Pain SensationDr. Hussein Farouk Sakr

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.

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.

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.

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.

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.

Mechanism of stimulation of pain receptors

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.

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.

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.

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 SlowOccurs within 0.1 sec Occurs within 1 sec.Continues for 1 sec. Continues for longer time.Well –localized Diffuse Afferent Aδ Afferent C unmylinatedCarried by the neospinothalamic tract

Carried by the paleospinothalamic tract

Pricking Burning Center in cerebral cortex Center in thalamusBlocked by pressure Blocked by L.A.Initiate withdrawal reflex Initiate autonomic and

emotional reflexes

Can not be summated Can be summated and become intolerable

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

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

Hyperalgesia

Primary SecondarySite 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 reflexStimulation 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:ConvergenceAfferent 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.

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.

Visceral Pain• Pain caused by stimulation of pain rectors located in viscera.• There are two types of visceral pain:

Parietal pain Visceral painPain 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

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

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.

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

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

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

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 the right iliac fossa.

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.

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.

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

Endorphins

Pain

Per

cepti

on

Pain Producing substances

Pain Inhibition