

› Irreversible pulpitis pain persists for several minutes to hours even after withdrawal of stimulus

PERIODONTAL PAIN› Can be dull aching› Inflammation along PDL› trauma from occlusion

FOOD IMPACTION› It is the forceful wedging of food into the

periodontium by occlusal forces› Causes dull gnawing type of pain› Cusps that tend to forcibly wedge food into

interproximal embrasures are known as Plunger cusps› Occurs due to open contacts or improper contours.

DENTINAL HYPERSINSITIVITY

› Sharp severe localized pain occurring due to cold, sweet food because of exposed dentine

› Pain lasts for few seconds & disappears after removing stimuli

› Exposure of dentine due to caries, fracture of tooth, attrition, erosion or abrasion, inadequate restorations in form of marginal leakage or improper base

CRACKED TOOTH SYNDROME› Pain on biting & releasing biting pressure

› Pain in particular occlusal position

BARODONTALGIA› Pain in tooth due to change in atmospheric pressure

› Change in the solubility of gases in blood

› Sea divers, decompression chambers

› & Mountaineers

Most pain assessments are done in the form of a scale. The scale is explained to the patient and they give a score. A rating is taken before administering any medication and after the specified time frame to rate the efficacy of treatment.

Number Scale

Patients rate pain on a scale from 0-10, 0 being no pain and 10 being the worst pain imaginable.

Faces Scale A scale with corresponding faces depicting

various levels of pain is shown to the patient and they select one.

FLACC SCALE

Used for neonates/infants or whom cannot verbalize / comprehend

Assessment 0 1 2

FaceSmiling/expressionless Frowning

Clenched jaw/Anguish

LegNormal movement/Relaxed Restless/Tense

Legs drawn up/Kicking

Activity None/Lying quietly Squirming/Tense movements

Arched back/Rigid/Jerking

Cry None Occasional whimper

Crying constantly/Screaming

Consolability RelaxedEasily distracted or reassured

Difficult to distract/reassure

Pain is termed Nociceptive (nocer – to injure or to hurt in Latin), and nociceptive means sensitive to noxious stimuli. Noxious stimuli activate nociceptors.

Nociceptors are sensory receptors that detect signals from damaged tissue or the threat of damage and indirectly also respond to chemicals released from the damaged tissue.

Nociceptors are free (bare) nerve endings found in the skin, muscle, joints, bone and viscera.

Recently, it was found that nerve endings contain transient receptor potential (TRP) channels that sense and detect damage. They transduce a variety of noxious stimuli into receptor potentials, which in turn initiate action potential in the pain nerve fibers.

The damage of tissue results in a release of a variety of

substances from lysed cells as well as from new substances

synthesized at the site of the injury.

Globulin and protein kinases

Arachidonic acid

Histamine

Nerve growth factor (NGF)

Substance P (SP) and calcitonin gene-related peptide

(CGRP)

Potassium - K+

Serotonin (5-HT), acetylcholine (ACh), low pH (acidic)

solution, and ATP

The nociceptive mechanism (prior to the perceptive event) consists of a multitude of events as follows:

Transduction:

This is the conversion of one form of energy to another. It

occurs at a variety of stages along the nociceptive pathway

from:

– Stimulus events to chemical tissue events.

– Chemical tissue and synaptic cleft events to

- Electrical events in neurones.

– Electrical events in neurones to chemical events at synapses.

Transmission:

Electrical events are transmitted along neuronal pathways,

while molecules in the synaptic cleft transmit information

from one cell surface to another.

Modulation:

The adjustment of events, by up- or down regulation. This can

occur at all levels of the nociceptive pathway, from tissue,

through primary (1°) afferent neuron and dorsal horn, to

higher brain centres.

Thus, the pain pathway as described by Descartes has had to

be adapted with time.

SENSORY NEURONS

First Order Second Order Third Order

Each sensory receptor is attached to a first order primary

afferent neuron that carries the impulses to the CNS.

The first order sensory neurons are in the dorsal root ganglia or

the sensory ganglia of cranial nerves.

The axons of these first-order neurons are found to have

varying thickness. It has long been known that a relationship

exists between the diameter of nerve fibers and their conduction

velocities. The larger fibers conduct impulses more rapidly than

smaller fibers.

40

Second Order Neuron

The primary afferent neuron carries impulse into the CNS

and synapses with the second-order neuron.

This second-order neuron is sometimes called a

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.

41

Third Order Neuron

Cell bodies of third order neurons of the nociception-

relaying pathway are housed in: the ventral posterior lateral,

the ventral posterior inferior, and the intralaminar thalamic

nuclei

Third order neuron fibers from the thalamus relay thermal sensory information to the somesthetic cortex.

42

It is often assumed that pain is a warning that damage

has occurred. But this is not strictly true.

So these are various theories being put forward on

how nerve impulses give rise to sensation of pain.

According to this view, pain is

produced when any sensory nerve is

stimulated beyond a certain level.

In other words pain is supposed to

be depended only on high intensity

stimulation.

But the Trigeminal system provides

an example against this theory. In

case of trigeminal neuralgia the

patient can suffer excruciating pain

from a stimulus no greater than a

gentle touch provided it is applied to

a trigger zone.

45

INTENSITY THEORY

• According to this view, pain is a specific modality equivalent to vision and hearing etc.

• Just as there are Meissner corpuscles for the sensation of touch,

• Ruffini end organs supposedly for warmth and

• Krause end organs supposedly for cold,

• so also pain is mediated by free nerve endings.

• But concept of specific nerve ending is no long tenable. The Krause and Ruffini endings are absent from the dermis of about all hairy skin, so it is certain that these structures cannot be receptors for cold and warmth.

Head and Rivers (1908) postulated the existence of two

cutaneous sensory nerves extending from the periphery to

the CNS.

The Protopathic system is primitive, yielding diffuse

impression of pain, including extremes of temperature and

is upgraded.

The Epicritic system is concerned with tough

discrimination and small changes in temperature and is phylogenetically a more recent acquisition.

This theory proposed by Melzack and Wall in 1965.

This theory of pain takes into account the relative in put of

neural impulses along large and small fibers, the small nerve

fibers reach the dorsal horn of spinal cord and relay impulses

to further cells which transmit them to higher levels.

The large nerve fibers have collateral branches, which carry

impulses to substantia gelatinosa where they stimulate

secondary neurons.

The substantia gelatinosa cells terminate on the smaller nerve

fibers just as the latter are about to synapse, thus reducing

activity, the result is, ongoing activity is reduced or stopped –

gate is closed, NO PAIN

The theory also proposes that large diameter fiber input has

ability to modulate synaptic transmission of small diameter

fibers within the dorsal horn.

Large diameter fibers transmit signals that are initiated by

pressure, vibration and temperature; small diameter fibers

transmit painful sensations.

Activation of large fiber system inhibits small fiber synaptic

transmission, which closes the gate to central progression of

impulse carried by small fibers.

The ascending pathways that mediate pain consist of three

different tracts:

THE NEOSPINOTHALAMIC TRACT,

THE PALEOSPINOTHALAMIC TRACT AND

THE ARCHISPINOTHALAMIC TRACT.

Each pain tract originates in different spinal cord regions

and ascends to terminate in different areas in the CNS.

PATHWAYS OF PAIN IN THE SPINAL CORD AND BRAIN STEM :

The first-order nociceptive neurons (in the DRG) make synaptic connections in Rexed layer I neurons

Axons from layer I neurons decussate in the anterior white commissure, at approximately the same level they enter the cord

And then ascend in the contralateral anterolateral quadrant

Most of the pain fibers from the lower extremity and the body below

the neck terminate in the ventroposterolateral (VPL) nucleus and ventroposteroinferior (VPI) nucleus of the thalamus,

which serves as a relay station that sends the signals to the primary cortex.

First-order nociceptive neurons make synaptic connections in Rexed layer

II (substantia gelatinosa) and the second-order neurons make synaptic

connections in laminae IV-VIII

Most of their axons cross and ascend in the spinal cord primarily in the

anterior region and thus called the Anterior spinal thalamic tract (AST)

and few remain uncrossed.

The above three fiber tracts are known also as the paleospinothalamic tract.

These fibers contain several tracts. Each of them makes a synaptic connection in different locations

mesencephalic reticular formation (MFR)

periaqueductal gray (PAG) also called as spinoreticular tract

tectum, and these fibers are known as the spinotectal or spinomedullary tractthe PF-CM complex (IL) also known as the spinothalamic tract .

The innervation of these three tracts is bilateral because some of the ascending

fibers do not cross to the opposite side of the cord

From the PF and CM complex, these fibers synapse bilaterally in the

somatosensory cortex (SC II-Brodman area)

The archispinothalamic tract is a multisynaptic diffuse tract or pathway

and is phylogenetically the oldest tract that carries noxious information

The first-order nociceptive neurons make synaptic connections in Rexedlayer II (substantia gelatinosa) and ascend to laminae IV to VII

From lamina IV to VII, fibers ascend and descend in the spinal cord via the

multisynaptic propriospinal pathway surrounding the grey matter to synapse with cells in the MRF-PAG area

Further multisynaptic diffuse pathways ascend to the intralaminar (IL) areas of the thalamus (i.e., PF-CM complex)

and also send collaterals to the hypothalamus and to the limbic system nuclei

These fibers mediate visceral, emotional and autonomic reactions to pain

Three major steps:

◦ Accurately identifying the location of the structure from which the pain emanates

◦ Establishing the correct pain category the is represented in the condition under investigation

◦ Choosing the particular pain disorder that correctly accounts for the incidence and behavior of the patient’s pain problem

I. The chief complaint

•A) location of pain

•B) onset of pain

•C) characteristics of pain

•D) aggravating and alleviating factors

•E) past consultation and/or other treatments

•F) relationship to other complaints

Ii. Past medical history

Iii. Review of systems

Iv. Psychological assessment

Pain sensations may be controlled by interrupting the pain

impulse between receptor and interpretation centers of brain.

This may be done :

1. Chemically

2. Surgically

Most pain sensations respond to pain reducing

drugs/analgesics which in general act to inhibit nerve impulse

conduction at synapses.

Occasionally however, pain may be controlled only by

surgery.

MANAGEMENT OF PAIN:

Pain perception control

1.Removing the cause

2. Blocking the path way

of painful impulses, Ex: GA/LA

3.Analgesics

- non narcotics

- narcotics

- NSAID`s

- muscle relaxants

- antidepressants etc.

Pain reaction control

1.Preventing pain

reaction

by cortical depression.

2.Using psychosomatic

methods.

Ex: Conscious sedation.

Behavior management

Raising the level of pain threshold

The purpose of surgical treatment is to interrupt the pain

impulse somewhere between receptors and innervations

centers of brain, by severing the sensory nerve, its spinal root

or certain tracts in spinal cord or brain.

Sympathectomy – excision of portion of neural tissue from

autonomic nervous system.

Cordotomy – severing of spinal cord tract, usually the lateral

spinothalamic.

Rhizotomy – cutting of sensory nerve roots.

Prefrontal lobotomy – destruction of tracts that connect the

thalamus with prefrontal and frontal lobes of cerebral cortex.

Transcutaneous Neural Stimulation (TNS)

With TNS, cutaneous bipolar surface electrodes are

placed in the painful body regions and low voltage

electric currents are passed.

Best results have been obtained when intense stimulation

is maintained for at least an hour daily for more than 3

weeks.

TNS portable units are in wider spread use in pain clinics

throughout the world and has been proved effective

against neuropathic pain.

• Pain is bad, but not feeling pain can be worse.

• Individuals with a congenital absence of pain receptors are extremely rare but not unknown. Such individuals are very poor at avoiding accidental injuries, and often inflict mutilating injuries on themselves.

• As a result, their life span is usually short. thus pain, although unpleasant, is a protective sensation with enormous survival value.

• The sensation of pain therefore depends in part on the patient past experience, personality and level of anxiety.

• Every day patient seeks care for the reduction or elimination of

pain.

• Nothing is more satisfying to the clinician than the successful

elimination of pain.

• The most important part of managing pain is understanding

the problem and cause of pain.

• It is only through proper diagnosis that appropriate therapy

can be selected.

Arthur C. Guyton, John E. Hall: Textbook of medical physiology, 11th

edition, Elsevier, 2006. C. Richard Bennett: Monheim’s Local Anesthesia and Pain control in

dental practice, 7th edition, CBS Publishers & distributors, 1990 Allan I. Basbaum, Diana M. Bautista, Grégory Scherrer, and David

Julius: Cellular and Molecular Mechanisms of Pain, Cell 139, October16, 2009, 267 -284.

Jeffrey P. Okeson: Bell’s Orofacial Pains The Clinical Management ofOrofacial Pain, 6th edition, Quintessence Publishing Co, Inc, 2005.

Bell’s Orofacial Pain. Fifth edition. Jeffrey P. Okeson Handbook of Pain Management. A clinical companion to Wall and

Melzack’s textbook of pain Mangement of Facial, Head and Neck Pain. Barry C. Cooper. Frank E.

Lucente Monheim’s Local Anesthesia and Pain control in Dental Practise. C.

Richard Bennett Diagnosis & management of facial pain- OMFS clinics of North

America– may 2000