Pain and Pain Pathways Final
Pain and Pain Pathways Final
Pain and Pain Pathways Final
Anjali Savita
MDS I
Dept of Conservative Dentistry and
Endodontics
“I don’t accept the maxim ‘there is no gain
without pain’, physical or emotional. I believe it
is possible to develop and grow with joy rather
than grief; however when pain comes my way, I
try to get the most growth out of it”
- Alexa Mclaughlin
Contents
Introduction Theories of pain
Definition Pain pathway of
History
Maxillofacial Region
Dental pain
Incidence
References
Related Terms
Characteristics of pain
Classification of pain
Pain receptors
Pathway of pain sensation
Introduction
Pain is the commonest symptom which physician are
called upon to treat.
Pain is an intensely subjective experience, and is
therefore difficult to describe.
Physiology of pain has taught us a lot about neural
function in general.
It has two universal features. First, its an unpleasant
experience. Second, it is evoked by a stimulus which is
actually or potentially damaging to living tissue.
That is why, although it is unpleasant, pain serves a
protective function by making us aware of actual or
impeding damage to the body.
Like all sensory experiences, pain has two components, the
first component is awareness of painful stimulus and second
one is emotional impact(or effect) evoked by experience.
While the awareness is localized to the area stimulated,
experience involve the whole being.
That is why when a finger is hurt, the whole person suffers.
Definition of Pain
Pain is “an unpleasant sensory and emotional experience
associated with actual or potential tissue damage, or described
in terms of such damage”.
- International association for the study of Pain.
Malignant
Non- malignant
Visceral Somatic pain /cancer
benign pain
pain
Musculo-
Superficial Deep Neuropathic
skeletal
ACUTE PAIN
Acute has a sudden onset, usually subsides quickly and is characterized by sharp,
localized sensations with an identifiable cause.
Lasts > 30 days and occurs after muscle strains and tissue injury such as trauma or
surgery.
A poorly treated pain can cause psychological stress and compromise the immune
system due to the release of endogenous corticosteroids
Acute pain is usually characterized by increased autonomic nervous system activity
resulting in psychological symptoms such as anxiety
Tachypnoea
Pallor
Diaphoresis
Pupil dilation
VISCERAL PAIN
Visceral pain is a type of nociceptive pain that comes from the
internal organs.
Unlike somatic pain it is harder to pinpoint, described as general
aching or squeezing pain
It is caused by the activation of pain receptors in the chest,
abdomen, or pelvic areas.
In cancer patients pain is caused by tumor infiltration,
constipation, radiation & chemotherapy.
SUPERFICIAL PAIN DEEP SOMATIC PAIN
Referred pain from remote Distant organs and Aching and pressing
pathologic sites structures
• TMJ pain
• Osseous pain
• Periodontal pain
AXIS II (psychologic conditions)
Mood disorders
Anxiety disorders
Somatoform disorders
Other conditions
• Psychologic factors affecting a medical condition
Pain Receptors
NOCICEPTORS or PAIN RECEPTORS are sensory receptors that
are activated by noxious insults to peripheral tissues.
The receptive endings of the peripheral pain fibres are free
nerve endings.
These receptive endings are widely distributed in the
Skin
Dental pulp
Periosteum
Meninges
SILENT
UNIMODAL POLYMODAL NOCICEPTORS
NOCICEPTORS NOCICEPTORS These receptors
These These receptors
activated at the
receptors time of
are sensitive to inflammation
respond several varieties
exclusively to only.
of noxious stimuli Upto 40% of C
one modality
i.e. either These do not have fibers and 30% of
noxious a specialized and Aδ fibers are
chemical or simple nerve silent
heat stimuli. endings in the nociceptors.
periphery.
NERVE FIBRES INVOLVED IN PAIN TRANSMISSION
A FIBRES C FIBRES
A – BETA A – DELTA
FIBRES FIBRES
Small & unmyelinated
Large Small Very slow conducting
Myelinated Lightly Respond to all types
Fast
Myelinated of noxious stimuli
conducting Slow Transmit prolonged
Low
conducting dull pain
stimulation Respond to Require high intensity
threshold heat, pressure, stimuli to trigger a
cooling & response
Respond to
chemicals
light touch
Sharp sensation
of pain
SENSITIZATION OF
SUBSTANCES EXITING NOCICEPTORS
STIMULATION OF
NCs HISTAMINE NOCICEPTORS BRADYKININ PGE2
POTASSIUM ATP
PGI2
The neurons of marginal nucleus & substantia gelatinosa form the II order neurons
Fibres from these neurons ascend in the form of the lateral spinothalamic tract
Fibres of fast pain arise from neurons of the marginal nucleus
SECOND ORDER The fibres of slow pain arise from neurons of substantia gelatinosa
NEURONS
The neurons of pain pathway are the neurons in Thalamic nucleus, reticular formation, tectum, gray matter
around the aqueduct of sylvius
THIRD ORDER Axons from these neurons reach the sensory area of cerebral cortex or hypothalamus
NEURONS
PAIN PATHWAYS
ASCENDING PAIN PATHWAY
DESCENDING INHIBITORY PAIN PATHWAY
Pain pathway of Maxillofacial region
5TH cranial nerve or trigeminal nerve is the principle
sensory nerve of head region.
Any stimulation in the area of trigeminal nerve is first
received by both myelinated and unmyelinated fibers,
and conducted as an impulse along afferent fibers of
ophthalmic, maxillary and mandibular branches into
semilunar and gasserian ganglion.
Pain impulse descend from the pons by spinal tract
fibers of trigeminal nerve through the medulla
MECHANISMS OF PAIN
Pain sensation involves a series of complex interactions
between peripheral nerves & CNS.
Pain sensation is modulated by excitatory and inhibitory
NTs released in response to stimuli.
Sensation of pain is composed of 4 basic processes
Transduction
Transmission
Modulation
Perception
TRANSDUCTION
Activation of nociceptor
Intense thermal and mechanical stimuli, noxious chemicals,
noxious cold
Stimulation of inflammatory mediators
Damaged tissue release bradykinin, potassium, histamine,
serotonin and arachidonic acid.
Arachidonic acid produce prostaglandins and leukotrienes.
TRANSMISSON
Process by which peripheral nociceptive information is
relayed to CNS.
First order neuron synapses with the secondary order neuron
from where impulse is carried to higher structures of brain.
Repeated or intense C fibre activation brings specific changes
on N-methyl-D-aspartate receptors resulting in central
sensitization, thus, response of second order neurons increases
as well as size of the receptive field also increases.
MODULATION
It is the mechanism by which transmission of impulse to the brain is
either inhibited or excitated.
Endogenous opioid peptides are naturally occurring paindampening
neurotransmitters and neuromodulators employed in suppression and
modulation of pain because they are present in large quantities in areas
of brain associated with these activities.
PERCEPTION
It is the subjective experience of pain. It is the sum of complex activities
in CNS that may shape the character and intensity of pain perceived and
ascribe meaning to pain.
PAIN THEORIES
Pain theories are proposed to offer the possible physiologic
mechanisms involved in pain. They are as follows
Specificity theory
Pattern theory
Neuro-matrix theory
Gate control theory
SPECIFICITY THEORY
Proposed by Johannes Muller in 1842.
According to this theory pain is a specific modality
equivalent to vision and hearing.
This theory states pain as separate modality evoked by
specific receptors(free nerve endings) that transmit
information to pain centers or regions in the forebrain
where pain is experienced.
PATTERN THEORY
Proposed by Goldscheider in 1894.
According to this theory pain sensation depends on Spatio-
temporal pattern of nerve impulse reaching the brain.
According to Woddell (1962) warmth, cold and pain are words
used to describe reproducible spatio temporal pattern or codes
of neural activity evoked from skin by changes in environment.
The precise pattern of nerve impulse entering the CNS will be
different for different regions, and will vary for person to person
because of normal anatomical variations.
NEUROMATRIX THEORY
This theory was put forward by MELZACK
This theory explains the role of brain in pain as well as the multiple
dimensions and determinants of pain.
According to this theory the brain contains a widely distributed neural
network called the body self Neuromatrix that contains somatosensory,
limbic, & Thalamocortical components
The body self Neuromatrix involves multiple input sources such as
Somatosensory inputs
Other impulses/ inputs affecting the interpretation of the situation
Various components of stress regulation systems
Intrinsic neural inhibitory modulatory circuits
GATE CONTROL MECHANISM
Proposed by MELZACK & WALL IN 1965.
According to this theory, the pain stimuli transmitted by
afferent pain fibres are blocked by GATE MECHANISM
located at the posterior gray horn of the spinal cord
If the gate is open pain is felt, and if the gate is closed pain
is suppressed
Impulses in A – δ & C – fibres can be blocked by
modulated by A – β activity that can selectively block
impulses from being transmitted to the transmission cells
in the spinal cord and then to CNS resulting in no pain
ROLE OF BRAIN IN GATE CONTROL MECHANISM