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DILU DAVISI IND YEAR POSTGRADUATE

PAIN CONTROL IN OPERATIVE DENTISTRY

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• HISTORY

• INTRODUCTION

• DEFINITION

• CHANGING CONCEPTS

• NEW DIMENSIONS

• PURPOSE OF PAIN

• CLASSIFICATION

• SOMATOSENSORY SYSTEM

• NEURAL PATHWAY OF PAIN

• THEORIES OF PAIN

FLOW CHART

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• CAUSES OF OROFACIAL PAIN

• DIAGNOSIS OF PAIN

• ASSESSMENT OF PAIN

• FACTORS THAT INFLUENCE PAIN

• DIFFERENTIAL DIAGNOSIS OF PAIN

• METHODS TO CONTROL PAIN

• CONCLUSION

• REFERENCES

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• Derived from Greek “Poin”; meaning “Penalty”

• Derived from Latin “Poena”; meaning “Punishment from God”

HISTORY

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• Chinese : Yin and Yang : 2 opposite forces & imbalance of system

• Egyptian : Dead spirits

• Buddhist of India : Reasoned it to frustrated desire & heart is root cause

• Greek : Brain as part of sensory & motor nervous system

Early Cultural Superstitions

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• Homer - Arrows Shot by the Gods

• Aristotle – distinguish five senses, considered pain to be Passion

of the Soul

• Plato – pain and pleasure arose from within and considered pain

to be an emotional experience than a localized body sensation

• Hippocrates – imbalance of body fluids

• Bible - Anguish of the Soul

• Freud - Solution to Emotional Conflicts

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• Probably - most fundamental and primitive sensation

• Distributed more or less all over the body

• Protective in nature and always indicates some serious trouble in the locality, such

as a structural damage or a serious functional or metabolic derangement

INTRODUCTION

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An unpleasant emotional experience associated with actual or potential tissue damage or described in terms of such damage.

International Association for the Study of Pain (IASP) (WHO)

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

Monheim

DEFINITION

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An unpleasant sensation that is perceived as arising from a specific region of the body and is commonly produced by processes which damage or are capable of damaging bodily tissue.

Fields

A more or less localized sensation of discomfort, distress, or agony resulting from the stimulation of specialized nerve endings."

Dorland's Medical Dictionary

The subject’s conscious perception of modulated nociceptive impulses that generate an unpleasant sensory and emotional experiences associated with actual of potential tissue damage or describe in terms of such damage.

Bell

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Pain is …

• protective mechanism

• localized sensation as a result of noxious stimulation

• now recognized as being more of an experience than a sensation

CHANGING CONCEPT OF PAIN

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Cognitive : Subject’s ability to comprehend & evaluate

Emotional : Represents the feeling that regenerated

Motivational : Drive to terminate

NEW DIMENSIONS TO PAIN

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• Protective mechanism for the body

• Tissue damage ignites individual’s reaction to pain stimulus

e.g. Skin ischemia - No pain - Desquamation

PURPOSE OF PAIN

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Depending on experience, pain can be classified as :

1. Experimental

2. Acute

3. Chronic

CLASSIFICATION OF PAIN

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Experimental

• Noxious stimuli causes a mild uncomfortable or painful sensation

Acute Pathological Pain

• Elicits a psychological or behavioral reaction

• The cause of this continuous pain is often unknown to patient

• May create anxiety, anger, physical gesture

• Usually alleviated with the help of professional care

Chronic Pathological Pain

• Complicated physical, behavioral and psychological problem

• Experience of persistent pain that last many months to years

• Little apparent cause & not self limiting

• Pain often increases over time & is aggravated by many factors

• Response is persistent anxiety, confusion, sleep disturbances, depression, disability

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Transient Pain

• Short duration• Severe• Self limiting

Acute

• Associated with postoperative, post injury

• More duration• Requires pharmacological

assistance(analgesics)

Persistent• Long term duration• Eg.: Cancer & neurogenic pain• Pharmacological assistance(analgesics) and

cognitive approach

Chronic or Disabling • Continue beyond expectation for disease

process• Pain and pain therapy dominate the life• Depression, anxiety

Depending On Duration

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Pain is also classified into two types :

FAST PAIN • Felt within about 0.1 second• Described as: sharp, pricking, acute, electric pain• Not felt in most deeper tissue of body

SLOW PAIN

• Begins only after 1 second or more & then increases slowly over many seconds & some times even minutes

• Slow burning, throbbing, nauseous, chronic pain• Associated with tissue destruction

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PHYSICAL CONDITIONS PSYCHOLOGIC CONDITIONS

SOMATIC PAINNEUROPATHIC PAIN

MOOD DISORDERS

ANXIETY DISORDERS

SOMATOFORM DISORDERS

OTHER CONDITIONS

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1. SOMATIC PAIN

• Superficial somatic pain• Cutaneous pain• Mucogongival pain

• Deep somatic pain• Musculoskeletal pain

• Muscle pain• Protective co-contraction• Delay onset muscle soreness• Myofascial pain• Myospasm• Myositis

• Temporomandibular joint pain• Ligamentous pain• Retrodiscal pain• Capsular pain• Arthritic pain

• Osseous and periosteal pain• Soft connective tissue pain• Periodontal dental pain

• Visceral pain

• Pulpal dental pain

• Vascular pain

• Arteritis

• Coritidynia

• Neurovascular pain

• Migraine with aura

• Migraine without aura

• Cluster headache

• Paroxysmal hemicrania

• Neurovascular variants

• Visceral mucosal pain

• Glandular, ocular and auricular pain

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2. NEUROPATHIC PAIN

• Neuropathic pain

• Episodic neuropathic pain

• Paroxysmal neuralgia

• Trigeminal neuralgia

• Glossopharyngeal neuralgia

• Geniculate neuralgia

• Superior laryngeal neuralgia

• Nervus intermedius

• Neurovascular pain

• Continuous neuropathic pain

• Neuritis

• Peripheral neuritis

• Herpes zoster

• Postherpetic neuralgia

• Deafferentation pain

• Neuroma

• Atypical odontalgia

• Sympathetically maintained pain

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PSYCHOLOGIC CONDITIONS

• Mood disorders

• Depressive disorders

• Bipolar disorders

• Mood disorders due to a medical condition

• Anxiety disorders

• Generalised anxiety disorder

• Post traumatic stress disorder

• Anxiety disorders due to medical condition

• Somatoform disorders

• Undifferentiated somatic disorders

• Conversion disorders

• Pain disorders

• Hypochondriasis

• Other conditions

• Malingering

• Psychologic factors affecting a medical condition

• Personality traits or coping style

• Maladaptive health behavior

• Stress related physiologic response

• Any other mental disorders not mentioned in this

classification

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1. Hyperreactive pulpalgia

a. Dentinal hypersensitivity

b. Hyperemia

2. Acute pulpalgia

a. Incipient

b. Moderate

c. Advanced

3. Chronic pulpalgia

a. Barodontalgia

PULPAL CAUSES OF PAIN

4. Hyperplastic pulpitis

5. Necrotic pulp

6. Internal resorption

7. Traumatic occlusion

8. Incomplete fracture

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PAIN OF NON-DENTAL ORIGIN

II) NEUROVASCULAR TOOTHACHE - ASSOCIATED WITH MIGRAINE VARIANTSCLINICAL FEATURES

1. Toothache is characterized by remission

2. Temporal behavior

3. Minor or no dental cause

I) MUSCULAR TOOTHACHE - TEMPORALIS, MASSETERCLINICAL FEATURES

1. Constant tooth ache which is non pulsatile

2. Not responsive to local provocation of the tooth

3. Pain increases with function of involved muscle

4. LA - not effective

5. LA of involved muscle - reduces toothache

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4. Following dental treatment - pain may spread to adjacent teeth, opposing teeth or entire face

5. Associated autonomic effects - nasal congestion, lacrimation, edema of eyelids and face

III) CARDIAC TOOTHACHECLINICAL FEATURES

1.Aching pain is cyclic

2.Pain is increased with physical exertion and exercise3.Toothache associated with chest pain4.Toothache decreased with nitroglycerin tablets5.Failure of toothache to respond to reasonable dental therapy

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IV) NEUROPATHIC TOOTHACHECLINICAL FEATURES

1. Pain is unilateral, severe, lacerating, shock - like2. Pain is provoked by a trigger3. Local anesthesia at the tooth will not reduce the pain

4. Local anesthesia at the trigger will reduce the attack

V) SINUS TOOTHACHECLINICAL FEATURES

1. Pressure below eyes

2. Increased pain with lowering of the head3. Increased pain with applied pressure over the sinus4. Local anesthesia of tooth not eliminating pain

5. Diagnosis confirmed by imaging studies

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V) PSYCHOGENIC TOOTHACHE CLINICAL FEATURES

1. Multiple teeth reported painful

2. Physiologic patterns of pain not applicable

3. Chronic pattern of pain

4. Lack of response to reasonable dental treatment

5. Not identifiable as any other pain condition

DIFFERENTIAL DIAGNOSIS HETEROTROPHIC REFERRED PAIN NEUROPATHIC PAINS PAINS OF CENTRAL ORIGIN

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SOMATOSENSORY SYSTEM

TYPES OF SENSATIONS

• The sensations are generally classified into four types :

a) Epicretic sensations

b) Protopathic sensations

c) Deep sensations

d) Special sensations

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A) Epicretic sensations

• Mild or light sensations

• These sensations are perceived more accurately

Fine touch or tactile sensation

Tactile localization

Tactile discrimination

Temperature sensation with finer range i.e., between 25 and 40°C

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B) Protopathic sensations

• Crude sensations or the primitive type of sensations

Pressure sensation Pain sensation Temperature sensation with a wider range

ie. Above 40°C and below 25°C

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C) Deep sensations

Sensations arising from the deeper structures beneath the skin and the visceral organs

Sensation of vibration or pallesthesia Kinesthetic sensation or kinesthesia Visceral pain arising from viscera

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D) Special sensations

• The special senses are : visual sensation

auditory sensations

gustatory (taste) sensation

olfactory (smell) sensation

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NEURAL PATHWAY OF PAIN

Given by Fields -1987 ; modified later by others

Fields divided the processing of pain from the stimulation of primary afferent nociceptors to the subjective experience of pain into four steps :

• TRANSDUCTION• TRANSMISSION• MODULATION• PERCEPTION

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I. Transduction: process by which noxious stimuli is converted to electrical activity in the appropriate sensory nerve endings

II. Transmission: refers to neural events that carry nociceptive input into CNS for proper processing. In this, first and second order neurons are involved

III. Modulation: refers to the ability of the CNS to control the pain transmitting neurons

IV. Perception: if the nociceptive input reaches the cortex, perception occurs. It is at this point the suffering and pain behavior begins

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TRANSDUCTIONis the activation of the primary afferent nociceptor

External stimuli• Intense thermal • Mechanical stimuli• Noxious chemicals• Noxious cold

Endogenous Chemical Substances (Inflammatory Mediators)

• Polypeptide bradykinin (BK)• Potassium• Histamine • Serotonin • Arachidonic acid

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• Activation of cutaneous C fibers causes their cell bodies to synthesize : • Neuropeptides• Substance P• Calcitonin gene–related peptide (CGRP)

WHICH IS RESPONSIBLE FOR PROLONGED PAIN

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NEU

ROTR

ANSM

ITTE

RS

SMALL (rapid acting)

Acetylcholine

NOREPINEPHRINE

SEROTONIN

GAMMA AMINOBUTYRIC ACID

GLYCINE

DOPAMINE

ASPARTATE

LARGE (slow acting)

Substance P

Endorphins

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Pain receptors

FIRST ORDER NEURONS

SPINAL CORD

Three classes of nociceptive afferent neurons provide the input whereby the brain perceives pain :

1. Mechanothermal afferents are primarily A∂ fibers : respond to intense thermal and mechanical stimuli

2. Poly modal afferent C fibres : conduct more slowly : respond to mechanical thermal and chemical stimuli

3. High Threshold mechanoreceptive afferents are chiefly A∂ Fiber normally respond to intense mechanical stimuli

First order neurons are the cells in the posterior nerve root ganglia

These neurons receive impulses of pain sensation from the pain receptors through their

dendrites and their axons reach the spinal cord

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• The fibers of fast pain sensation are carried by A∂

afferent fibers

• After reaching the spinal cord, the fibers synapse with

marginal cells in the posterior gray horn

• The fibers transmitting impulses of slow pain belong to C

type and these fibers synapse with substantia gelatinosa

in the posterior gray horn

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Sensory receptors

Spinal cord

Spinothalamic pathway

Thalamus & cortex

Muscle

1st order neuron Dorsal root

2nd order neuron

Interneuron 3rd order neuron

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There are 2 systems for processing the pain signals on their way to the brain :

1) The neospinothalamic tract for fast pain

2)The paleospinothalamic tract for slow pain

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TRANSMISSION Refers to the process by which

peripheral nociceptive information is relayed to the central nervous system by second and third order neurons

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SECOND ORDER NEURONS

• From spinal cord to the thalamus

• The marginal cells and the cells of substantia gelatinosa form the second order neurons

• Fibers from these cells ascend in the form of the LATERAL SPINOTHALAMIC TRACT situated near the gray matter

• Fibers of marginal cells for fast pain are long. Immediately after taking origin, the fibers cross the midline via anterior gray commissure, reach the anterolateral white column and ascend.

• These fibers form the NEOSPINOTHALAMIC TRACT, a part of lateral spinothalamic tract.

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• The third order neurons of pain pathway are the neurons of thalamic nucleus, reticular formation, tectum and gray matter around aqueduct of Sylvius.

• Axons from these neurons reach the sensory area of cerebral cortex

• Some fibers from reticular formation reach hypothalamus

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MODULATION

• Refers to mechanisms by which the

transmission of noxious information to the

brain is reduced

• Endogenous opioid system - pain modulation

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Brain Opiate System

• 1965, Reynold proposed presence of morphine like substances :

• Endorphins

• Enkephalins

• Dynorphin

• Believed to cause pre and post synaptic inhibition of type C and Aδ fibres

• Serotonin and norepinephrine also play a role in descending inhibitory pathway

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• Multiple areas of brain show opiate receptors

Enkephalin - brain stem and spinal cord

-Endorphine - hypothalamus and spinal cord

Dynorphin - brain stem and spinal cord

Intrinsic analgesic potency similar to morphine

• Abundance of opiate receptors present in brain in Amygdala & remainder of limbic

called Emotional or Visceral Brain

• Mediates integration of sensory information pertaining to pain & emotional behavior

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• Behave like morphine & bind to opiate receptors to obtund pain like morphine

• β endorphin - closely related to pituitary function

• The enkephalin & endorphins have antinociceptive effects

• Underlying mechanism not fully analyzed

Endorphins

β-Endorphin has approximately 80 times the analgesic potency of morphine

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• Secreted by nuclei that originate in median raphe of the brain stem & project to many areas of brain & spinal dorsal horn.

• Released when necleus raphe magnus in brain stem stimulated by sensory input

• Released by blood platelets, synthesized in CNS

• Potentiate endorphin – analgesia

Serotonin

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• The pain receptors adapt very little OR not at all

• As the pain stimulus continues, excitation of the pain fibers becomes progressively greater

• Increase in sensitivity of pain receptors is called hyperalgesia

• Significance : keeps the person apprised of a tissue damage stimulus as long as it persists

Nonadapting Nature Of Pain Receptors

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• Pain impulses are believed to be conducted into the central nervous system by two types of nerve fibers, which are classified by the size and speed at which they conduct the impulse

PATHWAYS OF PAIN SENSATION

NERVE FIBRES

A

Aα

13 to 20μm70 to 120 m/s

Aβ

6 to 13 μm40 to 70 m/s

Aγ

3 to 8 μm15 – 40 m/s

Aδ

1 to 5 μm5 to 30 m/s

C

0.5 to 1μm0.5 – 2 m/s

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CENTER FOR PAIN SENSATION

• The center for pain sensation is in the post central gyrus of parietal cortex.

• Fibers reaching hypothalamus are concerned with arousal mechanism due to pain stimulus.

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Referred Pain

• The pain is not felt over the area where the viscus is situated but felt some where else

• Felt in the area where the viscus was situated in the embryonic life

e.g.• Pain of heart - left arm, neck• Pain of center of diaphragm - tip of shoulder• Lower molar to ear

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FEATURES OF REFERRED PAIN

Wholly spontaneous

Not accentuated by provocation of site

Ceases immediately if primary pain is arrested

Felt in superficial or deep structures

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Theories Of Referred Pain• The two most popular theories are

1) Convergence – Projection

2) Convergence - Facilitation

1. Convergence-Projection Theory:

• This is the most popular theory

• Primary afferent nociceptors from both visceral and cutaneous neurons often converge onto the same second-order pain transmission neuron in the spinal cord

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Brain having more awareness of cutaneous than of visceral structure through past experience, interpret the pain coming from the regions served by cutaneous afferent

fibersEXAMPLE (Milne et al 1981)

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2. Convergence – Facilitation Theory:

• Similar to convergence – projection theory

• Believed that the internal organs were insensitive to stimuli and that they created a irritable focus on the spinal cord leading to R.P.

• Did not hold good

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Afferent fiber is bifurcated before connecting to the dorsal horn

3. Axon-Reflex

4. Thalamic Convergence

Referred pain is perceived as such due to the summation of neural inputs in the brain

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Dental condition that causes head and neck pain 1. Hypersensitive dentin2. Cracked tooth syndrome3. Pulpal and periapical system4. Barodontalgia

Oral condition that cause head and neck pain.1. PDL disease pain2. TMJ disturbance3. MPDS4. Bruxism5. Pain from cysts and tumour dry socket6. Traumatic neuron

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Pathway From Dental Pulp To Cortex :- (mand molar)Once the nociceptors located in the pulp activated

the impulse is carried into the CNS by primary afferent neuron in the mandibular branch of 5th nerve

GASSERIAN OR TRIGEMINAR GANGLION

Nucleus CaudalisNucleus Oralis may also play important role

Fast pain Slow pain

Thalamus Reticular formation

Sensory cortex

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THEORIES OF PAIN

• Peripheral free nerve endings mediate pain to the central apparatus

• Direct line from receptor to the brain

• Pulling one end of the rope causes a ring on the other end of the bell

• No morphological basis

Specificity Theory Descartes - 1664

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Intensity Theory :Mumford & Newton-1971

• Pain is caused when nerve is stimulated beyond certain level

• Pain is non-specific sensation

• Depends on high intensity stimulation

• e.g., application of heat is pleasant ; but more heat causes burning

• Intensity of stimulation is a factor in causing pain

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Protopathic & Epicritic Theory

Head & Rivers 1908

• Two groups of sensory nerves from periphery to CNS

• Protopathic – primitive, yielding diffuse impression of pain & temperature

• Epicritic- concerned with touch & small changes in temperature

• These groups do not exist

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Pattern Theory

Goldscheider 1894

• Pain is produced by intense stimulation of non-specific receptors

• Pain sensation depends on spatiotemporal pattern of nerve impulse reaching brain

• spatio-temporal:- warmth, cold, pain

(according to Weddel 1955)

• Pattern of nerve impulse entering the brain will be different for different regions

• Designation of sensation as hot, cold, tingling etc., is somewhat arbitrary since there are many grades in between

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GATE CONTROL THEORY Melzack & Wall 1965

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• Proposed by Ronald Melzack and Patrick Wall in 1965 & in 1982

• Described psychological mechanism by which psychological factors can affect the experience of pain

• Neural gate can be open & close - modulate the pain

• Gates are located in spinal cord• Allow to pass directly to the brain• Altered prior to being forwarded to the brain (for instance, influenced by

expectations)• Prevented from reaching the brain (eg: by hypnosis-induced anesthesia)

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Although the theory may be simply stated, its ramifications are extremely complex

Gate Control Theory postulates :

1. Information about the presence of injury is transmitted to the central nervous system by small peripheral nerves

2. Cells in the spinal cord or nucleus of the fifth cranial nerve, which are excited by these injury signals, are also facilitated or inhibited by other large peripheral nerves that also carry information about innocuous events (for example, temperature or pressure)

3. Descending control systems originating in the brain modulate the excitability of cells that transmit information about injury

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Large-diameter fiber input has the ability to modulate synaptic transmission of small-diameter fibers within the dorsal horn

• Large diameter fibers transmit impulsesat a greater rate of speed than do small diameter fibersinitiated by pressure, vibration, and temperature

• Small diameter fibers transmit noxious or painful sensations

• Intentional stimulation of the large fiber system results in inhibition of synaptic transmission within the smaller, pain producing fibers • Acupuncture and

• transcutaneous electrical nerve stimulation (TENS)

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Factors Involving In Opening & Closing Of Gate

• Amount of activity in pain fibers

• Amount of activity in other peripheral fibers

• Message that descend from brain

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Factors that open the gate• Physical conditions

o Extent of injuryo Inappropriate activity level

• Emotional conditionso Anxiety or worryo Tensiono Depression

• Mental conditionso Focusing on paino boredom

Conditions that close the gate• Physical conditions

Medications Counter stimulation

• Emotional conditions Positive emotions Relaxations, rest

• Mental conditions Intense concentrations or

distraction Involvement and interest in life

activities

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CAUSES OF OROFACIAL PAIN

1. Local Pathosis of Extracranial Structures – can arise from: a. Tooth pulp, periodontium, periradicular structures, gingiva, mucosa

b. Salivary gland disorders – mumps , acute parotitis (children) - mucus plug, sialolith (adults) - Sjogren’s syndrome(inflammation)

c. Ear pain – otitis media, otitis externa, mastoiditis

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d. Sinus & paranasal pain – maxillary, frontal & ethmoid sinusitis

e. Tongue

f. Eyes

g. Temporomandibular joint articular disorders – polyarthritis, disc derangements,

osteoarthritis, dislocations, fractures

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2. Intracranial causes –

a. Neoplasm

b. Aneurysm

c. Meningitis

d. Hematoma / hemorrhage

e. Edema

f.Abscess

g. Angioma

h. Cerebrovascular accidents

I. Venous thrombosis

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3. Referred pain from remote pathologic sites – can be from:

a. Heart – angina pectoris , myocardial infarction

b. Thyroid – inflammation

c. Carotid artery – inflammation , other causes

d. cervical spine – inflammation , trauma , dysfunction

e. muscles – myofascial trigger points

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4 . Neurovascular causes –

a. Migraine

b. Cluster headaches & chronic paroxysmal hemicrania

c. Headaches with vascular disorders – arteritis, hypertension

d. headaches with substance exposure or withdrawal – nitrates, alcohol, narcotics,

caffeine

e. Headaches with metabolic disorders – hypoxia, hypoglycemia, dialysis

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5. Neuropathic causes – a. Paroxysmal - Trigeminal neuralgia - Glossopharyngeal neuralgia - Nervus intermedius neuralgia - Occipital neuralgia - Neuroma b. Continuous - Postherpetic neuralgia - Post – traumatic neuralgia - Anesthesia dolorosa

6. Causalgic pain – reflex sympathetic dystrophy - arises from sympathetic nervous system

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7. Muscular pains – a. Myospasm painb. Myositis painc. Local myalgia – unclassifiedd. Myofascial pain - tension – type headaches - coexisting migraine and tension-type headaches

8. Unclassifiable pains / atypical facial pains

a . Atypical odontalgiab. Burning mouth syndrome

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HISTORY1. Chief complaint – a) Location of Pain b)Onset Of Pain – associated with other factors - progression c)Characteristics of Pain - Quality - Behaviour - Intensity - Concomitant symptoms - Flow of the pain d)Aggravating / Alleviating Factors e)Past Treatments2. Past Medical History3. Psychologic Assessment

DIAGNOSIS OF PAIN

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CHARACTERISTICS OF PAIN

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CLINICAL EXAMINATION

1. General examination

• Vital Signs

• Cranial Nerve Evaluation

• Eye / Ear Evaluation

• Cervical Evaluation

• Balance Coordination

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2. Muscular examination

• Pain & Tenderness

• Trigger Points & Pain Referral

3. Masticatory Evaluation

• Range Of Mandibular Movements

• Temporomandibular Joint Evaluation

• Oral Structures ( Teeth, Periodontia, Occlusion )

4) Other Diagnostic Tests

• Thermal Test

• Pulp Vitality Test

• Imaging

• Laboratory Tests

MRICT

ULTRASOUNDSINGLE PHOTON CT

POSITRON ELECTRON TOMOGRAPHY

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Locating the source of pain – DIAGNOSTIC BLOCKS

LA at site of pain fails to reduce pain

LA at source of pain reduces the pain at

the source as well as the site

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ASSESSMENT OF PAIN

Numerical Rating Scale 0-10 Scale

Visual Analog Scale Mark point on 10 cm line

McGill Pain Questionnaire Pt. identifies terms describing pain from 20 sets of words

West Haven Yale Multidimensional Pain inventory

Language skills52 questions assessing various aspects

of pain

Faces Scale Pictures of Faces ranging from smiling to crying indicating level of discomfort

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FACES SCALE

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• A visual analog scale is a line that represents a continuum of a particular experience, such as pain

• The most common form used for pain is a 10 cm line, whether horizontal or vertical, with perpendicular stops at the ends

• The ends are anchored by “No pain” and “Worst pain imaginable”

1. Visual Analog Scale:

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• Patients are asked to place a slash mark somewhere along the line to indicate the intensity of their current pain complaint.

• For scoring purposes, a millimeter ruler is used to measure along the line and obtain a numeric score for the pain ratings.

• Children as young as 5 years are able to use this scale.

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• It is a verbal pain scale that uses a vast array of words commonly used to

describe a pain experience.

• The words are listed in 20 different categories in order of magnitude

from least intense to most intense and are grouped according to

distinctly different qualities of pain.

• The patients are asked to circle only one word in each category that

applies to them.

2.McGill Pain Questionnaire

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• First 10 categories represent different sensory descriptors that cover

various temporal, spatial, pressure, and thermal qualities of pain

• Next five categories are affective or emotional descriptors

• Category 16 is evaluative (ie, how intense is the pain experience)

• Last four categories are grouped as miscellaneous.

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• To score the questionnaire, the words in each category are given a numeric value

• The first word in each category ranks as 1, the second as 2, etc

• The scores for each category are added up separately for the sensory, affective, evaluative, and miscellaneous groupings

• Then the total number of words chosen is also noted

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• Biological • Genetic variations leads differences in amount & type of neurotransmitters.

• Previous pain experience

• Gender

• Cognitive • Younger –report greater level of pain

• Older children understand the meaning of pain• Upto 3 months- no understanding of pain but memory is present• By 6 month respond to pain by anger• By 20 months anger becomes more dominant

Factors That Influence Pain

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• Psychologial • Feeling of lack of control - intensify pain perception

• Sociocultural• Difference in perception exist among different cultural group

• Parents perception & response to their child’s pain strongly influence child’s perception & his reaction to pain

Are Indians and Females Less Tolerant to Pain? An Observational Study Using a Laboratory Pain Model Med J Malaysia Vol 64 No 2 June 2009

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Thresholds for Sensation and Pain

• Three thresholds for sensation and pain help in understanding the experience of pain :

1. Sensory threshold

2. Pain threshold

3. Pain tolerance/response threshold

Psychologic Factors Modifying Pain

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• First time the subject reports perception of any sensation is termed the

"sensory threshold."

• This is defined as the lowest level of stimuli that will cause any response

• Pain threshold : As the current is increased, the sensation becomes

stronger until the subject states that it is painful.

• Neurologically, when the summation of firing of primary afferent

nociceptive fibers reaches a certain point, pain is perceived

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Pain tolerance

• If the intensity of the electrical current is increased above pain threshold, a level

of pain will be reached that the subject can no longer endure.

• At this point, the individual makes an attempt to withdraw from the stimulus.

• The range between the pain threshold and response threshold is termed a

person's tolerance to pain

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Differential Diagnosis of Pain

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SITE OF PAIN REFERRAL INVOLVED TEETH

Frontal region Maxillary incisors

Nasolabial area Maxillary canineMaxillary premolars

Temporal region Maxillary 2nd premolar

Below mandibular molar area Maxillary 2nd & 3rd molar

Ear Mandibular molars

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Mental region Mandibular incisor , canine & premolar

Angle of mandible Mandibular first & second molar

Midramal region Mandibular second pre molar

Superior laryngeal area Mandibular 3rd molar

Maxillary premolar Maxillary canine

Maxillary molars Maxillary canineMandibular premolars

Mandibular premolars Maxillary canineMaxillary premolars

Mandibular first premolar Mandibular first and second molar

Glick DH 1962115

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Pulpal And Periapical Pain

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Hypothetical Mechanism For Pain In Pulp

1. Cholinergic neurotransmitters(Ach) – found in pulp

2. ANS :

The neurotransmitters elaborated by autonomic efferent in inflamed pulp

Bradykinin level during inflammation increases significantly

3. Adrenergic neurotransmitters (histamine) released from inflamed pulp

(mast cell)

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4. Prostaglandin :

• Present in inflamed tissue

• Create pain by direct irritation of nerve endings

• Alerts the sensors to kinin

• Bradykinin in minute conc. evokes pain

5. Cyclic AMP – cGMP

• Nerve stimulated – increased amount of c AMP – hyperpolarization of nerve –

decreased transmission of nerve impulse

• cGMP – depolarization of neurons – increased neuronal excitability

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6.Lowered O2 tension

• Decreased O2 tension - nerve impulses fired rapidly

• Pulpal ischemia - cell injury

• Outer membranes, subcellular mitochondria, lysosomes damaged

• Accumulation of Ca++ ions and release of enzymes that break down cell

components

• Reduced O2 tension in pulp

• Stimulation of sympathetic and parasympathetic nerves in blood vessels of

pulp, during this period generate pain

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7.Increased Intrapulpal pressure – Inflammation

Increased temperature

Increased intrapulpal pressure

Pain

8.Specific infection of pulp and P.A. tissue• Responsible for transmitting or modulating nerve impulses

• Therefore may be related to pain or pulpitis.

This theory is still unclear

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METHODS OF PAIN CONTROL

1. Removing the cause

2. Blocking the pathway of painful impulses

3. Raising the pain threshold

4. Preventing pain by cortical depression

5. Using psychosomatic methods

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Method Of Control Of Pain In Restorative Dentistry

• Gaining confidence of the patient : fear - pain

• Sharp instruments employed with skill and confidence

• Use of cooling devices

• Use of obtundents

• Preventing desiccation of the dentin

• Local anesthesia

• General anesthesia

• Newer methods of pain control

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• Supra periosteal infiltration

• Regional nerve block : depositing suitable local anesthetic solution close to a main nerve

trunk preventing afferent impulses from traveling centrally beyond that point

Local Anesthesia

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• Posterior superior alveolar nerve

• Anterior superior alveolar nerve

• Greater palatine

• Nasopalatine

Maxillary Anesthesia

• Inferior alveolar nerve block

• Incisive nerve block

• Mandibular block

• Vasirani Akinosi technique (closed mouth technique)

Mandibular Anesthesia

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• Intra Osseous Anesthesia

• Intra Ligamentary Anesthesia

• Intra Septal Anesthesia

• Intra Pulpal Anesthesia

Additional Local Anesthetic Procedures

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• Anesthetize soft tissue and bone overlying the apical region of the tooth through local infiltration

Intraosseous injection

Intraseptal infiltration• 27 gauge 1 inch needle

• More successful in younger patients - less density of bone

Intrapulpal injection• Used when all other techniques have failed or during endodontic therapy as an

adjunct• Most commonly on mandibular molars, but not exclusively• Intense, instantaneous pain is usually felt by the patient

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• Conscious sedation

• Nitrous oxide gas

General Anesthesia

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• General anesthesia should not be administered in dental clinics which

are not equipped with :

• Surgical grade suction unit

• Medication kit including oxygen to tackle any anesthetic complications

• Adequate floor assistance

• Large comfortable area for recovery of the patient

• Access to medical emergency services

Precautions

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• Patients with acute inflammatory lesions in which local anesthetic is likely to be effective

• Over - reactive patients

• Patients who experience repeated fainting after intra-oral injections patients who are intolerant of drill noises

• Children who are uncooperative

• Patients who experience a hyperactive gagging reflex

• Patients with cardiovascular conditions, in whom mental stress should be avoided

• Patients with neuro/psychological disorders or emotional instability

• Patients with histories of convulsions and fits

• Patients who are handicapped with involuntary muscular movements or spasms, or who have inability to communicate adequately

Indications

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Advantages

Practically universally accepted

Increased safety

Adverse reactions less frequent

Adverse reactions less severe

Oral sedation

Disadvantages

× Slow onset of action (15 - 30) minutes

× Long duration of action (3 - 4hr)

× Inability to rapidly increase or decrease of

sedation

× Patient require escort from office

Drugs which can be used for sedation include diazepam, triazolam, zaleplon, lorazepam, and hydroxyzine

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Advantages

Rapid onset of action

Ability to titrate to ideal level of sedation

Ability to rapidly increase or decrease sedation level

Total clinical recovery within 3 to 5 minutes

Ability to discharge most patients without need for adult escort

Inhalation Sedation

Disadvantages

× Cost and size of equipment

× Requirement for education in proper use of inhalation

sedation

Potential Complications:

× Chronic exposure of low level of nitrous oxide

× Abuse potential of nitrous oxide

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• A favorable mental attitude may be established through suggestions of relaxation.

• Better control over patients habits such as talking, rinsing.and oral tissue tension

Hypnosis

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DRUGS COMMONLY USED TO MANAGE ACUTE DENTAL PAIN

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NSAIDS CONSIDERED SAFE

Paracetamol

Ibuprofen

Naproxen

Paracetamol with codeine

Dental Pain during Pregnancy

ANALGESICS TO AVOID

Aspirin

Ibuprofen

Naproxen

Codeine

ANTIBIOTICS CONSIDERED SAFE

Penicillin

Amoxicillin

Cephalexin

Clindamycin

Metronidazole

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• Preoperative oral NSAID, one hour before start of treatment

• Local anesthetic of choice for pain control during surgery

• Bupivacaine or etidocaine HCL administration at END of procedure immediately prior to dismissal of patient

• Continue oral NSAIDs on timed basis for number of days deemed appropriate

• Postoperative telephone call evening of appointment

Pain Management Protocol

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• Vibrotactile devices

• Computer controlled LA delivery system

• Jet injectors

• Safety dental syringes

• And devices for IO anaesthesia

NEWER PAIN CONTROL METHODS

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1. Vibraject : attached to normal syringe, high frequency vibration

2. DentalVibe : It is a cordless, rechargeable, hand held device that delivers soothing, pulsed, percussive micro-oscillations to the site where an injection is being administered

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• Accupal :

• CCLAD : Incorporated computer technology to control the rate of flow of the anesthetic solution through the needle

• WAND

• Comfort Control Syringe

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• SYRIJET

• MEDJET

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• Stabident system : 2 parts: a perforator, a solid needle that perforates the cortical plate of bone with a conventional slow-speed contra-angle handpiece, and an 8 mm long, 27-gauge needle that is inserted into this predrilled hole for anesthetic administration

• X-tip :Composed of a drill and guide sleeve.

• IntraFlow :

Newer Intraosseous LA

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PAIN THERAPY FOR OROFACIAL PAIN

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MANAGEMENT OF OROFACIAL PAIN – THERAPEUTIC MODALITIES

1. Pharmacological therapy• Analgesic agents – NSAIDs & narcotic agents• Anesthetic agents – topical / injectable local anesthetics• Anti – inflammatory agents• Anticonvulsants• Muscle relaxants• Antidepressants• Anxiolytic• Antihistamine• Others – clonidine ; baclofen ; gabapentine ; tramadol ; NMDA

receptor antagonist

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OPIOIDS

Opioid analgesics bind to opioid receptors

& causes decrease in neurotransmission

by several mechanisms

Morphine ; codeine

Pentazocine ; butorphanol

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ANTIINFLAMMATORY AGENTS

Acts by preventing formation of

prostaglandin E by inhibiting the

cycloxygenase pathway

Aspirin, NSAIDs, Corticosteroids

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ANESTHETIC AGENTS

Acts by blocking conduction in the sodium (Na) channel

Uses:a. To arrest primary pain inputb. To interrupt pain cycling c. To resolve myofascial trigger point activityd. To induce a sympathetic blockade in cases of : - reflex sympathetic dystrophy - herpes zoster - postherpetic neuralgia

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ANTICONVULSANTS

Action is by blocking sodium channel & suppressing neuronal discharge

- CARBAMAZEPINE (Tegretol)- exerts analgesic effects by central potentiation of adrenoreceptor & by increasing the nor-adrenergic output

- PHENYTOIN SODIUM (Dilantin)

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ANXIOLYTIC AGENTS

BENZODIZEPINESBARBITURATES

Their action is on GABA – a RECEPTORS

MUSCLE RELAXANTS

Act by CNS depression

- CYCLOBENZAPRINE has anticholinergic activity & works on the neuromuscular junction to reduce electrochemical signals

-SUCCINYLCHOLINE CHLORIDE

-METHOCARBAMOL

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ANTIDEPRESSANTS

It acts by inhibiting the reuptake & storage of Neurogenic amines : - SEROTONIN - NOREPINEPHRINE - AMITRIPTYLINE

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ANTIHISTAMINES

They may have some analgesic activity by virtue of reduction of histamine released in the area of inflammation - DIPHENHYDRAMINE - HYDROXYZINE - PYRILAMINE

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SURGICAL MANAGEMENT OF OROFACIAL PAIN – TRIGEMINAL NEURALGIA

- interruption of pain pathways between center & periphery achieved by:-

EXTRACRANIALLY :1. Alcohol block in peripheral nerve

2. Peripheral neurectomy – supra / infra orbital - lingual - inferior alveolar nerve ( Ginwalla’s tech.)

3. Electrosurgery

4. Cryosurgery

5. Selective radiofrequency thermocoagulation

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INTRACRANIALLY:1. Alcohol blockade of the gasserian gangloin

2. Radio – frequency thermocoagulation of gasserian ganglion

3. Retrogasserian rhizotomy

4. Medullary tractotomy

5. Midbrain tractotomy

6. Intracranial sensory nerve root decompression - jannetta’s approach - dandy’s approach

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OTHER ADJUVANT THERAPIES

1. Acupuncture

2. Placebos

3. Ultrasound

4. Deep heat

5. Massage

6. Hypnosis

7. Physical activity

8. Exercises

9. Counselling

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• WHO analgesic ladder

• Pain is a diagnostic challenge. A doctor should be aware of the physiologic and psychological aspects of pain and anxiety as it applies to the patient. There is a vast array of diseases that manifest with painful symptoms clinically.

• Adequate clinical assessment and diagnosis are the keys to successfully manage such painfull conditions.

CONCLUSION

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1. Bell’s orofacial pain – Jeffrey P.Okeson.

2. Pain control in dentistry – Samuel Seltzer3. DCNA -PAIN 19784. Orofacial pain- J. M. Mumford5. Relief of pain in clinical practice – Samson Lipton

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Understanding medical physiology.- Bijlani- 3rd edition.Textbook of medical physiology.- Guyton and hall - 10th edition.Clinical oral physiology.- Timothy S Miles.Essentials of oral physiology.- Robert M Bradley.Management of temporomandibular disorders and occlusion.- Jeffrey P okeson- 5th editionOral bioscience.- David B Fergusion

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1. REVIEW OF MEDICAL PHYSIOLOGY- GANONG

2. CONCISE MEDICAL PHYSIOLOGY- CHAUDHRI

3. TEXT BOOK OF MEDICAL PHYSIOLOGY :GYTON AND HALL

4. TEXT BOOK OF MEDICINE :DAVIDSON

5. TEXT BOOK OF ENDODONTICS : INGLE

6. PATHWAYS OF PULP : COHEN

7. MONEIHM’s LOCAL ANESTHESIA : C R BENNET

8. ESSENTIALS OF MEDICAL PHYSIOLOGY : K. SEMBULINGAM

THANK YOU

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