PAIN, PAIN PATHWAYS AND

PAIN CONTROL
Introduction
Definition of pain
Terminology
Basic consideration of
nervous system
Classification of pain
Pain pathways
Orofacial pain

Dual nature of pain
Referred pain
Theories of pain
Control 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 pain
ALLOLDYNIA: pain that occurs without noxious stimulation at
the site of pain
ANALGESIA: that decreases the sensitivity to pain
NOCICEPTOR: 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.
Neuropathydisturbance of function or pathologic
change in a nerve
Pain threshold-lowest stimulus intensity at which a
subject perceives pain
Paresthesiaan abnormal,altered sensation
Dysesthesiaan unpleasant abnormal sensation
Noxious stimulitissue damaging stimuli that causes
pain.



RECEPTORS

CNS SPINAL CORD


MEDULLA NEURONS

HIGHER THALAMUS
CENTERS

CORTEX


COMPONENTS 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
Acetylcholine
1 most common neurotransmitter
2 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 neuron
Norepinephrine
1. secreted by neurons whose cell bodies are located in the
brain stem and hypothalamus
2 excitatory neurotransmitter

Serotonin
1.secreted by nuclei located in the Median Raphe of the
brain stem
2. peripherally algonenic agent related to vascular pain
syndromes
3. in CNS involved in endogenous nociceptive
mechanisms thought to potentiate endogenous endorphin
analgesia
Others
Glutamate and Aspartate excitation
Gamma amino butyric acid, glycine , dopamine
inhibitory

SLOW ACTING NEUROTRANSMITTERS



Substance P
1 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
Pain
Somatic
Visceral
Eg. Angina
pectoris /
peptic ulcer
intestinal coli
Superficial
From skin &
subcutaneous
tissues
Eg. Superficial
cuts, burns
Deep
From
Muscles/
bones /
joints/
Eg. 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 pain
Slow pain---begins only after a second
burning ,aching,throbbing,nauseas pain ,chronic pain

Chronic
Acute
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
pain fibers transmit
mainly mechanical and
acute thermal pain.
They terminate mainly
in lamina I (lamina
marginalis of the
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 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 7
th
9
th
and 10
th
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
processes
1. Transduction
2. Transmission
3. Modulation
4. Perception

Theories of pain
Specificity theory.
Descartes 1644-straight through channel
Muller 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
substance which are produced within the human
body and act like opium alkaloids
Endogeneous opioid peptide combine with their receptors

There are three receptors, mu, kappa, delta
Mu receptors are present most abuntantly in the brain
Kappa 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 history
Clinical examination
A thorough knowledge

Sir william osler what u dont know , u dont 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 measure
There 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 get
The 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 dentistry
In the past
Research at university of pittsburgh
This 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 causedesirable,
Blocking the pathway of painful impulsesmost
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 methodpt 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 analgesics


Pain is not a sensation,
it is an experience.