PAIN, PAIN PATHWAYS PAIN, PAIN PATHWAYS AND PAIN CONTROLAND PAIN CONTROL

IntroductionDefinition of painTerminology Basic consideration of nervous systemClassification of painPain pathways Orofacial pain

Dual nature of painReferred painTheories of painControl of pain

Introduction

1. Pain is an unpleasant experience

2. Seriously impairs the lives of millions of people.

3. In 1984, Bonica reported that nearly 1/3rd of the

population

4. This results in loss of billions annually in health

care services, loss of work, decreased productivity

and disability compensation

5.The clinical management of pain

Definition

“An unpleasant emotional experience usually initiated by

a noxious stimulus and transmitted over a specialized

neural network to the central nervous system where it is

interpreted as such.”

TERMINOLOGY

ALGOGENIC: causing painALLOLDYNIA: pain that occurs without noxious stimulation at the site of painANALGESIA: that decreases the sensitivity to painNOCICEPTOR: a sensory receptor preferentially sensitive to noxious or potentially noxious stimuli.ODONTALGIA: pain that is felt in a tooth.

Neuralgia –pain in the distribution of a nerve.Neuropathy—disturbance of function or pathologic change in a nervePain threshold-lowest stimulus intensity at which a subject perceives painParesthesia—an abnormal,altered sensationDysesthesia—an unpleasant abnormal sensationNoxious stimuli—tissue damaging stimuli that causes pain.

RECEPTORS

CNS SPINAL CORD

MEDULLA NEURONS

HIGHER THALAMUS CENTERS

CORTEX

COMPONENTS OF THE PAIN PATHWAYCOMPONENTS OF THE PAIN PATHWAY

Receptors

Are highly specialized structures.Emerge the afferent sensory nerves.First structures in the sensory path of pain.Specific receptors respond to specific stimuli

Receptors

- ruffini end organs

- pacinian corpuscles

free nerve endings

- merkels corpuscles

Type of neurons

Depending on their functions and location

They can be classified as                                                               i.Afferent neuron : Conducts nerve impulse towards the CNS                                                             ii.Efferent neuron : Conducts nerve impulse peripherally                                                          

Types of sensory neurons  i. First order  ii. Second order   iii.Third order                                                            

Type A fibres:

Alpha 70-120m/s, 12-20um.

Beta 40-70m/s, 5-12um

Gamma 10-50m/s, 3-6um

Delta 6-30m/s, 2-5um

Type B fibres 3-15m/s, <3um

Type C fibres 0.5-2.0m/s, 0.4-1.2um

CLASSIFICATION OF NERVE FIBRES

SYNAPSE OR SYNAPTIC JUNCTION

It is a unique junction that mediates the transfer of info

from one neuron to the next, or neuron to an effector cell

Transmitter vescicles

The neurochemicals that transmit impulses

across synaptic clefts.

Rapidly acting neurotransmitters

Slow acting neurotransmitters.

Neurotransmitters

Acetylcholine1 most common neurotransmitter2 secreted by neurons in the brain, those innervating the

skeletal muscle, preganglionic neurons of ANS , pre and postganglionic neurons of parasympathetic and sympathetic nervous system

3. has an excitatory effect on post synaptic neuronNorepinephrine

1. secreted by neurons whose cell bodies are located in the brain stem and hypothalamus

2 excitatory neurotransmitter

Serotonin1.secreted by nuclei located in the Median Raphe of the

brain stem2. peripherally algonenic agent related to vascular pain

syndromes3. in CNS involved in endogenous nociceptive

mechanisms thought to potentiate endogenous endorphin analgesiaOthers

Glutamate and Aspartate excitationGamma amino butyric acid, glycine , dopamine

inhibitory

SLOW ACTING NEUROTRANSMITTERS

Substance P1 Polypeptide composed of 11 amino acids

  released at the central terminals of primary nociceptive

neurons and act as transport substances

2.Centrally it act as an excitatory neurotransmitter for

nociceptive impulse

3.Its modulating action on pain is both rapid and short-lived

4.Its concentration is highest in the most severely inflamed

joints.

1. Endorphins

a.       Are polypeptides, behave like morphine

b.      They are displaced from their receptors by morphine antagonist Naloxone.

c.       Bind to morphine receptors to obtund pain.

d.      Important contributors to pain threshold & pain tolerance.

2. Bradykinin

a. Is an endogenous polypeptide that consists of a chain of 9 amino acids

b. Released as a part of inflammatory reaction

c. Powerful vasodilator

d. It requires the presence of prostaglandins to act    

Classification of Pain

PainPain

SomaticSomatic VisceralVisceralEg. Angina Eg. Angina

pectoris / pectoris / peptic ulcer peptic ulcer intestinal coliintestinal coliSuperficialSuperficial

From skin & From skin & subcutaneous subcutaneous tissuestissues

Eg. Superficial Eg. Superficial cuts, burnscuts, burns

DeepDeep

From From Muscles/Muscles/bones / bones / joints/ joints/

Eg. FractureEg. Fracture

Referred pain Pain perception and pain reaction are at different

sites.

Psychogenic pain Is an unpleasant sensation that has no organic

basis.originates wholly in the mind.In some cases, this pain is a symptom of deep underlying neurosis of which the patient himself may be unaware.

PAIN

FAST PAIN SLOW PAIN

Fast pain ---0.1 seconds sharp pain,pricking,acute ,electric painSlow pain---begins only after a second burning ,aching,throbbing,nauseas pain ,chronic pain

ChronicAcute

CLASSIFICATION OF OROFACIAL PAIN

The pain signals take 2 different pathways to the brain.

  PAIN PATHWAY 

 

 

 

Neo Spinothalamic PaleoSpinothalamic

Tract Tract

NEOSPINOTHALAMIC PATHWAY (Transnmission of fast pain)

The fast type a-delta The fast type a-delta pain fibers transmit pain fibers transmit mainly mechanical and mainly mechanical and acute thermal pain. acute thermal pain. They terminate mainly They terminate mainly in lamina I (lamina in lamina I (lamina marginalis of the marginalis of the dorsal horns)dorsal horns)

PALEOSPINOTHALAMIC

PATHWAY(Transmission of slow chronic pain)

The paleospinothalamic system

transmits pain mainly carried in

the peripheral slow-chronic type-C

pain fibres, although it does

transmit some signals from type A-

delta fibres as well.

The peripheral fibres

terminate almost entirely in

laminas II and III of the dorsal

horns, which together are called as

substantia gelatinosa.

Somatic inputs from the face and oral structures do not enter the spinal cord by way of spinal nerves. Instead, sensory input from the face and mouth is carried by way of the fifth cranial nerve, the trigeminal nerve.

Orofacial Pain PathwayOrofacial Pain Pathway

Trigeminal pathway is only one of the many pathways

that carry orofacial nociception to the brain.

Nociceptive impulses from the face and mouth may be

mediated centrally by way of afferent neurons that pass through

the 7th 9th and 10th cranial nerves as well and also visceral

afferents that descend through cervical sympathetic chains.

The cell bodies of the

trigeminal afferent neurons are

located in the large gasserion ganglion.

This region of the brain stem

is structurally very similar to the

dorsal horn of the spinal cord.

NEURAL PATHWAYS OF PAIN

Fields has described that the subjective

experience of pain arises by four distinct

processes1.      Transduction2.      Transmission3.      Modulation 4.      Perception

Theories of pain

Specificity theory.Descartes 1644-straight through channelMuller 19 century –theory of information transmission only by way of sensory nerves.Von frey---sp. Cutaneous receptors ,free nerve endings,pain centre-exist,responsible

- Specificity theory cannot explain

a) Any pathologic pain produced by mild noxious

stimuli.

b) Referred pain that can be triggered by mil

innocuous stimulation of normal skin.

c) Do not explain the paroxysmal episodes of pain

produced by mild stimulation of trigger zone in

trigeminal neuralgia.

Pattern theory

• 1894 goldscheider was the first –stimulus intensity and

central summation

• particular patterns of nerve impulses that evoke pain are

produced by summation of sensory input within drg.

• Pain results when total output of cells exceeds a critical

level.

Touch + pressure + heat.

Gate control theory

Characteristics of Pain

1) Threshold and intensity.

2) Adaptation.

3) Localization of pain.

4) Emotional accompaniment.

5) Influence of the rate of damage on the intensity of pain.

Dual nature of pain

Pain perception physioanatomical process similar to all healthy individuals.

Pain reaction psychophysiological process. varies from individual to individual.

MODULATION

The concept of modulation is extremely important in

understanding the patients experience of pain .It is based on

the principle that neural impulses ,rising to the higher centers

that are termed painful can be altered by a process called as

inhibition

Pain modulation takes place in the following areas

1. Pain modulation in the trigeminal spinal tract

nucleus

2. Transcutaneous electrical nerve stimulation

3. Pain modulation in reticular formation

4. Pain modulation of the descending inhibitory

system

PAIN IN THE TRIGEMINAL SPINAL TRACT

NUCLEUS

Tip of dorsal horn of the spinal cord - substantia gelatinosa

substantia gelatinosa neurons were

proposed to inhibit transmitter release

from primary afferent neurons, thus

inhibiting the impulse carried by the

primary afferent neuron .

The myelinated afferents were proposed to excite the

inhibitory interneurons

This in turn reduce the activity of pain transmission neuron

TRANSCUTANEOUS ELECTRICAL NERVE

STIMULATION [TENS]

The chief product of the gate control theory was the

introduction of transcutaneous electrical nerve stimulation as a

therapeutic modality

The rationale of TENS is based on the antinociceptive effect of

stimulating cutaneous sensory nerves

An interrupted periodic current of very low intensity at

a frequency of 50 to 100Hz is used

The stimulation is usually below what is required to

activate A-delta and C nociceptive fibers

The effect is immediate and usually disappears rapidly

Pain relief is localized to the segment stimulated,

Serotonin and dynorphin are released when superficial cutaneous

nerve are stimulated

Instinctive act of grabing, holding ,pressing or rubbing exemplifies

this effect

Pain reducing remedies are of this category

e.g.: massage analgesic balms ,counter irritants mustard plasters,

hot and cold compresses, vibration,hydrotherapy,and vapocoolant

therapy

PAIN MODULATION IN RETICULAR FORMATION

Reticular formation is a portion of the brain stem that contains a

number of nuclei that can either excite or inhibit the incoming

impulses

Reticular formation controls the overall activity of the brain

Pain signal in particular , increase the activity in this area and

strongly excite the brain to attention

PAIN MODULATION OF THE DESCENDING INHIBITORY SYSTEM

3 major components

1.periaqueductal and

periventricular areas.

2.raphe magnus nucleus

3.inhibitory complex located in

dorsal horn of spinal cord.

These fibers at their terminals , secrete either serotonin or enkephalin as neurotransmitter and

they are called as serotogenic or enkephalinergic neurons.

Endorphins and encephalins are the two Endorphins and encephalins are the two

substance which are produced within the human substance which are produced within the human

body and act like opium alkaloidsbody and act like opium alkaloids

Endogeneous opioid peptide combine with their receptors

There are three receptors, mu, kappa, deltaMu receptors are present most abuntantly in the brainKappa are present particularly in the substantia gelatinosa rolandi [SGR]Combination of enkephalin or endorphin with mu and kappa leads to inhibition of pain perception

Referred pain: - Heterotropic pain that is felt in an

area innervated by a nerve different from the one

that mediates the primary pain.

Diagnosis

Accurate and detailed historyClinical examinationA thorough knowledge

Sir william osler “what u don’t know , u don’t diagnose”

Signs and symptoms**clinical features

1) Its character, eg. Sharp, dull, throbbing, burning or stabbing.

2) The site or sites from which it arises, and to which it travels.

3) Its timing, when did the first attack occur its frequency & duration.

4) The provoking factors.5) The relieving factors.6) Associated phenomena eg., swelling, discharge,

bruxism, trismus.7) Does the patient suffer from anxiety or depression?8) The current and previous general medical history and

drug therapy.

The history should include

HOW TO MEASURE PAIN

Pain measurement is a complex and controversial psycho physiologic measureThere is no simple method of measuring pain. Pain intensity can be measured by using ratings such as

VISUAL ANALOG SCALE (VAS). A VAS consists of a 10cm line on which 0 no pain 10 pain as bad as it can getThe VAS are sensitive to treatment effects, can be incorporated into

pain diaries and can be used with children.Disadvantage: the multidimensional aspects of pain are not well

measured

Control of pain

Most important aspect of practice of dentistryIn the pastResearch at university of pittsburghThis should no longer be the fact

1) Removing the cause

2) Blocking the pathway of painful impulses.

3) Raising the pain threshold

4) Preventing pain reaction by cortical depression.

5) Using a psychosomatic methods.

1 and 2 affect pain perception.

4 and 5 affect pain reaction.

3 affect pain perception and pain reaction.

Following are methods of pain control

Removing the cause—desirable,Blocking the pathway of painful impulses—most widely used method in dentistry,drug –analgesic property –injected-in proximity to the nerve involved.Raising pain threshold---pharmacological action,drugs raise the pain th centrally –interfere with pain reaction.Cortical depression---general anaesthesia.Psychosomatic method—pt in properframe of mind,gain faith and confidence,well informed,once they are secure ,tolerate pain to a greater degree.

Methods of Pain Control

Action of anti-inflammatory analgesicsAction of anti-inflammatory analgesics

“Pain is not a sensation,it is an experience”.