pain sensation. hussein farouk sakr
Post on 23-Feb-2017
31 Views
Preview:
TRANSCRIPT
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
top related