The document provides an overview of pain pathways, including definitions, classifications, theories, components, and genetics involved in pain transmission. It discusses the various structures and pathways involved in pain processing, from nociceptors and receptors in tissues, to nerve fibers, neurotransmitters, the spinal cord, brainstem, thalamus, and cortex. Both ascending and descending pain pathways are described. Finally, the document outlines assessment and management approaches for acute and chronic pain.

1. PAIN PATHWAYS
Dr.L Vasavi reddy
I MDS

2. CONTENTS
Introduction
Definition
History
Incidence
Classification
Theories of pain pathways
Components of pain transmission
Neural pain pathways
Pain pathways
Genes involved in pain transmission
Applied aspects
Management of pain

3. INTRODUCTION:
• Pain and fear of pain continue to be strongest motivation of patient to seek dental
care
• The head and face are subjected to chronic persistent or recurrent pain more often
than any other part of the body
• Therefore, the dentist responsibility in managing the pain is two fold, first is the
diagnosis and second is therapy for which knowledge on pain pathways is essential

4. HISTORY
• The word pain is derived from ‘poine’ meaning penalty or payment, which certain
religious segments have translated it s synonyms for punishment
• Homer thought that pain was result of arrows shot by god
• Aristotle was the first to distinguish five physical senses considering “pain as
passion of soul”
• Plato described pain as emotional experience more than a localized body
disturbance
• John Bonica- father of pain

5. DEFINITIONS
• Pain is an unpleasant sensory and emotional experience associated with
actual or potential tissue damage or described in terms of such
damage( by International Association for Study of Pain)
• An unpleasant emotional experience usually initiated by noxious
stimulus and transmitted over a specialized neural network to the
central nervous system where it is interpreted as such (Monheim)

6. CLASSIFICATION
According
to pain
intensity
Mild Moderate Severe
According to onset
Spontanoues
Induced
Triggered

7. ACCORDING TO TEMPORAL
RELATION AND DURATION
Intermitte
Continuou
Protracted
Intractable
Reccurent
Remission
periodic

8. ACCORDING TO QUALITIES OF PAIN
Steady pain
Paroxysmal
pain
Bright pain
Dull painItching pain
Pricking
Stinging

9. ACCORDING TO
PAIN
LOCALIZATION
Localised Diffuse
Radiating
Lancinating
Spreading
Enlarging
migrating

11. Fast pain is felt within about 0.1
second after a pain stimulus is applied.
It is also described by many
alternative names, such as sharp pain,
pricking pain, acute pain, and electric
pain.
Slow pain begins only after 1 second or
more and then increases slowly over
many seconds and sometimes even
minutes.
Slow pain also goes by many names,
such as slow burning pain, aching pain,
throbbing pain, nauseous pain, and
chronic pain.
Slow painFast pain

12. THEORIES OF PAIN
• Specificity Theory of
Pain:
Each modality (touch and
pain) is encoded in
separate pathways.
• Intensive Theory (Erb,
1874)
Rather, the number of
impulses in neurons
determines the intensity of
a stimulus.

13. • Pattern Theory of Pain
posits that somatic sense
organs respond to a
dynamic range of
stimulus intensities.
• Gate Control Theory of
Pain proposes that both
large (A-fibers) and small
(C-fibers) synpase onto
cells in the substantia
gelatinosa (SG) and the
1st central transmission
(T) cells.

14. OTHER THEORIES:
Central Summation Theory (Livingstone,
It proposed that the intense stimulation
resulting from the nerve and tissue damage
activates fibers that project to internuncial
neuron pools within the spinal cord creating
abnormal reverberating circuits with self-
activating neurons.
The Fourth Theory of Pain (Hardy, Wolff,
Goodell, 1940s)
It stated that pain was composed of two
components: the perception of pain and the
reaction one has towards it.
Sensory Interaction Theory
(Noordenbos, 1959)
It describes two systems involving
transmission of pain: fast and slow
system.
Biopsychosocial Model of Pain
It states that pain is not simply a
neurophysiological phenomenon, but also
involves social and psychological factors.

15. LEVELS OF PAIN PROCESSING
Nociception: it refers to noxious stimulus originating from sensory receptor.
Pain: it is an unpleasant sensation perceived by cortex as a result of nociceptive input
Suffering: it refers to phenomenon of how human reacts to pain.
Pain behavior: refers to patients audible and visual actions that communicate his
suffering to others

16. COMPONENTS OF PAIN
TRANSMISSION
Receptors
Nerve fibres
Neurotransmitters
Spinal cord
Medulla
Thalamus
Cortex

17. SENSORY RECEPTORS
At distal terminals of afferent
nerves are specialized sensory
receptors that respond to
physical or chemical stimuli.
When they are adequately
stimulated, impulse is
generated in primary afferent
neuron which is carried
centrally to CNS
They are classified as:
• Exteroceptors
• Proprioceptors
• interoceptors

18. Exteroceptors
Merkels corpuscles
Meissner’s corpuscles
Ruffini’s corpuscles
Krause’s corpuscles
Free nerve endings
Proprioceptors
Muscle spindles
Golgi tendon organs
Pacinian corpuscles
Periodontal mechano receptors
Free nerve endings
Interoceptors
Pacinian corpuscles
Free nerve endings

19. NOCICEPTORS
• Nociceptors are receptors in tissues which are activated specifically by painful stimuli.
• The tissue area for which the nociceptor is responsible is receptive field.
• This ‘noxious’ information is transduced by the receptors into an electrical signal and
transmitted from the periphery to the central nervous system along axons.
• There are two types of nociceptors:
A) high-threshold mechanoreceptors (HTM), which respond to mechanical deformation
B) polymodal nociceptors (PMN), which respond to a variety of tissue-damaging inputs:
hydrogen ions (protons) 5-hydoxytryptamine (5-HT) cytokines bradykinin histamine
prostaglandin
• Nociceptors are the free nerve endings of nerve fibres.

20. NEURONS
Nerve fibers can be classified based on different criteria:
1. Depending on number of axons present, unipolar, bipolar
or multipolar
2. Histologically, as myelinated or non-myelinated
3. Functionally, as afferent (sensory) or efferent (motor).
4. Based on diameter and conduction velocity which is known
as Gasser and Erlanger’s classification.
5. Based on the type of neurotransmitter released from their
terminals as adrenergic, cholinergic, dopaminergic, etc.

23. • First order neurons: these are primary afferent neurons
attached to sensory receptors that carry impulses to CNS
• They are three types of afferents: mechanothermal( A delta),
high threshold meachano receptive (A delta), polymodal(c
fibres)
• Second order neurons: these are transmission neurons
• There are three types of second-order neurons in the dorsal
horn: nociceptive specific (NS) - respond selectively to high-
threshold noxious stimuli - found in laminae II and III wide
dynamic range (WDR) - respond to a range of sensory stimuli -
found in laminae V and VI low-threshold (LR) - respond solely
to innocuous stimuli.
• Third order neurons: Third order neurons are in the subcortical
areas. Fibers of these neurons carry the sensory impulses from
subcortical areas to cerebral cortex.

24. SPINAL CORD
• The dorsal horn of the
spinal cord is the site
where the primary
afferent fibres synapse
with second-order
neurons.
• It is also where complex
interactions occur
between excitatory and
inhibitory interneurons
and where descending
inhibitory tracts from
higher centres exert their
effect

25. • The dorsal horn is divided into laminae (called Rexed
laminae).
• Lamina II is also known as the substantia gelatinosa and
this extends from the trigeminal nucleus in the medulla,
to the filum terminale at the caudal end of the spinal
cord.
• C fibres terminate in lamina II and Ad fibres terminate in
laminae I and V.
• Ab fibres (light touch and vibration) enter the cord
medial to the dorsal horn and pass without synapse to
the dorsal columns.
• They give off collateral branches to the dorsal horn
which terminate in several laminae (IIIeV). They also
synapse directly with terminals of unmyelinated C fibres
in lamina II. Laminae II and V are important areas for the
modulation and localization of pain.

26. MEDULLA
• Medulla has a region made up of both
white and gray matter called reticular
formation.
• It is the centre for various nuceli formation
• Reticular formation plays an important
role in monitoring the impulses that travel
the brain.
• It controls the overall activity of brain
either by enhancing or inhibiting the
impulses.

27. THALAMUS
• Thalamus acts as relay
station for most of the
communication between
brain stem, cerebellum and
cerebrum.
• As the impulses arrive at
thalamus it makes
assessment and direct the
impulses to appropriate
regions in higher centres
for interpretation and
response.

28. CORTEX
• Brain areas for perception of pain:
• Sub cortical areas: hypothalamus,
limbic system and thalamus
• Cortical areas: S1 and S2 in the
somatosensory cortex. Insula and the
anterior cingulate cortex

29. NEUROTRANSMITTERS
OF PAIN
• they bathe the nociceptors,
activating and sensitizing them.
• Prostaglandins and bradykinin
sensitize nociceptors to activation
by low-intensity stimuli.
• Histamine and 5-HT cause pain
when directly applied to nerve
endings.
• Hydrogen ions and 5-HT act directly
on ion channels on the cell
membrane, but most of the others
bind to membrane receptors and
activate second-messenger systems
via G proteins.

31. RECEPTOR POTENTIAL
• It leads to development of local
circuit which is later transmitted as
action potential
• It doesn’t obey all or non
phenomenon

32. ACTION POTENTIAL

33. NEURAL PAIN PATHWAYS
Transduction: Noxious stimuli
leads to electrical activity in the
appropriate sensory nerve
ending.
Transmission: Neural event that
carry the nociceptive input into
the central nervous system for
proper processing.
Modulation: Neural impulses
(nociceptive) are changed or
altered before reaching the
higher centers (Cortex).
Perception: Interaction of the
(cortex, thalamus, and limbic
system) higher centers.

34. PAIN PROCESSING
PATHWAYS
• It includes ascending and
descending pathways
• In ascending pathways spino
thalamic and spino reticular
pathways play a major role in
pain transmission to higher
centres.
• Spino thalamic pathways
includes neo spinothalamic and
paleospino thalamic tracts

35. ASCENDING TRACTS

36. NEOSPINOTHALAMIC
TRACT
• Neurotransmitter - Glutamate
• A∂ fibres transmit mechanical and thermal pain.
• Termination in the spinal cord : Lamina I
(Lamina
Marginalis) of the dorsal horn.
• Excite second-order neurons

37. fast type A𝛿 pain fibers
there excite second-order neurons, to long fibers that cross immediately
to the opposite side of the cord through the anterior commissure and
then turn upward, passing to the brain in the anterolateral columns.
terminate
reicular areas of
the brain stem
ventrobasal complex
along with the dorsal
column–medial lemniscal
tract
for tactile sensations.
terminate in the posterior
nuclear
group of the thalamus, which
transmit the signals to
somatosensory cortex.
terminate mainly in lamina marginalis of the dorsal horns

38. Capability of the Nervous System to Localize Fast Pain in the Body.
The fast-sharp type of pain can be localized much more exactly in the different
parts of the body than can slow-chronic pain.
It is believed that glutamate is the neurotransmitter substance secreted in the
spinal cord at the type A𝛿 pain nerve fiber endings.

39. PALEOSPINOTHALAMIC TRACT
• Type C fibres
• Neurotransmitter – Glutamate and
Substance P
• Termination in spinal cord : Lamina II
and Lamina III (Substantia
Gelatinosa)

40. type C pain fibers, transmit some signals from type
A𝛿 fibers
peripheral fibers terminate in the spinal cord almost
entirely in laminae II and III of the dorsal horns,
which together are called the substantia gelatinosa.
pass first through the anterior commissure to the
opposite side of the cord, then upward to the brain in
the anterolateral pathway.
reticular nuclei of the medulla, pons, and
mesencephalon;

41. DESCENDING PAIN
PATHWAY
• Analgesic pathway that interferes with pain
transmission is often considered as
descending pain pathway
• At synaptic level, analgesic fibers release
neurotransmitters and inhibit the pain
transmission before being relayed to brain.
• Neurotransmitters released by the fibers of
analgesic pathway are serotonin and opiate
receptor substances namely enkephalin,
dynorphin and endorphin.

42. FACIAL PAIN PATHWAY
• Facial pain is mainly mediated by trigeminal
nerve

43. Special Capability of Pain Signals to Arouse Overall Brain Excitability.
Electrical stimulation in the reticular areas of the brain stem and in the intralaminar
nuclei of the thalamus, the areas where the slow-suffering type of pain terminates, has a
strong arousal effect on nervous activity throughout the entire brain.
In fact, these two areas constitute part of the brain’s principal “arousal system,”.
This explains why it is almost impossible for a person to sleep when he or she is in
severe pain.

44. GENES INVOLVED IN PAIN

45. APPLIED ASPECTS
1. Analgesia :Analgesia means loss of pain sensation.
2. Hyperalgesia :Hyperalgesia is defined as the increased sensitivity to pain sensation.
3. Paralgesia :Abnormal pain sensation is called paralgesia.

46. ASSESSMENT OF PAIN
Acute pain Chronic pain
The Brief Pain Inventory (BPI)
0–10 NRS
The BPI also asks the patient to rate how
much pain interferes with seven aspects of
life:
(1) general activity
(2) Walking
(3) normal work
(4) relations with other people
(5) Mood
(6) Sleep
(7) enjoyment of life. The BPI asks the
patient to rate the relief they feel from the
current pain treatment.

47. OTHERS
• McGill pain questionnaire
• Grade chronic pain severity scale
• Quantitative sensory testing

48. Sensory stimulation
Analgesics
pychologicalMedcinal therapy
Electro acupuncture
Neo epinephrine blockers
Anti histaminics
tranqulizers
Anti microbials
Analgesic balm
Anti convulsant
Anti inflamatory
Anti deppresant
nuerolytics
Non narcotic
narcotic
adjuvant
To arrest primary pain
output
Interruption in pain cycle
Symapthetic blockage
Trigger point therapy
Dietary supplements
cutaneuous
Local anesthesia
Transcutaneous
percutaneou
Trigger point therapy
Deep heat therapy
exercise
Management of pain

49. REFERENCES:
• Bell’s Orofacial pains
• Guyton textbook of medical physiology
• Sembhulingam physiology text book
• Burkets oral medicine
• Anil Ghom oral medicine
• A K JAIN textbook of physiology
• Moayedi M, Davis KD. Theories of pain: from specificity to gate control. J
Neurophysiol 109: 5–12, 2013.
• The anatomy and physiology of pain by Charlotte E Steeds