PHYSIOLOGY &

PATHOPHYSIOLOGY OF PAIN
WIWI J - LABORATORY OF ANESTHESIOLOGY
& INTENSIVE THERAPY RS SAIFUL ANWAR MALANG

WHAT IS PAIN?
According to the International Association for the Society of Pain,

Pain is an unpleasant sensory and emotional experience

associated with actual or potential tissue damage, or
described in terms of such damage.
Nyeri adalah persepsi sensorik & pengalaman emosional
yg tidak menyenangkan yang berhubungan dengan
kerusakan jaringan yg aktual atau potensial atau yang
dideskripsikan dengan kerusakan yg serupa.
(Loeser,
2011)

AETIOLOGY : WHAT CAUSES PAIN ?

Pain can be due to a wide variety
of
diseases, disorders and conditions
that range from a mild injury to a
debilitating disease
(Williams,
2011)

ACUTE PAIN
The terms acute and chronic refer exclusively to the time course
of the pain, irrespective of aetiology (Craft, Gordon, and Tiziani, 2011,
p.144).

Acute Pain:

Usually lasts less than 3 months

Sudden onset
Usually know the cause of the pain
Usually well defined
Predicable ending (healing)
Can lead to chronic pain if left untreated

Examples : cut to the finger, broken bone

CHRONIC PAIN
Chronic Pain :
Persistent or recurring pain
Continues for more than 3 months
May last for months or even years
Can be difficult to diagnose and treat
Primary goal is not total pain relief but reducing pain relief

Examples include: arthritis and back pain

PRESENTATION OF PAIN
Acute

Chronic

Often obvious distress

Can be sharp, dull, shocklike,
tingling,
shooting,
radiation, fluctuating in
intensity, and varying in
location (occur in timely
relationship
to
noxious
stimuli)
Comorbid conditions not
usually present
May see HTN, increased
HR, diaphoresis, pallor

Can appear to have no

noticeable suffering
Can be sharp, dull, shocklike,
tingling,
shooting,
radiation, fluctuating in
intensity, and varying in
location (do NOT occur in
timely
relationship
to
noxious stimuli)
Symptoms may change
over time
Usually NO obvious signs

PAIN THRESHOLD
Pain Threshold is the lowest point at which pain can be felt
Entirely subjective
May vary from person to person but changes little in the
same individual over time.

PATHOPHYSIOLOGY
Pain is not a disorder or disease.
A consequential reaction by the body to noxious
stimuli.
Injury
Disease

Pain incorporates
Cognition
Emotion
Behaviour

Simple pathway to the brain;

Transduction
Transmission
Perception
Modulation

PAIN PATHWAYS :
1. Painful Stimuli or tissue damage activate
specialized nerve cells (nociceptors), which in
turn send pain signals to the spinal cord.
2. Pain signals enter the dorsal horn of the spinal
cord, where some are increased or decreased
by the interneuron before continuing up to the
brain.
3. Thoughts, feelings and beliefs change the pain
signals into the individuals experience of
PAIN".
4. Certain parts of the brain generate signals that
travel back down the spinal cord to reduce or
increase pain signals at the interneuron.

PATHOPHYSIOLOGY
Transduction
Process by which afferent nerve endings participate in
translating noxious mechanical, chemical or thermal impulses
into nociceptive impulses.
Strong physical stimuli and disease processes cause chemical
release.
Once activated the chemicals bind to specific receptors.
chemicals such as bradykinin, cholecystokinin and prostaglandins,
activate or sensitize nearby nociceptors
Lead to the generation of Action Potentials (AP)

TRANSDUCTION

PATHOPHYSIOLOGY
Transmission
1st Order Sensory Neurons
Located in the dorsal root ganglia in the posterior of the spinal
cord.
APs are conducted to the CNS primarily via two types of primary
afferent neurons
A delta Fibres "Epricritic Pain"
C Fibres "Protopathic Pain"

2nd Order Sensory Neurons

The impulse crosses the spinal cord and ascends to the thalamus
and branches to the brainstem nuclei via central transmission.
Messages cross the cord and ascend to the thalamus via the
Spinothalamic pathway, heading to the somatosensory cortex,
the insula, frontal lobes and limbic system.

A-DELTA AND C FIBRES

Nerve fibre

Appearance
Type of Pain Epicritic

Information
carried

Sharp pain
(fast pain)
Temperature

Protopathic

Dull pain
(slow pain)
Temperatur
e
Itch

Diameter
(micrometr
es)

1-5

0.2-1.5

Speed of
signal
conduction

5-35 m/sec

0.5-2.0
m/sec

A delta Fibres
"Epricritic Pain"
Mechanical message
Sharp, Fast pain
Thin Myelinated fibres increase
speed of processing

C Fibres
"Protopathic Pain"
Mechanical and Thermal
Stimuli
Slow, dull, long lasting pain
Unmyelinated fibres, slower
response

PERIPHERAL TRANSMISSION

Peripheral transmission

An electron micrograph showing

large myelinated A
small lightly myelinated A fibres
unmyelinated fibers C Fibres.

SYNAPTIC TRANSMISSION

Synaptic
transmission
Action potential synapse at
the dorsal horn of the
spinal cord
Neuroactive excitatory and
inhibitory
neurotransmitters are
released
Lead to generation of
action potentials and
central transmission of pain
signals to higher centres.

PATHOPHYSIOLOGY
Perception
When noxious stimuli is recognised.
Multiple areas of the brain
3rd Order Sensory Neurons
To the higher brain centres of

m Limbic system

Frontal cortex, primary sensory cortex of the post central gyrus of

parietal lobe

Sensory-Discriminative Response
result of activity in the somatosensory and the insular cortex
allows the person to identify the type, intensity and bodily location of the
noxious event.

Affective-Emotional Response
Mediated by the limbic system.
Defines the response and associated behaviour.

PATHOPHYSIOLOGY
Modulation
Dampening or amplifying pain-related neural signals.
Descending input from the brainstem influences central nociceptive
transmission in the spinal cord.

Descending inhibition of nociception through the release of

neurotransmitters such as serotonin, norepinephrine and endogenous
opioids.
Gate Control Theory (Melzack and Wall, 1965)
The body can reduce or increase the degree of perceived pain through
modulation of incoming impulses at a gate located in the dorsal horn of the
spinal cord.
The integration determines whether the gate will be opened or closed, either
increasing or decreasing the intensity of the ascending pain signal.
Psychological variables in the perception of pain, including motivation to
escape pain, and the role of thoughts, emotions, and stress reactions in
increasing or decreasing painful sensations.

Sites of Action
Peripherally

Medications

(at the nociceptor)

Cannabinoids, NSAIDs, Opioids, Tramadol,

Vanilloid receptor antagonists(i.e., capsaicin)

Peripherally Local
anesthetics,

Anticonvulsants (except the gabapentinoids)

(along the nociceptive nerve)

Centrally
(various parts of the brain)

Acetaminophen Anticonvulsants (except the

gabapentinoids), Cannabinoids. Opioids, Tramadol

Descending Inhibitory
pathway in the spinal
cord

Cannabinoids, Opioids, Tramadol, Tricyclic

antidepressants, SHRIs

Dorsal horn of the

spinal cord

Anticonvulsants, Cannabinoids, Gabapentinoids,

NMDA receptor antagonists, Opioids,. Tramadol,
Tricyclic antidepressants, SNRIs

THANK YOU - TERIMA KASIH

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