What is Pain
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Transcript of What is Pain
Andi Husni TANRA
Professor of Anesthesiology
Department of Anesthesiology, IC and Pain Management
Faculty of Medicine Hasanuddin University
Makassar
Introduction to Pain
2
Poisons
Tissue damage
Release of mediators
Stimulation of nociceptors
Transmission to CNS
What is pain?
How do we feel pain? In normal situation!
Noxious
stimulus
Nociceptors
Transduction
Conduction
Modulation
Transmission Pain
Perception
Stimulate
Regarding to the function of pain.
TWO KINDS OF PAIN
*Good Pain, is an alarm symptom, tell us that something
wrong in our body Acute Pain, pain with nociception
(nociceptive pain). alarm protection.
Disini nyeri seperti bel rumah bunyi kl ada tamu
*Bad pain, is a disease entity, no nociception,
nothing wrong but patient feel severe pain makes patient
suffering Chronic Pain.
Disini nyeri seperti bel rumah yg korsleting tidak ada
tamu tapi bel rumah bunyi terus.
The word “pain” derives from latin word “poena” meaning“punishment”.
congenital insensitivity to pain ( chennelopathy)
CHRONIC PAIN vs ACUTE PAIN
Chronic pain is misleading or over simplistic. The key distinction between acute & chronic is not the DURATION of pain, but
chronic pain is pain that PERSIST
BEYOND HEALING BEYOND NOCICEPTION BEYOND EXPECTION
DIFFICULT TO TREAT. (symptom is disproportionate) NO BIOLOGICAL MEANING. IT CAUSED SUFFERING AND BEHAVIOR CHANGES Bad Pain
Phantom Limb Pain After limb amputation
Two type of pain syndrome
Stump pain
Phantom pain
The incidence of phantom pain varies
from 50% - 85%
About 40% of amputees having
severe phantom pain
ACUTE PAIN
Acute pain is pain that
Associated with tissue damage or nociception.
Has biological meaning.
Has tendency to recover as nociception is vanished.
Symptom is slightly proportionate.
It caused protection for further damage Good
Pain
Prototipe dari acute pain postoperative pain
Clinical Features
of Postoperative Pain
ALLODYNIA
HYPERALGESIA
PATHOPHYSIOLOGICAL PAIN
(CLINICAL PAIN)
Vanished after
healing process finished
So pain, between acute & chronic pain
is absolutely different ;
Different in etiology
Different in pathophysiology
Different in diagnosis
Different in treatment
HAROLD MERSKEY (psychiatrics) proposed
definition of pain, which was accepted by
IASP (International Association for Study of Pain 1979)
PAIN IS “AN UNPLEASANT SENSORY AND EMOTIONAL EXPERIENCE
ASSOCIATED WITH ACTUAL OR POTENTIAL TISSUE DAMAGE, OR
DESCRIBED IN TERM OF SUCH DAMAGE”
Nyeri adalah perasaan sensorik dan emosional yang tidak menyenangkan
akibat adanya kerusakan jaringan yang nyata atau yang berpotensi rusak
atau tergambarkan seperti kerusakan tersebut.
The problem lies in the word unpleasant.
Pain is more than unpleasant.
The great merits of this definition
1. Pain is unpleasant sensory and unpleasant emotional
experience. Kata tidak menyenangkan harus ada nyeri
2. Pain usually associated with actual tissue damage
Nociceptive pain or acute pain PAIN WITH
NOCICEPTION
3. Pain may occur with potential tissue damage (noxious
stimulus) PHYSIOLOGICAL PAIN withdrawal- reflex.
4. Pain is described in term of such damage, although nothing
wrong in his/her body but patient feel severe pain,
PAIN WITHOUT NOCICEPTION CHRONIC PAIN
Classification of Pain
Based on Duration: Acute and Chronic.
Based on Clinical Context:
• Postsurgical
• Malignancy related
• Neuropathic
• Degenerative .
Based on Organ
- Headache
-Pelvic pain
-Lowback pain Based on Pathophysiological -Mechanism :
- Nociceptive pain
- Neuropathic pain
Most Accepted Classification:
Nociceptive pain = tissue injury
(Acute pain) Somatic Pain
Visceral Pain
Neuropathic pain = nerve injury
(chronic Pain)
Mechanism of Nociceptive pain.
Noxious
stimulus
Nociceptors
Transduction
Conduction
Modulation
Transmission Pain
Perception
Stimulate
Nociceptive Pain is pain that generated
from nociceptors. Nyeri yang dibangkitkan
dimulai dari nosiseptor
1. NOCICEPTORS
What is a nociceptor? reseptor nyeri
Nociceptors are peripheral sensory neurons that respond selectively to noxious stimuli (Stimulus kuat).
Or A number of receptors/channels that sense damage
VR1 - vanilloid receptor family ASICs - respond to low pH P2X receptors - respond to ATP TRPs receptors – respond temp. Chemical sensors - prostaglandins,
Diciptakan Tuhan guna melindungi diri kita dari bahaya.
TRPVs ASICs TRPs P2X
capsaicin
H+
PGs
EPs
cold warm ATP
COX1/2
ATP
heat
Na+, K+,
Ca2+
channels
DRG
C-fibre
Tissue damage and pain in the periphery
Mechanical?
2. SENSORY NERVE
AFFERENT
Sensory afferent n.f.
connecting receptors to
the CNS
(Centripetal)
Motor afferent n.f. is
connecting CNS to
muscle or gland
(centrifugal).
Sensory Nerve
Afferent
Anatomy of peripheral sensory nerve fibers
A
A C
Dorsal Horn
Dorsal root
ganglion
Peripheral sensory
Nerve fibers
A
A
C
Large
fibers
Small
fibers
Two sensory afferent neurons 1. Large myelinated A fibers, very fast conduction velocity. Respond to
innocuous stimuli
2. Small myelinated A & C unmyelinated fibers, have slow conduction
velocity. Respond to noxious stimuli
Modified by AHT
A
A
C Lateral
Nucleus
proprius
Marginal layer Substantia
gelatinosa Medial
Afferent Synaptic in DHN
Characteristic of A and C-fiber
Polimodal
Nociceptors
A Fiber Rapid Conduction
C-Fiber Slow Conduction
Mechano Thermal
Nociceptors
Glu
First Pain
Secound
Pain
Glu
sP
Two distinct responses to a noxious stimulus
FIRST PAIN and SECOUND PAIN
• First pain: sharp and pricking,
well-localised and brief.
Responded by
mechanoreceptors , conveyed
by Ad fiber.
• Second pain: dull and diffuse
and prolonged . Responded by
polimodal nociceptors ,
conveyed by C fiber C Fiber
A Fiber
First Pain
Secound Pain
Modified by AHT
Although in normal condition A fiber does not response to
noxious stimuli, but it plays a big role in NORMAL
SENSATION.
The Role of A fiber
Without A fiber, any noxious stimuli will perceive
as BURNING PAIN (TN, HZ)
A
1. TRANSDUCTION 2. CONDUCTION
Role of nociceptors and
primary afferent neurons
are:
Process whereby noxious
stimuli are translated
into electrical activity at
the sensory endings of
nerve Heat
Chemical
TRANSDUCTION
TRANSDUCTION
Pressure
1. TRANSDUCTION PROCESS (NOCICEPTORS ACTIVATION and CONDUCTION)
Action Potential
Na+
Ca++
TRP Peptides-
sP, CCK,
CGRP
Ca++ TRP
Generator
Potential
Traumatic
Mediators-
K+, H+,
ATP,PGE
Neural
Mediators-
Epine,
Norepine
Local &
Vescular
Mediators-
Bradykinin,
Cytokines
Histamine,
5HT.
In Creased
Synthesis
Pro
Inflammatory
Cytocaines
-(IL) 1
-IL-6
Modified by AHT
R. Sinatra 2007
“Noxious Soup”
Tissue
Injury
TRP (Transient Receptor Potential) Ion
Channel is a Transducer molecules.
K+ K+
Ca2+
Na+
1. Transduction
4. Transmission 2. Spike Initiation
3. Propagation (conduction)
Modified Meliala, 2006
Transduction and Conduction Process
Mechanical
Thermal
Chemical
Transduction
Conduction
Modulation
Transmission
Persepsion
Neuron I
Neuron II
Neuron III
Modified by AHT
3. MODULATION in DHN
Lehmann, K. A.: From the first stimulus to pain memory. UN. Cologne, 2000
Dorsal Horn neurons of SC Plays a big role in pain perception
Is the first gate to control pain.
Nociception (Pain) is born in DHN
36
Modulation in Dorsal Horn Neurons
Done by Descending neurons & Interneurons
37 Modulation at DH
Postsynaptic
Opioid
Receptors
(-)
(+)
Glutamate
Receptors
Enkephalinergic
Interneuron
(Inhibitory)
Descending
Enkephalinergic
Fiber (Inhibitory)
Presynaptic Opioid
Receptors
(-)
Primary
Nociceptive
Fiber
Spinal Sensory
Neuron
ENK ENK
ENK
ENK
SITES OF ENKEPHALIN BINDING IN SPINAL CORD.
PLAYED BY DESCENDING INHIBITORY AND INTRNEURON INHIBITORY FIBER
Modified by AHT
Modulation
Peranan Modulasi dalam kehidupan
Peran modulasi inilah yang membuat persepsi nyeri menjadi sangat subyektif.
Ransangan yang sama dirasakan berbeda oleh tiap orang. ( latar belakang yang berbeda)
Bahkan R yang sama dirasakan berbeda oleh orang yg sama kr kondisi emasionalnya berbeda.
Suatu Nyeri mamiliki 3 dimensi;
1. Cognitive ( dimana dan intesitas nyeri)
2. Affective ( arti dari suatu nyeri)
3. Emotional ( atensi thp nyeri )
Pain is very Subjective
feeling
Pain has multidimensional experience
1. sensory – discriminative
Identifies the intensity, type and location of pain
2. Affective – motivational
Assessing the injury the meaning of injury
3. Emotional – behavioral component
Attention, mood and behavioral due to pain
1. MODULATION 2. TRANSMISSION
Thus, the role of DHN, is the place
where interaction between afferent
ascendern input and descedern
input.
4. ASCENDING PATHWAYS
Spinothalamic
tract Peripheral
nerve
Dorsal Horn
Dorsal root
ganglion
Pain
Medulation
Ascending
input
Descending
modulation
Peripheral
nociceptors
Trauma
Adapted from Gottschalk A et al. Am Fam Physician. 2001;63:1981, and Kehlet H et al. Anesth Analg. 1993;77:1049.
Conduction
Modified by AHT
Transduction
5. DESCENDING MODULATING
PATHWAYS
Descending
pathways
Ascending
pathways
Brain is a huge
Pharmacetucal
Factory.
Dorsal homs Opioids
NRM LC
PAG
Cortex
Opioids
Descending Modulatory
Systems
5-HT - - Enkephalin - Norepinephrine
Modified by AHT
Begitu kuatnya proses
Desendern sehingga orang ini
seperti tidak punya Otak.
Perception is on the brain, so
No brain no pain.
Pain
Perception Brain
Noxious perception?
A number of theories:
1. Specificity theory by Descartes
(16 century)
2. Gate control theory by Melzack
and Wall (i965)
3. Sensitization theory by Woolf et
al (1990 an)
How pain perception is processed, still obscured, and Where pain perceptions in the brain still unclear.
Limbic Cortex
Sensory Cortex
Thalamus
SS
SS
Pain was faithfully
transmitted from
periphery to brain
1. Specificity theory
Descartes (17th Century)
Modified by AHT
NO BRAIN, NO PAIN
2.GATE CONTROL THEORY by MELZACK and Wall
Ascending Action
System
Large
fibers
Central
Control
Descending
Modulation
Small
fibers Dorsal Horn “Gate”
The Gate control theory of pain processing. T = Second-order transmission cell; SG = substantia
gelatinosa cell.
Modified by AHT
Prof. Hyodo
Prof. Hyodo
3.Sensitization theory , by Woolf et in 1990
:After the tissue injury, sensitization in the
periphery and centrally ns is occurred.
HYPERALGESIA : RANGSANG KUAT YANG NORMAL
DIRASAKAN NYERI KINI LEBIH NYERI
ALLODYNIA: RANGSANG LEMAH YANG NORMAL TIDAK
TERASA NYERI KINI TERASA NYERI
After tissue damage it occurs peripheral
and central sensitization
Increasing Stimulus Intensity
Stimulus response alteration observed with hyperalgesia
No Pain
Allodynia
“Hyperalgesia” Normal
Response
Worst Pain
Tissue Injury Arachidonic Acid
Prostaglandine
Pain
CycloOxyganase
Enzym
-Aspirin
-Ibuprophen
-Ketoprophen
-Ketorolac
-Etc.
Nonsteroidal Anti Inflammatory Drugs (NSAID)
- Paracetamol not NSAID
Anti
Primary hyperalgesia
Secondary hyperalgesia
(allodynia)
So, there are three
possibilities how do
we feel pain.
1. Nociception with Pain
Pain
CNS
Nociception exp. normal situation
Noxious stimulus with Pain
Inhibition
Excitation
Modulation
Pain
CNS
Nociception Noxious stimulus without Pain
Inhibition
Excitation
Example:
Stress Induced Analgesia
X
Modulation
2. Nociception without pain
Pain
CNS
Nociception Pain without noxious stimulus
Inhibition
Excitation
Example: Phantom Pain
Neurophatic Pain
X
Modulation
3. Pain without nociception
New concepts of
ACUTE PAIN TREATMENT
Modify by AHT
Ketamin
Acetaminophen
Transduction
Transduction Modulation
Perception
Transmission
Modulation
Target Point of Analgesic Agents
SEKIAN Terima Kasih Banyak
Semoga Ada Manfaatnya