how the pain pathway works ? how to learn it easy and simple way of presentation

1. PAIN PATHWAY
PARVA DAVE
M.PHARM SEM- 2
KBIPER

2. WHAT IS PAIN ?
Pain is a difficult word to define
Patients use different words to describe pain
eg.
Aching, Pins and needles,Pricking, Biting

3. 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
IASP – International Association for the
Study of Pain 2011

4. PAIN IS..
Pain is
subjective
protective
and it is modified by developmental, behavioural,
personality and cultural factors
It is a symptom
Associated signs are crying, sweating, increased heart
rate, blood pressure, behavioural changes etc

5. Measurement of pain
It is difficult to describe pain although we know what it
is
It is difficult to measure pain
visual analogue scale (VAS) is used

6. PAIN TERMINOLOGY
Hyperalgesia
Increased pain from a stimulus that normally provokes pain
Hyperaesthesia
Increased sensitivity to stimulation, excluding the special
senses (increased cutaneous sensibility to thermal sensation
without pain )
Paraesthesia
An abnormal sensation, whether spontaneous or evoked
Anaesthesia
A loss of sensation resulting from pharmacologic depression
of nerve function or from neurological dysfunction
Neuralgia
Pain in the distribution of a nerve or nerves
Analgesia
Absence of pain in response to a normally painful stimulus
Allodynia
Pain due to a stimulus that does not normally provoke pain

7. PAIN TERMINOLOGY
Neuropathic Pain
Pain caused by a lesion or disease of the somatosensory
nervous system
Nociceptive pain
Pain that arises from actual or threatened damage to non-
neural tissue and is due to the activation of nociceptors
Visceral pain
Pain arising from visceral organs (e.g., heart, lungs,
gastrointestinal tract, liver, gallbladder, kidneys, bladder).
Neuropathy
A disturbance of function or pathological change in a nerve: in
one nerve, mononeuropathy; in several nerves, mononeuropathy
multiplex; if diffuse and bilateral, polyneuropathy
Nociception
The neural process of encoding noxious stimuli
Noxious stimulus
A stimulus that is damaging or threatens damage to normal
tissues.

8. STIMULI
Physical
pressure etc
Electrical
Thermal
cold, hot
Chemical
H+, lactic acid, K+, histamine, bradykinin, serotonin,
leucotrines, acetylcholine, proteolytic enzymes, capsiacin
Prostaglandins (PGE2)
Cannot directly stimulate nociceptors
Increase the sensitivity of nociceptors for other stimuli (decrease the
threshold)

9. RECEPTORS
 There are no specialised receptors
 Pain receptors are called nociceptors
 A sensory receptor that is capable of transducing and
encoding noxious stimuli
 Nociceptors are free nerve endings
 Free nerve endings are distributed everywhere
 both somatic and visceral tissues
 except brain tissue and lung parenchyma

10. RECEPTORS
Nociceptors are very slowly adapting type
Different types of nociceptors
Some respond to one stimulus
Some respond to many stimuli (polymodal)
Some may not respond to the standard stimuli
(silent nociceptors)
they respond only when inflammatory substances are
present
Capsaicin receptor (TRPV1 receptor)
Respond to capsaicin, heat, low pH
Stimulation leads to painful, burning sensation

11. CLASSIFICATION OF PAIN
Based on source/ location/ referral & duration
ACUTE PAIN /
TRAUMATIC PAIN
CHRONIC PAIN
VISCERAL
/SPLANCNIC
PAIN
SOMATIC PAIN MALIGNANT PAIN
OR
CANCER PAIN
NON – MALIGNANT
PAIN
OR
BENIGN PAIN
SUPERFICIAL PAIN
OR
CUTANEOUS PAIN
DEEP SOMATIC
PAIN
MUSCULOSKELETAL
PAIN
NEUROPATHIC PAIN

12. Nerve pathways carrying pain signals to the
brain
Pain signals enter the spinal cord
First synapse is present in the
dorsal horn of the spinal cord
Then the second order neuron
travels through the lateral
spinothalamic tracts

13. afferent fibres
two types
A (thin myelinated)
C (unmyelinated)

14. Nociceptive Pathways
Fast
A Delta Fibers
Glutamate
Neospinothalamic
Mechanical, Thermal
Good Localization
Sharp, Pricking
Terminate in VB
Complex of Thalamus

15. SENSORY NEURONS
SUPERFICAL
1ST
NEURONE synapses
2ND
NEURONE
fibersfromthethalamus
3RD
NEURONE

16. Pathophysiology of pain
Pain sensations could arise due to
Inflammation of the nerves (neuritis)
Injury to the nerves and nerve endings with scar
formation (disk prolapse)
Injury to the structures in the spinal cord, thalamus or
cortical areas that process pain information (spinal
trauma)
Abnormal activity in the nerve circuits that is perceived
as pain (phantom limb pain)
Nerve invasion, for example by cancer (brachial
plexopathy)

18. central connections
substantia
gelatinosa
Neurotransmitter at the first synapse of the pain
pathway is substance P
afferent fibre enters the spinal cord
synapses in laminae ii,iii
substantia gelatinosa

19. From the site of pain generation, i.e. from the periphery, the
pain senses are carried by Aδ & C fibres.
Their cell bodies are situated in the dorsal root ganglion.
The central processes of the neuron, lying in the ‘sensory root’
of the spinal nerve enter the dorsal horn to terminate in the SG
( Substantia gelatinosa), situated in the tip of dorsal horn.
From the SG, next order ( i.e. 2nd order) neuron arises, crosses
to the opposite side, then moves up through the white matter
of spinal cord to reach the brain.
ascending pathway

20. i) Most of these 2nd order neurons travel up as spinothalamic
tract (STT), then ultimately terminate in the proper area of
thalamus, from these specific nuclei of thalamus, next order
neurons arise to terminate on the cerebral cortex, at areas SI
& SII as well as cingulate gyrus (which is the key area for
production of some emotions).
At SG, there is a synapse between 1st order & 2nd order
neuron. Also there is synapse of 2nd & 3rd order neuron at
thalamus.
The NT (neurotransmitter ) at the synapse between Aδ fiber
& 2nd order neuron at SG is glutamate while the NT between
C fiber & 2nd order neuron (slow pain) at SGR is substance
P.

21. Other 2nd order neurons, from SG also are known, & they
also cross to the opposite side to reach different areas of
brain.
The tip of dorsal horn, particularly the SG plays a key role
in modification of pain perception. It is called a gate. As a
gate can be shut/ partially opened/ fully opened to control
incoming traffic, so also behaves the SG controlling the
incoming traffic of pain.

22. ascending pathway
• crosses the midline
• ascends up as the lateral spinothalamic tract
Pain
lateral
spinothalamic
tract
C fibre
substantia
gelatinosa

23. PAIN PATHWAY

24. SUB PATHWAYS OF PAIN
• Spinothalamic - Major
Neo- Fast (A Delta)
Paleo- Slow (C Fibers)
• Spinoreticular
• Spinomesencephalic
• Spinocervica(MostlyTactile)
• Dorsal Columns (Mostly Tactile)

25. FAST PAIN
Neospinothalamic Tract for Fast Pain
The fast type A(δ) pain fibers transmit mainly mechanical
and acute thermal pain.
They terminate mainly in lamina I at the dorsal horn and
these excite second order neurons of the neospinothalamic
tract.

26. SLOW PAIN
Paleospinothalamic tract for Slow Pain
This pathway transmits pain mainly from peripheral slow
chronic Type C pain fibers.
In this pathway, the peripheral fibers terminate almost entirely
in lamina II and III of dorsal horns of spinal cord, together
called as substantia gelatinosa.

27. CONTD..
Axons of secondary neurons emerge from the spinal nucleus,
cross the midline and ascend to join fibers of mesencephalic
nucleus to form trigeminal lemniscus or spinothalamic tract
of 5th nerve.
These tracts continue upward and terminate in the postero
ventral nucleus of thalamus. From here it is transmitted to
posterocentral convolutions of cortex.

29. P
A
I
N
P
A
T
H
W
A
Y

30. Descending pain modulatory system
several lines of experimental evidence show
the presence of descending pain modulatory
system
stimulus produced analgesia (Reynolds)
stimulation of certain areas in the brain stem was known to
decrease the neuronal transmission along the spinothalamic
tract
discovery of morphine receptors
they were known to be present in the brain stem areas
discovery of endogenous opioid peptides
eg. Endorphines, enkephalins, dynorphin

31. midbrain
pons
medulla
spinal cord
periaqueductal
grey nucleus
nucleus raphe
magnus
substantia gelatinosa

32. THEORY OF PAIN
Intensity theory
touch
pain
There are two
different
pathways for
touch and pain
Specificity theory
touch pain
There is a single pathway for touch
and pain
Less intensity produces touch
Increased intensity produces pain

33. GATE THEORY
This explains how pain can be relieved very quickly by a neural mechanism
First described by P.D. Wall & Melzack (1965)
“There is an interaction between pain fibres and touch fibre input at the spinal
cord level in the form of a ‘gating mechanism’

34. GATE THEORY
Pain is felt
gate is
openedWhen pain fibre is stimulated, gate will
be opened & pain is felt

35. GATE THEORY
When pain and touch fibres are stimulated together, gate will be closed
& pain is not felt