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Pain Pathways: Understanding the Physiology and Classification of Pain
1. Pain and Pain Pathways
Anjali Savita
MDS I
Dept of Conservative Dentistry and
Endodontics
2. “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
4. 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.
5. 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.
6. 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.
“An unpleasant emotional experience usually initiated by
noxious stimulus and transmitted over a specialized neural
network to the CNS where it is interpreted such as.”
- Monheim’s textbook of local anaesthesia
7. History
Derived from Latin word “poena” meaning punishment from
God.
Homer thought pain is due to arrows shot by God.
Aristotle who was first to distinguish five physical senses
considered pain to “ the passion of the soul” that somehow
resulted from intensification of other sensory experience.
Plato contented, pain and pleasure arose from within the
body.
Bible makes reference to pain not only in relationship to
injury and illness but also an anguish of the soul.
8. Incidence of Pain
According to Cohen- it was found that 21.8% of adult in the united states
experiences orofacial pain symptoms within 6 months of study.
The most common pain was toothache, which was estimated to have
occurred in 12.3% of the population.
Dental pain is highly prevalent among children, the association being most
apparent in lower socioeconomic groups with reduced access to care.
The prevalence of dental pain was 35% among all pain.
Dental pain has been associated with many factors, such as low
socioeconomic status, high levels of dental caries and restricted access to
dental services.
10. Characteristic of Pain
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 Weber-
Fechner’s Law.
As per this law magnitude of sensation felt is directly
proportional to log of intensity of stimulus
11. Adaptation
Pain receptors show no adaptation, so the pain continues as
long as receptors are stimulated.
Localization of pain
Pain sensation is somewhat poorly localized, however
superficial pain is comparatively better localized than deep pain.
Influence of the rate of damage on intensity of pain
If rate of damage(tissue injury) is high, intensity of pain is also
high.
13. 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
Tachycardia with hypertension
Pallor
Diaphoresis
Pupil dilation
14. 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.
15. SUPERFICIAL PAIN
It is also known as
cutaneous pain.
It arises from superficial
structures such as skin &
subcutaneous tissues.
It is a sharp, bright pain
with a burning quality and
may be abrupt or slow in
onset.
DEEP SOMATIC PAIN
It originates in deep body
structures such as
periosteum, muscles,
tendons, joints & blood
vessels
Strong pressure, ischemia,
tissue damage act as stimuli
for brain damage
Radiation of pain from
original site of injury occur.
16. CHRONIC PAIN
Chronic pain is defined as pain lasting longer than 3 to 6
months.
It begins when pain persists after the initial injury has
healed.
It is persistent or episodic pain of duration or intensity
that adversely affects the function and well being of the
patient.
It may be nociceptive, inflammatory, neuropathic or
functional in origin.
17. It occurs in 60-90 % of patients
with cancer.
Pain can be related to the tumor
or cancer therapy or may be
idiosyncratic.
Pain may also be found at the
metastasized regions and
treatment interventions may
activate peripheral nociceptors.
Pain can be somatic/visceral
CHRONIC NONCANCER PAIN
Pain may last for many years
and is considered progressive in
nature.
May be nociceptive, neuropathic
or mixed in nature.
CHRONIC MALIGNANT PAIN
18. NEUROPTHIC PAIN
Neuropathic pain is a result of an injury or malfunction of the
nervous system.
It is described as
Aching
Throbbing
Burning
Shooting
Tenderness/ sensitivity of skin
20. MUSCULOSKELETAL PAIN
This a type of chronic non cancer pain occurring due to
musculoskeletal disorders such as
Rheumatoid arthritis
Osteoarthritis
Fibromyalgia
Peripheral neuropathies
21. BASED ON TRANSMISSION
FAST PAIN
Felt about 0.1 sec after a
painful stimulus is applied.
It is described as sharp pain,
pricking pain, acute & electric
pain
Fast sharp pain is not felt in
most deeper tissues of the
body.
Due to activation of Aδ fibres
SLOW PAIN
Usually begins after 1 sec or
more and may range from
seconds to minutes.
Described as slow, burning,
aching, throbbing, nauseous
pain and chronic pain
Associated with tissue
destruction.
Due to activation of C fibres
22. OTHER TYPES OF PAIN
REFERRED PAIN
Pain that originate due to
irritation of a visceral organ and
felt not in organ but in some other
somatic structure as well which
has innervated by the same neural
segment.
Usually applies to pain that
originates from the viscera
E.g. The pain associated with MI
commonly is referred to the left
shoulder arm, neck & chest.
BREAKTHROUGH PAIN
Pain is intermittent, transitory.
Usually lasts from minutes to
hours and can interfere with
functioning.
E.g. Neuropathic pain, Lower
back pain
23.
24. Practical clinical classification of cranio facial pain
General Classification Origin of Pain Quality of Pain
Extra cranial Structure Craniofacial region varies
Referred pain from remote
pathologic sites
Distant organs and
structures
Aching and pressing
Intracranial pathosis Brain and related
structures
Varies
varies
Neurovascular Blood vessels Throbbing, Pulsing,
Pounding
25. General Classification Origin of Pain Quality of Pain
Neuropathic Sensory nervous
system
Shooting, sharp,
burning pain
Causalgic Sympathatic nervous
system
Burning
Muscular Muscles Deep aching, tight
27. AXIS II (psychologic conditions)
Mood disorders
Anxiety disorders
Somatoform disorders
Other conditions
• Psychologic factors affecting a medical condition
28. 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
29.
30.
31. SILENT
NOCICEPTORS
These receptors
activated at the
time of
inflammation
only.
Upto 40% of C
fibers and 30% of
Aδ fibers are
silent
nociceptors.
UNIMODAL
NOCICEPTOR
S
These
receptors
respond
exclusively to
one modality
i.e. either
noxious
chemical or
heat stimuli.
POLYMODAL
NOCICEPTORS
These receptors
are sensitive to
several varieties
of noxious stimuli
These do not have
a specialized and
simple nerve
endings in the
periphery.
32. NERVE FIBRES INVOLVED IN PAIN TRANSMISSION
A FIBRES
A – BETA
FIBRES
Large
Myelinated
Fast
conducting
Low
stimulation
threshold
Respond to
light touch
C FIBRES
Small & unmyelinated
Very slow conducting
Respond to all types
of noxious stimuli
Transmit prolonged
dull pain
Require high intensity
stimuli to trigger a
response
A – DELTA
FIBRES
Small
Lightly
Myelinated
Slow
conducting
Respond to
heat, pressure,
cooling &
chemicals
Sharp sensation
of pain
33.
34. NEURO TRANSMITTER S INVOLVED IN PAIN
ACTIVATION OF NOCICEPTORS BY INTERACTING WITH OTHER
CHEMICAL MEDIATORS
PGI2
LTs
SUBSTANCES EXITING NCs
HISTAMINE POTASSIUM
ATP
STIMULATION OF
NOCICEPTORS BRADYKININ
DISCHARGE OF PAIN
RELEASING SUBSTANCES
BY NOCICEPTORS
SUBSTANCE – P
GLUTAMATE
SENSITIZATION OF
NOCICEPTORS
PGE2
PGI2
35. PATHWAYS OF PAIN SENSATION
The pathways of pain sensation are as follows
Pathway from skin & deeper tissues
Pathway from face – pain sensation is carried by trigeminal nerve
Pathway from viscera – pain sensation from thoracic &
abdominal viscera are transmitted by sympathetic nerves & from
oesophagus, trachea & pharynx by glossopharyngeal nerves
Pathway from pelvic region – conveyed by sacral
parasympathetic nerves
36. PATHWAY FROM SKIN & DEEPER TISSUES
FIRST
FIRST ORDER
NEURONS
These are the cells in the posterior nerve root ganglia, receive impulses from pain receptors through dendrites
These impulses are transmitted through the axons to spinal cord
Impulses are transmitted by Aδ fibre or C fibres
SECOND ORDER
NEURONS
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
The fibres of slow pain arise from neurons of substantia gelatinosa
THIRD ORDER
NEURONS
The neurons of pain pathway are the neurons in Thalamic nucleus, reticular formation, tectum, gray matter
around the aqueduct of sylvius
Axons from these neurons reach the sensory area of cerebral cortex or hypothalamus
39. 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
40.
41. 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
42. 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.
43. 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.
44. 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.
45.
46. 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
47. 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.
48. 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.
49. 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
50. 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
51. ROLE OF BRAIN IN GATE CONTROL MECHANISM
Gates in spinal cord are
open
Pain signals reach the
thalamus through lateral
spinothalamic tract
Signals are processed in
thalamus
Signal are sent to sensory
cortex & perception of
pain occurs in cortex
Signals are sent from
cortex back to spinal cord
and the gate is closed by
releasing pain relievers
such as opioid peptides
Minimizing the
severity & extent of
pain
52.
53. Tooth pulp pain
Exposure of dentinal tubules causes toothache &
other non noxious sensation.
Both Aδ & C fibers respond to stimuli in dentine
Transmission of stimuli across dentin, mediated by
movement of fluid in dentinal tubules.
Fibers terminate at medullary dorsal horn &
synapse and also at trigeminal sensory nucleus
54. From trigeminal nucleus send to thalamus & sensory
cortex.
Pulpal innervation are capable of regenerating &
reinnervating
55. Conclusion
Anxiety is determinant for pain during dental care & pain
is related to local anesthetic procedures. There are
evidences that dentists attitude are determinants for pain.
56. References
Essential of oral physiology- Robert M Bradley
Textbook of medical physiology- Guyton & Hall
Essential of medical physiology- K.Sembulingam & Prema Sembulingam.
Textbook of human physiology- S Chand
Determinants of painful experience during dental treatment- Ruth Suzanne et al
Rev.Dor 2012;13(4)
Case report study on Brown sequard syndrome- Ponachi et al Neurology Asia
2007;12;65-67
Anatomy, physiology & pharmacology of pain- Ryan Moffat, Colin P.Rae anesthesia
& intensive care medicine; 2010;12(1)