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ANATOMY and PHYSIOLOGY

of PAIN.
OBJECTIVES
Nociceptors.
Primary afferent neuron
Dorsal horn Neurons
Ascending pathway
Descending control of pain
Pathophysiology
Peripheral Sensitization
Central Sensitization
Pain perception.
What is Pain.
Pain can be defined as the conscious awareness of
actual or potential tissue injury.
Pain is involving:
1. Nociceptors activation by mediators released from
injured tissue and nerves'.
2. Afferent transmission /conduction to the spinal cord and
processing within the dorsal horn and supra spinal
center.
3. Pain perception is depend on the net result of
interaction between Acendern in put and decendern
control.
4. In general, pain is an alarm mechanism to protect our
body.
Anatomy
Primary afferent neurons
1. Sensory afferent neurons have a unipolar cell body.
2. They are classified into 3 major groups (A,B,C),
according to the fiber size.
3. Group A is further sub-classified into 4
subgroups (A, A, A).
4. Sensory afferent that respond to noxious
stimulation include myelinated A, or unmyelinated
C- fiber.
5. Most A and all C fiber originate as free nerve
endings which is called NOCICEPTORS
Classification
of
Peripheral
nerve

5
1. NOCICEPTORS
What is a nociceptor?

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,
5HT etc
Tissue damage and pain in the periphery
ATP
capsaicin
Mechanical?
heat DRG
COX1/2

H+
cold ATP
PGs warm

C-fibre
TRPVs ASICs EPs TRPs P2X
Na+, K+,
Ca2+
channels

sensitize, activate
Nociceptors;is characterized
by their response;
1. A-delta Mechanothermal nociceptors
Respond to mechanical and thermal stimuli.
display rapid conduction.
Produced first pain and well localized.
Ad fibers respond to this naciceptors.

2. C-fiber Polimodal nociceptors


Respond to mechanical, thermal and chemical.
Slow conduction.
Produced second pain and diffuse.
C fibers respond to this receptor.
Exist in many tissues, skin, muscle, pariosteum, joints, and viscera, except brain.
Characteristic of A and C-fiber

A Fiber
Mechano Rapid Conduction Glu
Thermal
Nociceptors First Pain First
Pain
Secound Pain

C-Fiber
Slow Conduction Glu
Polimodal
Nociceptor sP
Secound
Pain
2. PERIPHERAL SENSORY
AFFERENT FIBERS
Anatomy of peripheral sensory nerve fibers

Large myelinated A

Small myelinated A
Unmyelinated C
A

C A
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

Large
fibers A

Dorsal root
ganglion Dorsal Horn
A
Small
fibers
C Peripheral sensory
Nerve fibers

Modified by AHT
The Role of A fiber
Although in normal condition A fiber does not
response to noxious stimuli, but it plays a big
role in NORMAL SENSATION.

Without A fiber, any noxious stimuli will perceive


as BURNING PAIN (TN, HZ)
Peripheral fibre systems SENSATIONS

SP & CGRP
I NS
peripheral dorsal root IIo
endings ganlgia IIi
III

IV
A
heavily
low V
intensity
myelinated WDR

non-noxious fast conducting


stimuli VI
A
thinly myelinated
intermediate
high intensity
conducting
noxious
stimuli C X
unmyelinated
slow conducting VII

INPUTS
VIII
IX
REFLEXES
It is important to know that two
distinct responses to a noxious
stimulus FIRST PAIN and SECOUND PAIN

First pain: sharp and


pricking, well-localised
and brief. Responded by
A Fiber mechanoreceptors ,
First Pain
conveyed by Ad fiber.
Secound Pain Second pain: dull and
diffuse and prolonged .
Responded by polimodal
C Fiber nociceptors , conveyed by
C fiber

Modified by AHT
Role of nociceptors
and primary afferent
neurons are:

1. TRANSDUCTION
2. CONDUCTION
Noxious Soup
TRANSDUCTION PROCESS
(NOCICEPTORS ACTIVATION)
Local &
Vescular
Mediators- Action Potential
Ca++
Bradykinin,
Cytokines Peptides- TRP Na+
Histamine, sP, CCK,
5HT. CGRP

Traumatic
Tissue Mediators-
Injury K+, H+,
ATP,PGE

In Creased Neural
Synthesis Mediators- TRP Ca++
Pro Epine,
Inflammatory Norepine
Generator
Cytocaines
-(IL) 1
Potential
-IL-6
TRP (Transient Receptor Potential) Ion
Channel is a Transducer molecules. Modified by AHT
R. Sinatra 2007
Pain Perception

Pain

Descending
modulation Dorsal Horn

Ascending Dorsal root Conduction


input ganglion

Transduction
Spinothalamic Peripheral
tract nerve

Trauma
Peripheral
nociceptors

Adapted from Gottschalk A et al. Am Fam Physician. 2001;63:1981, and Kehlet H et al. Anesth Analg. 1993;77:1049.
Modified by AHT
3. DORSAL HORN NEURONS
Dorsal Horn of Spinal cord
Plays a big role in pain perception
Is the first gate to control pain
Nociception (Pain) is born in DHN

Lehmann, K. A.: From the first stimulus to pain memory. UN. Cologne, 2000 21
Dorsal Horn Neurons
Is highly organized center of neurons
The place where afferent input is processed.
The place where terminal endings of primary afferent ( first
order neuron) and receiving neurons (second order neurons)
synapse.
Where interaction between excitatory and inhibitory
system.
Two types of second order nociceptive neurons are found in
DHN.
1. NS (Nociceptive-Specific Neurons )
2. WDR (Wide-Dynamic Range Neurons)
Targets of Primary Afferent Neurons in
the posterior gray (dorsal) horn

NS

WDR

Transmission at DH 23
NS : Respond exclusively to noxious stimuli from A
& C fiber.
WDR :
Respond to both noxious and innocuous stimuli.
May receive afferent input from skin, muscle, joint
and visceral nociceptors referred pain.
Low frequency stimulation of C fiber lead to
gradually increase WDR discharge, until
continuous discharge wind up.
These responsible by NMDA receptors, while
AMPA receptors responsible for short-lasting
depolarization (brief pain).
Neurotransmitters and receptors
on Dorsal Horn

Modulation at DH 25
NEUROTRANSMITTERS
Primary afferent neurons may release one or more excitatory
Amino acid (EAA) such as:
Glutamate
Aspartate, or
Peptide such as
Substance P Neurokinin A
CGRP (Calcitonin Gene-Relate Peptide)
CCK (Cholecystokinin) Somatostatin
Bombezine etc.
EAA mediated rapid short-duration depolarization of second
order neurons.
Peptides produce a delayed and long lasting depolarization.
4. ASCENDING PATHWAYS
Ascending Pathways
5 ascending pathways have been recognized.
1. SPINOTHALAMIC TRACT
Discriminative pathway location of pain
2. SPINORETICULAR TRACT
Emotional aspect of pain (suffering pathway)
3. DORSAL HORN COLUMN TRACT
Transmission of visceral pain
4. SPINOMESENCEPHALIC TRACT
Behavioral response
5. SPINOHYPOTHALAMIC TRACT
Sensationl from the skin, lips & sex organs
SSC FLC SPINOTHALAMIC TRACT
Neo Spino Thalamic Tract direct to
Cortex and
Thalamus
VPL MT
Thalamus SSC Localizing and
discriminative information withdrawal
reflex.
Hypothalamus Pleo Spino Thalamic Tract FLC (Frontal
and Pituitary Sympathetic
PAG Outflow Limbic Cortex) Affecting circulation,
Hypothalamic- respiration, endocrine, emotional,
Midbrain
Pituitary Outflow
behavioral responses (fear, anxiety,
LC
helplessness, avoidance).

Ascending Descending
Peripheral
Pathaways Pathaways
Nociceptor

Brainstem NRM
C-Fiber Sensory
Afferent

NSTT

PSTT Delta Sensory


Afferent

Spinal Cord
Sympathetic
Efferent

A-Alpha Motor
Efferent
Response Cortical
- anxiety
- fear
- apprehension

Response Suprasegmental
- neurohumoral response
- catecholamines
- cortisol
- dll.

Response Segmental
- muclespasm
- vasospasm
- bronchospasm
- decreased gastrointestinal
motility
Response Local
-release pain substances
-inflammation
RESPONSES TO NOXIOUS STIMULI INDUCED BY AN ABDOMINAL SURGERY
5. DESCENDING MODULATING
PATHWAYS
Descending Modulating
Pathways
Those ascending pathways is modulated by descending
modulating pathways in several higher centers;
CEREBRAL CORTEX
THALAMUS
HYPOTHALAMUS
BRAINSTEM/ MIDBRAIN
Periaqueductal gray (PAG)
Nuclei raphe magnus
Locus ceruleus
Sub ceruleus
SPINAL CORD
SSC FLC

Cortex and
Thalamus
VPL MT

Hypothalamus
and Pituitary Sympathetic
PAG Outflow

Hypothalamic-
Pituitary Outflow
Midbrain
LC

Ascending Descending
Peripheral
Pathaways Pathaways
Nociceptor

Brainstem NRM
C-Fiber Sensory
Afferent

NSTT

PSTT Delta Sensory


Afferent

Spinal Cord
Sympathetic
Efferent

A-Alpha Motor
Efferent
SEROTONIN
NEOREPINEPHRINE
Modulation
Descending Pain Control
Cortex
Brain Hypothalamus
Thalamus

Releases
Midbrain PAG Endogenous opioids
GABA
NE

Releases
Brain stem NRM Serotonin
NE

Inhibit
Spinal cord DHN WDR neurons Analgesia
NS neurons
NO BRAIN, NO PAIN
Role of DHN, is the place
where interaction between
afferent ascendern input
and descedern modulation
pain control.

1. MODULATION
2. TRANSMISSION
Perception Pain Perception

Pain

Medulation
Descending
modulation Dorsal Horn

Ascending Dorsal root Conduction


input ganglion

Transduction
Spinothalamic Peripheral
tract nerve

Transmission Trauma
Peripheral
nociceptors

Adapted from Gottschalk A et al. Am Fam Physician. 2001;63:1981, and Kehlet H et al. Anesth Analg. 1993;77:1049.
Modified by AHT
PAIN PERCEPTION
How pain perception is processed, still obscured, and
Where pain perceptions in the brain still unclear.

Noxious perception?
Pain A number of theories:
Perception Brain
SS
1. Specificity theory by Descartes
(16 century)
SS Limbic Cortex

Sensory Cortex
Thalamus
2. Gate control theory by Melzack
and Wall (i965)
3. Sensitization theory by Woolf
et al (1990 an)
1. Specificity theory
Descartes
(17th Century)

Pain was
faithfully
transmitted
from
periphery to
brain
Modified by AHT
2.GATE CONTROL THEORY by MELZACK and Wall

Central Descending
Control Modulation

Large
fibers

+
+ Ascending Action
SG T
System

+

Small
fibers Dorsal Horn Gate

The Gate control theory of pain processing. T = Second-order transmission cell; SG = substantia
gelatinosa cell.
Modified by AHT
3.Sensitization theory by Woolf
After the injury sensitization in the periphery
and centrally is occurred. (Hyperalgesia and
allodynia).
Pain perception is the net process starting
from:
Nociceptor activation
Neural conduction
Spinal transmission
Noxious modulation
Limbic & frontal cortical perception
So, there are three
possibilities how do
we feel pain.
Noxious stimulus with Pain
Pain

Inhibition
CNS Modulation
Excitation

Nociception exp. normal situation


Nociception with Pain
Noxious stimulus without Pain
Pain
X Inhibition
CNS Modulation
Excitation

Example:
Nociception Stress Induced Analgesia

Nociception without pain


Pain without noxious stimulus
Pain

Inhibition
CNS Modulation
Excitation

X Example: Phantom Pain


Nociception Neurophatic Pain

Pain without nociception


6. Peripheral Sensitization
Activation of neciceptor
Nociceptive stimulation

Axon reflex
Primary afferent nerve
vessel

Nocicepto
Redness
r Swelling
Pain
Fever
PGE2
K+HH+ + HT Hist. PGI2 BK NOR
LTB4
Tissue Platelet Mast Membrane Kininogen
cell cell phospholopid

Tissue damage
Chemical intermediaries in nociceptive transduction

produces pain in effect on primary


substance source man afferent

potassium damaged cells ++ activate

serotoin platelets ++ activate

bradykinin plasma kininogen +++ activate

histamine mast cell + activate

prostaglandins arachidonic acid-damaged cell sensitize

leukotrienes arachidonic acid-damaged cell sensitize

substance primary afferent sensitize

Pain: Howard L. Fields p.32


Primary Hyperalgesia
Immuno Cells
Cell injury
Kinins Cytokines Cannabioids
H+ Neurotrophins Opioids
K Histamine Adenosine
5HT
Prostaglandin
Bradikynin

Nociceptors NO
Kinins
Vasculature
Neuropeptides
Primary Afferent Neurones

Prostaglandins
Sympathetic Efferent Neurones
7. Central Sensitization
NMDA RECEPTOR / CHANNEL
IS BLOCKED BY Mg ion

Ca
Na Na
NKr
Gly NMDA AMPA

Mg
Zn PCP

PKC

K K Dickenson, 1994
3 conditions are needed to release Mg
blockade.
NMDA is binding by Glu, Gly and Long depolarisation
Mg
SP Glu Glu
Ca
Na Na
NKr
Gly NMDA AMPA

DEPOLARIZATION
Zn PCP

PKC

K K Dickenson, 1994
When NMDA channel is open large of
Ca and Na influx into the cell
Mg
SP Glu Glu
Ca
Na Na
NKr Gly NMDA AMPA

DEPOLARIZATION
Zn PCP

PKC

K K

Increased excitability
Long term changes Ca
Cell death Dickenson, 1994
Central sensitization Processing in Spinal Cord

Inhibitory
Interneuron

Nociceptor NE

Terminal ending MU

Glu SP SP -
Glu SP
Post Synaptic Membrane of
the Spinal Sensory Neuron
Na+
Na+
Glu Ca++
Glu + SP

Glu Mg++ NMDA

AMPA
Receptor
Receptor NK-1
Receptor
MU
-
Kainate
Receptor Second Messenger
Na+ Fast Prime Slow Prime Formation, (cAMP, PKA)

NMDA Receptor: Requires voltage Ca++


mRNA synthesis, and
dependent priming for activation -
upregulation of inducible
enzymes/ protein
Worst Pain

Hyperalgesia Normal
Response

No Pain
Allodynia

Increasing Stimulus Intensity

Alteration responses due to peripheral & Central sensitization


Nerve fibers
diameter velocity
nerve fiber funtion myelin
/
proprioceptive
motor 12 20 70 120
Tactile sense
A 5 12 70 80
pressure +
spindle fiber 36 15 80
pain temperature 25 12 30
B sympatheic preganglionic 3 3 15 +

d.r. pain 0.4 1 0.5 2


C
S sympathetic postganglionic0.3 1.3 0.7 2.3
Spontaneous Allodynia
Tissue damage Hyperalgesia
pain

PERIPHERAL
ACTIVITY CENTRAL
SENSITIZATION

Decreased Increased
Nerve damage threshold to spontaneous
peripheral Expansion of activity
stimuli receptive
field
Inadequate postoperative
pain management

May produce long term


synapse potentiating in
term of Central sensitization .
Consequence of Prolonged
Central sensitization

Under treatment of postoperative pain


Collapse of the body's pain defenses
Central sensitization

Pain disease
Sandkhler, J.: Preventing Pain Memory. MMW 2002; Special edition 2 62
VISCERAL PAIN
1. Neurophytiological thinking about pain in
general has been dominated by
Sherrington's approach.
PAIN AS PHYSICAL ADJUNCT OF A
PROTECTIVE REFLEX
IT HAS A SURVIVAL VALUE
(Sherrington 1926)
Cara pandang ini berlaku pada Sopratic Pain, tapi toh
pada Visceral Pain
Looks likely that Visceral Pain is not playing a role as
survival protection.
NATURE OF VISCERAL PAIN
2. 1. Is the most common form of pain produced by
disease and one of the most frequent reasons for
patients to seek medial attention.
2. Mechanism of visceral pain is less well understood
than somatic pain. (visceral pain research started
1990)
3. The more we know about mechanism of somatic
and visceral pain, the more realized that these two
processes, while heaving many common features,
also have important differences.
4. Visceral pain is evoked by a stimulus which may not
evoke in somatic pain.
5 CHARACTERISTIC OF VISCERAL PAIN
3. 1. Is not evoked from all visceral (liver, kidneys
or lungs do not have any sensory unless
adjacent structures are also affective.
2. Is not liked to visceral injury.
3. Is referred to other location.
4. Is diffuse and poorly location.
5. Is accompanied by method and autonomic
reflex.
THE DIFFERENT OF
SOMATIC AND
VISCERAL PAIN.
1. Visceral pain can not be evoked
from all visceral.

Some Visceral organs such as the liver, kidneys


or lungs do not evoked any sensory feed back,
unless adjacent structures are also affected (e.g.
cancer in these organs).
We dont know why pain can be evoked by
certain internal stimuli, such as renal or biliary
calculi.
Visceral pain is usually evoked by stimuli that
cause strong contractions of smooth muscle or
ischemic of the viscous.
2. Visceral pain is not linked to
internal injury
Some forms of injury, such as ischemic or inflammation can
evoked visceral pain however these stimuli will not always trigger
pain when applier to certain viscera.
In general visceral pain can be evoked by the following stimuli:
1. Spasm of the smooth muscle in hollow visceral.
2. Distention of hollow visceral.
3. Ischemia.
4. Inflammatory states.
5. Chemical stimuli.
6. Traction, compression and twisting of the mesenteries.
While cutting, crushing or buring which may produce severe
pain of applied in somatic again but not in visceral organ.
3. Visceral pain can be referred to other
locations.

Many form of visceral pain are felt in regions


of the body other than the organ whose
stimulation cause the pain e.g.
The pain of angina is a characteristic
example.
Pain produced by cardiac ischemia will be
felt into left shoulder and arm.
4. Visceral pain is diffuse and poorly
location.

All form of visceral pain are poorly localized and most


are felt in are as considerably larger than the size of
the originating viscous.
It is also a common experience that as the pain
becomes more intense, somatic area in which pain is
felt becomes larger (intestinal pain is felt vaguely
over the entire abdomen).
A classical exception to the poor localization of
visceral pain is the pain of gastro-duodenal peptic
ulcer, which some patients are able to pinpoint to
epigastria with a fingertip.
5. Visceral pain is accompanied by intense
motor and autonomic reflexes.
All form of pain, coetaneous and visceral, will generate
neurophysiologic response include motor and autonomic
reflex. (these response called pseudaffective reaction by
Sherrington 1906)
These response, clinically shows as muscle contractures
and spasm accompanied by tachy cardia BP, sweating
and change motility which contribute greatly to the
patients discomfort. These pseudaffective reaction makes
patients looke more ill than they would be without them.
Walaupun reflex ini memiliki arti klinik, namun tidak bisa
menjadi alasan untuk tidak segera memberi analgetik agar
motor and autonomic responses dapat ditekan to make
patient comfort.
WIDE
WIDE DYNAMIC
DYNAMIC RANGE
RANGE SPINAL
SPINAL
NEURON
NEURON
Glutamate
C
(Subs P)

A NMDAr
Glutamate
A
Glutamate
+ Wind-up Brain
Gene induction

Inhibitory
GABA
-
Fibers
Glycine
Opioids
NA, 5HT
DECENDING CONTROL

All decending control, particularly


endogenern opioid (70%) will.
1. Inhibit pre synaptic release of algesic
neurotransmitters. (glutamate or peptide)
2. Suppression of second order neurons (WDR
and NSD at postsynaptic neurons).
What PAIN is?

What the textbooks


would have you believe
about pain
Noxious (painfull)
stimulus to the body

Tissue
Injury
Descending
Cortex
Modulatory Systems

PAG
Opioids
Opioids

NRM LC

5-HT - - Enkephalin - Norepinephrine

Opioids
Opioids
Dorsal homs

Modified by AHT
Two distinct sensations
(dual pain sensation)

Pain intensity

early sharp, relatively brief


Afiber=first pain pricking sensation

C fiber=second pain
later dull, somewhat
prolonged sensation

Time

Injury
Limbic Cortex

Sensory Cortex
Thalamus
Trauma

Descending Ascending
Pathway Pathways
Central Grey
Nociceptor
Mid Brain
Dorsal
Horn
Noxious Fiber

Spinal Cord
Motor Efferent
Adapted from Julius & Basbaum.
Nature 2001;413(6852):203
Pain Processing in Spinal Cord

Inhibitory
Interneuron

NE
Nociceptor
Terminal ending MU

Glu
SP SP -
Glu
SP
Post Synaptic Membrane of
the Spinal Sensory Neuron

Na+
Na+
Glu
Glu
Mg++
+ SP

Glu NMDA

AMPA
Receptor
Receptor NK-1
Receptor
MU
-
Kainate
Receptor Second Messenger
Na + Fast Prime Slow Prime Formation, (cAMP, PKA)

NMDA Receptor: Requires voltage Ca++


mRNA synthesis, and
dependent priming for activation -
upregulation of inducible
enzymes/ protein

Modified by AHT
NOCICEPTIVE TRANSMISSION

Glu
( SP )
NMDA r

(CGRP)

NO
AA

C-fiber Dorsal Horn Neuron


Cortical structures
It has been long to divide higher neural center
in pain processing into 2 parts:
Somatosensory cortex sensory discriminative
pain
Cingulate cortex affective pain
However, this is maybe an oversimplification,
the role of cortex in PAIN PERCEPTION
remains unclear.
( Philip Siddal )
PAG
( Periaqueductal gray )
Play a big role in pain control modulation,
it may releases:
Endogenous opioids
Enkephalin
Endorphine
Dynorphine
GABA (gamma amino butiric acid)
Norepinephrine
Noxious afferent fibers
A myelinated fiber
Responds to noxious stimuli
C unmyelinated fiber

Both have
free nerve
endings

Nociceptors
ACUTE (NOCICEPTIVE)
PAIN PATHWAYS
A nociception has at least 4 components

1. TRANSDUCTION
2. CONDUCTION
3. TRANSMISSION
3. MODULATION
4. PERCEPTION
Neuron III Persepsion

Transduction

Mechani Conduction/
cal Transmission
Transmission
Modulation
Neuron II
Therm
al
Neuron I
Chemic
al

Modified by AHT
1.TRANSDUCTION (NOCICEPTOR ACTIVATION)

Defines as noxious stimuli are converted into a


calcium ion-(Ca2+) mediated electrical
depolarization within the distal nociceptor
endings.

Note!
Ca++ ion channels is a Generator Potential (gear)
Na+ ion channels is like accelerator (gas)
Ka+ ion channels is like breaker (rem) in automobile.
Transduction and Conduction Process

Ca2+

K+
K+

Na+

1. Transduction 3. Propagation (conduction)


2. Spike Initiation 4. Transmission

Modified Meliala, 2006


TRANSMISSION (spinal
transmission)
Refers to the transfer of noxious impulses
from primary nociceptors cells in the dorsal
horn neurons.
Ad and C fibers are the axons of unipolar
neurons that have distal projections known as
nociceptive field.
Two nociceptive fields in dorsal horn neurons;
1. Nociceptive-specific neurons (NS)
2. Wide dynamic range (WDR)
MODULATION (noxious modulation)

Refers to pain- suppressive mechanism within the spinal


cord dorsal horn neurons and at higher levels of the
brainstem and midbrain.
In the spinal cord, this intrinsic breaking mechanism
inhibits oxious transmission at the first synapse
between the primary noxious afferent and second
order WDR and NS neurons.
Thereby reducing spinothalamic relay of noxious
impulses.
Spinal modulation is mediated by spinal-inter neurons
and terminal descending inhibitory.
Pharmacologic Modalities of
acute pain management
Cyclo-oxygenase inhibitors
Non-specific COX inhibitors(classical NSAIDs)
Selective COX-2 inhibitors, the coxibs
Acetaminophen is probably COX-3
Local anesthetics
Opioids
NMDA antagonists
Ketamine, dextromethorphan
Anti-convulsants
Gabapentin, Pregabalin
What is pain?

Poisons
mechanical , thermal , chemical

Tissue damage

Release of mediators
Hydrogen and potassium ions,
neurotransmitters, kinins, prostaglandins

Stimulation of nociceptors

Transmission to CNS
via afferent pathways
94
Pain
Tissue damage - inflammation
or nociceptive pain
Nerve damage - neuropathy
Headache/period
Central pain
Cancer pain

Co-existence

Acute
Chronic

Most accepted classification:


Nociceptive pain (Acute pain)
Neuropathic pain
mixed pain
psychologic pain
Perception Pain Perception

Pain

Modulation
Descending Conduction
modulation Dorsal Horn Conduction
Ascending Dorsal root
input ganglion

Transduction
Spinothalamic Peripheral
tract nerve
transmission
Trauma
Peripheral
nociceptors

Adapted from Gottschalk A et al. Am Fam Physician. 2001;63:1981, and Kehlet H et al. Anesth Analg. 1993;77:1049.
Modified by AHT
Multimodal Analgesia
OPIOID
- Systemic
PERCEPTION - Epidural
- Subarachnoid
Pain Ketamin, Tramadol,
agonist
LOCAL ANESTHETIC
COX-2, COX-3?
- Epidural
MODULATION -Subarachnoid
Descending
modulation Dorsal Horn -Peripheral nerve block
Ascending
input CONDUCTION/
TRANSNISSION Steroids
LA
COX-1
Spinothalamic
COX-2
Peripheral
tract TRANSDUCTION
nerve
TRANSMISSION

Trauma
Peripheral
nociceptors

No single drug can produce optimal analgesia without adverse effect


Adapted from Gottschalk A et al. Am Fam Physician. 2001;63:1981, and Kehlet H et al. Anesth Analg. 1993;77:1049. Modified by AHT
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