Pain sensation Pain receptors cutaneous pain visceral pain referred pain pain control system

1. Pain Sensation
Dr. Hussein Farouk Sakr

2. Pain Sensation
• Pain is defined as unpleasant discomfortable sensation which when
sever enough is associated with emotional disturbances.
• Significance:
1- Warning signal for tissue damage.
2- Evoke protective reaction: allow the subject to react, get rid and
avoid the reexposure to the injurious agent.

3. Pain Sensation
Reactions
Somatic reactions
Withdrawal reflex
Increased Neuro-
Muscular
excitability
Reflex spasm of
the nearby
muscles
Autonomic Reactions
Sever cutaneous,
deep pain and
visceral pain 
parasympathetic
stimulation
Mild to moderate
cutaneous pain
 sympathetic
stimulation.
Emotional
reactions
worry, anxiety
and depression.

4. Pain Receptors:
• Free Nerve endings (nociceptors) which respond to painful stimuli
that cause tissue damage.
• Classification:
1- Mechanical Pain Rs: respond to strong mechanical stimulus the
produces tissue damage.
2- Chemical Pain Rs: respond to injurious chemical stimuli.
3- Thermal Pain Rs: respond to tissue damage caused by thermal
changes (> 45 and < 10o C).
4- Polymodal: Can respond to any noxious stimuli.

5. Pain Receptors:
• Distribution:
• Pain Rs are widely distributed in the skin, S.C. tissue and in the serous
membrane as dura, peritoneum and pleura.
• Pain Rs decrease to some extent in the deep organs and viscera.
• They are completely absent in the parynchematous organs like the
liver, lung, brain and kidney, so pain arising from these structures will
not appear except after involvement of the serous membranes.

6. Mechanism of Stimulation
Pain Rs are stimulated by tissue damage  that cause
release of chemical substances called Pain Producing
Compounds.
Pain Producing compounds include:
Direct Stimulators: include K+, Histamine, Sertonine, and
Bradykinin are the most potent stimuli for the pain Rs.
Sensitizers: include PGE2 and substance P and they
increase the sensitivity of pain Rs and so they decrease
their threshold.
Substance P is released from the somatic antidromic nerve
causing:
1- V.D. of arterioles  production of spreading flare.
2- Histamine release from the mast cells 
Increases sensitivity of pain Rs.

7. Mechanism of stimulation of pain receptors

8. Non Adaptation of Pain Rs
• Pain receptors are non adapting receptors because they showed
increased sensitivity to their stimulus (Hyperalgesia).
• Non adaptation of Pain receptors produces protective function to
keep the individual informed about the tissue damage and enforces
him to get rid from the noxious agent.

9. Pain threshold
• It is lowest intensity of stimulus that
produces pain when applied for
sufficient period of time.
• Can be detected by using the radiant
heat that produces heating of the
skin.
• The majority of individuals begins to
perceive pain at 450C and all
individuals perceive pain at 470C.
• Peoples do not show significant
differences in their sensitivity to pain,
but there are significant differences in
their emotional reactions.

10. Pain Qualities
• Pricking or cutting pain: sharp, well localized, it is usually cutaneous.
• Burning pain: poorly localized and cutaneous.
• Aching pain: diffuse originating from deep structures.
• Throbbing Pain: characterized by the fluctuating intensity with arterial
pulsation.
• Colicky pain: visceral pain arising spasmodic contractions of the walls
of hollow viscera.

11. Cutaneous pain
• Pain caused by stimulation of the
pain receptors in the skin and S.C.
tissue present in 2 forms
Types of cutaneous pain
Fast Slow
Occurs within 0.1 sec Occurs within 1 sec.
Continues for 1 sec. Continues for longer time.
Well –localized Diffuse
Afferent Aδ Afferent C unmylinated
Carried by the neospinothalamic
tract
Carried by the
paleospinothalamic tract
Pricking Burning
Center in cerebral cortex Center in thalamus
Blocked by pressure Blocked by L.A.
Initiate withdrawal reflex Initiate autonomic and
emotional reflexes
Can not be summated Can be summated and become
intolerable

12. Sensory pathway
• Fast cutaneous pain is carried by
anterolateral system
• First order neuron A delta fibers
terminate on the dorsal horn
nuclei.
• Second order neuron ascend
through the anterolateral system
to reach the postero- ventro
lateral nucleus of the thalamus
• Third order neuron terminates
on the primary sensory cortex.
Sensory pathway of cutaneous pain

13. Hyperalgesia
• Abnormal condition in which the skin reaction to pain is altered or
increased sensitivity of the skin to pain.
Primary hyperalgesia
Non painful stimulus is felt as painful
Secondary hyperalgesia
Painful stimulus is felt as sever pain

14. Hyperalgesia
Primary Secondary
Site In the red inflamed skin around the site of injury. In the healthy skin around the injured area
Change Non painful stimulus is felt as painful Painful stimulus is felt as sever pain
Mechanism
Local axon reflex
Stimulation of the pain receptors leads to release
of substance –P from the somatic antidromic
nerve producing:
- V.D. of arterioles  production of spreading
flare.
- Histamine release from the mast cells.
- Increases sensitivity of pain Rs.
Convergence-Facilitation theory:
Convergence
Afferent from the healthy area converge on the same
neurons that receive pain signals from the injured area
Facilitation:
Impulses from the injuired area cause a state of
stimulation in the central neurons (↑↑↑ excitability)
 magnification of the pain impulses arising from the
area of secondary Hyperalgesia.
Onset 30-60 minutes following cutaneous injury Earlier
Associated with
Mainly with cutaneous pain. With cutaneous, deep and visceral pain.

15. Deep Pain
• Pain arising from stimulation of pain receptors in deep structures, as joints,
ligaments ,tendons, muscles and periostium of bone.
• It is usually caused by ischemia and inflammation
• It is poorly localized and dull aching in character
• It is associated with
1-Depressor effects (sickening reaction) as a result of parasympathetic
stimulation in the form of nausea, decrease heart rate and drop of blood
pressure which may lead to fainting.
2- Reflex spasm of the nearby muscle to limit the movement of the affected
part to minimize pain.
3- Hyperalgesia (tenderness) in the affected deep tissue.

16. Visceral Pain
• Pain caused by stimulation of pain rectors located in viscera.
• There are two types of visceral pain:
Parietal painVisceral pain
Pain arising from the parietal layer of
serous membrane and from the
retroperitoneal organs are carried by both
Aδ & C afferent fibers to reach to the dorsal
horn of the spinal cord to reach C.N.S.
Pain arising from the viscera or visceral
layer of the serous membrane is carried by
the C- afferent fibers which carried by the
autonomic afferent to the dorsal horn of
the spinal cord to reach C.N.S.
Parietal pain is well localized. It is pricking
and sharp
Visceral pain is poorly localized. It is colicky,
burning and even biting

17. Visceral Pain Causes
• Spasmodic contraction of hollow viscus (colic): the rhythmic contraction
of the smooth muscles in the wall of the viscera compress the blood
vessels  decrease blood flow accumulation of metabolites 
increased production of pain producing substances such as lactic acid and
Bradykinin  stimulation of pain Rs.
• Overdistention of hollow viscus: mechanicl overstretch of the wall.
• Ischmia: decrease blood flow accumulation of metabolites  increased
production of pain producing substances such as lactic acid and Bradykinin
 stimulation of pain Rs.
• Chemical irritation: as in peptic ulcer there excess HCL production with
destruction of the gastic mucosa.
• Inflammation: which lower the threshold of pain Rs

18. Ischemic Pain
• Pain caused by the accumulation of the metabolites as a result of
decreased blood flow to muscular organ
• Examples:
1. Angina Pectoris: caused by coronary insufficiency during physical activity,
the cardiac muscle is suffering from O2 lack and inadequate perfusion 
accumulation of metabolites.
2. Intermittent Claudication: caused by decreased blood flow to the skeletal
muscles in patients with atherosclerosis of the blood vessels of the leg.
So, during exercise there is insufficient blood supply to the muscle 
accumulation of metabolites.
3. Muscle Spasm: when the muscle contracts continuously  compression
and occlusion of its blood vessels  insufficient blood supply to the
muscle  accumulation of metabolites.

19. REFERRED PAIN
• Pain which is felt away from its original side.
• It is felt in the area of the skin (dermatome) supplied by the same
segment of the spinal cord that supply the diseased viscus.
• Mechanism of referred pain: Convergence- Projection theory

20. Convergence- Projection theory
• Convergence: Afferent fibers
from the injured viscus
converge on the same higher
centers that receive pain signals
from the site of reference in the
skin.
• Projection: Brain is accustomed
to receive pain signals from the
skin and the stimulation of the
pain centers in the cerebral
cortex means tissue damage in
the skin. Angina pectoris pain is felt in the left shoulder, left are and forearm

21. Convergence- Projection theory
• So, when the same afferent
fibers from viscera conduct
impulses to the brain and are
not different from the somatic
pain impulses.
• Than brain can not detect the
origin and the pain is felt as it
is arising from the skin area
which is supplied by the same
segment of the spinal cord
that supplies the diseased
viscus.
Convergence- Projection theory

22. Cardiac Pain Root of neck Left shoulder Left arm. Left forearm. Left
hand.
Esophageal pain Pharynx , lower neck and epigastrium.
Gastric pain To the epigastrium
Biliary and gall
bladder pain
To the tip of right scapula, right shoulder or even to the
epigastrium.
Renal colic To the inguinal canal and in loin
Uterine Perineum, suprapubic region and lower part of the back.
Appendicitis Early: to the area around the umbilicus.
Late if the parietal peritoneum is affected  localized in

23. Pain Control System
• Special areas in the brain and spinal cord concerned with the
inhibition of the transmission of pain signals and reduce pain
sensation.
It is located in:
1. Periaquiductal gray area around the
aqueduct of sylvius in the midbrain and
pons
2. The raphae magnus nucleus in lower pons
and upper medulla.
3. The nucleus reticularis
paragigantocellularis in medulla.
4. Pain inhibitory complex neurons located
at the tip of the dorsal horn.
Mechanism of activation:
The hypothalamus stimulates  the
Periaquiductal gray area which produce
inhibition of the GABA releasing neurons in the
medulla  (dysinhibitory) stimulation of the
release of sertonine from the raphae magnus
nucleus  stimulation of the Pain inhibitory
complex located at the dorsal horn 
hyperpolarization of the nerve terminal of the
afferent neuron  decrease release of the
chemical transmitter.

24. What is opioids?
Exogenous opioid is morphine.
Endogenous opioids are enkephalin, endorphins and dynorphins.
The endogenous group is the specific chemical transmitter for the opiate receptors  analgesia (pain
relief).
What are opioid receptors?
Delta (δ), Kappa (k) and Muta (μ).
Enkephalin delta receptors.
Endorphins  muta receptors.
Dynorphins  Kappa receptors.
They stop the transmission of pain impulses in CNS.

25. Pain Receptors
Dorsal root ganglion
Spinal cord
Brain Stem
Thalamus
Cerebral Cortex
Hypothalamus
Limbic system
Midbrain (PAG)
Raphae Magnus Nucleus of pons
Endorphins
GABA
Serotonin
Pain Inhibitory complex
Pain Producing substances
PainInhibition