PAIN – SOME FACTS
Dr. S. Parthasarathy
MD., DA., DNB, MD (Acu), Dip. Diab. DCA, Dip. Software
statistics
DEFINITION

An unpleasant sensory and emotional
experience associated with actual or potential
tissue damage, or described in terms of such
damage.

ISSP definition
SOME SAY AS
An unpleasant sensation, occurring in varying
degrees of severity as a consequence of injury,
disease, or emotional disorder.
 pain always has a subjective component

MARGO MCCAFFREY

Whatever the patient says hurts.
WHAT IS NOCICEPTION ??

Nociception is the activation of a nociceptor by
a potentially tissue-damaging (noxious)
stimulus. It is the first step in the pain pathway
WHAT IS A NOCICEPTOR ??

nociceptor is a specialized, neurologic receptor
that is capable of differentiating between
innocuous and noxious stimuli

Terminals of A delta and C fibres
ANALGESIA

Patient has no pain

But the noxious stimulus is there

Anaesthesia – all sensory modalities gone

While analgesia – only pain
PARAESTHESIA

Abnormal sensation

Spontaneous or evoked
Painful or painless
 Painful paraesthesia is dysaesthesia
 Formication is a form of paresthesia in which
the patient feels as though bugs are crawling

ANAESTHESIA DOLOROSA
pain is felt in an area that is otherwise numb or
desensitized
Trigeminal neuralgia
Trigeminal nerve is ablated
no sensation
but suddenly shooting pain comes

HYPERPATHIA
hyperpathia refers to an abnormally intense
pain response to repetitive stimuli.
 Usually hyperpathic area of skin is not sensitive
to a simple stimulus but over responds to
multiple stimuli
 Pin prick

ALGOGENS

Histamines, substance P, potassium, and
prostaglandins, bradykinin, 5 HT are examples
of algogenic substances

Produced or injected – nociception
HYPERALGESIASHIFT OF THE STIMULUS PAIN RESPONSE
CURVE TO THE LEFT

P
A
I
n


stimulus


Primary
Pain to a non noxious
stimulus in the area of
injury
Pharyngitis – swallowing –
painful
Secondary
Pain to a non noxious
stimulus in the area by the
side or encircling the injury
PRIMARY
Starts within minutes
 Area of injury
 Sensitive to heat and
mechanical
 Peripheral
sensitization

SECONDARY
Delayed onset
 Wider area
 Only thermal
 Central role

PRIMARY HYPERALGESIA – MECHANISMS
Expansion of receptive field of nociceptor
 Sensitization of nociceptor
 Loss of central inhibition

Increased CAMP levels
 Activation of protein kinase C

SECONDARY HYPERALGESIA
Antidromic release of algogens
 Dorsal horn neurons – sensitive
 WDR neurons – plastic changes

Sometimes irreversible
 Post op pain - !!!

SENSITIZATION
 shift
of the
stimulus - nerve
fibre response
curve to the left
F
I
B
r
e
s
stimulus
SENSITIZATION
Sensitization is a state in which a peripheral
receptor or a central neuron either responds to
stimuli in a more intense fashion than it would
under baseline conditions or responds to a
stimulus to which it is normally insensitive.
Sensitization occurs both at the level of the
nociceptor in the periphery and at the level of
the second-order neuron in the spinal cord
CLASSIFY
PAIN
TYPES OF PAIN
Nociceptive
 Somatic
 Visceral

 Nonnociceptive
Peripheral
 Central
 Psychogenic

NOCICEPTIVE – SOMATIC
Dull or sharp
 Localized
 Increased with movement


Eg. Tooth ache
SKIN, MUSCLE, BONE, JOINT ETC….
VISCERAL NOCICEPTION
autonomic sensations
including nausea,
vomiting, and
diaphoresis.
There are often
cutaneous referral
sites
NEUROPATHIC

burning, electrical, and numbing

Intervening normal
Sudden
 Post herpetic, trigeminal, glossopharyngeal

CENTRAL PAIN
Central pain syndrome is a neurological
condition caused by damage or malfunction in
the Central Nervous System (CNS) which
causes a sensitization of the pain system.
Trauma, tumors, stroke, Multiple Sclerosis,
Parkinson's disease, or epilepsy .
 Pain can either be relegated to a specific part
of the body or affect the body as a whole.

DEJERINE ROUSSY SYNDROME

severe, persistent, paroxysmal, often
intolerable, pains on the hemiplegic side, not
yielding to any analgesic treatment
THEORIES HAVE BEEN PROPOSEDNEUROPATHIC PAIN
that state there are specific cellular and molecular
changes that affect membrane excitability and
induce new gene expression after nerve injury,
thereby allowing for enhanced responses to future
stimulation.
 the ectopic impulses of neuroma, changes of
sodium and calcium channels in injured nerves,
sympathetic activation, and deficient central
inhibitory pathway contribute to the mechanisms
of neuropathic pain

PSYCHOGENIC PAIN
Psychogenic pain, also called psychalgia, is
pain that is caused by increased, or prolonged
by mental, emotional, or behavioural factors
 Headache, back pain, or stomach pain are
some of the most common types of
psychogenic pain.
 It accompanies or induced by social rejection,
broken heart, grief, love sickness, or other such
emotional events.

PSYCHOGENIC PAIN
No nociception
 No neuropathic mechanism

But some evidence of psychologic symptoms to
meet criteria for somatoform pain disorder,
depression,
 Usually chronic

WHY DO WE NEED TO CLASSIFY PAIN ??

Origin of pain

Treatment modalities

Prognosis
TEMPORAL CLASSIFICATION
Acute
 Acute pain is temporally related to injury and
resolves during the appropriate healing period
 Chronic
 pain that persists for more than 3 months or
that outlasts theusual healing process.
 Recurrent
 Duodenal ulcer

OTHER CLASSIFICATIONS
Etiology
 Arthritic
 Cancer
 Site
 Appendix
 Mastitits

HISTORY AND THEORY
Aristotle believed that pain was due to evil spirits
entering the body through injury,
 Hippocrates believed that it was due to an
imbalance in vital fluids.
 it was thought that pain originated outside the
body, perhaps as a punishment from God
 In 1644, René Descartes theorized that pain was
a disturbance that passed down along nerve fibers
until the disturbance reached the brain

THEORIES OF PAIN - SPECIFICITY THEORY
body has a separate sensory system for
perceiving pain just as it does for hearing and
vision— Von Frey (1895)
 and this system contains its own special
receptors for detecting pain stimuli, its own
peripheral nerves and pathway to the brain,
and its own area of the brain for processing
pain signals

SPECIFICITY THEORY


when someone pulls
the rope to ring the
bell, the bell rings in
the tower.
Proved not correct
PATTERN THEORY- GOLDSCHNEIDER (1920)
there is no separate system for perceiving pain,
receptors for pain are shared with other senses,
such as of touch.
 people feel pain when certain patterns of
neural activity occur.

OTHER THEORIES
Wilhelm Erb's (1874) "intensive" theory, that a
pain signal can be generated by intense
enough stimulation of any sensory receptor,
has been soundly disproved
 Central processing theory
 Inputs – same but the central processing
differs to produce pain

MELZACK WALL GATE CONTROL THEORY

pain stimulation is carried by small, slow fibers
that enter the dorsal horn of the spinal
cordWall highlighted that pain messages are
carried by the specific nerve fibres
that can be blocked before reaching the brain
by the actions of other nerves and
psychological factors
THE GATE OPENS AND CLOSES
THE GATE CONTROL THEORY
The gate control theory states that non painful
stimulus such as distraction competes with the
painful impulse to reach the brain.
 This rivlary limits the number of impulses that
can be transmitted in the brain by creating the
hypothetical gate
 Distraction – mechanical , endorphins,
psychological
 Only theory – multifaceted pain approach

THE IDEA IS

if the large fibers remain un stimulated,
the pain signal will be propagated, but if
they are activated, they act as an
electrical gate, blocking the transmission
of pain up the C fiber.

How is pain perceived ??
TYPES OF FIBRES MYELIN –
DIA MM
VELOCITY MM/S
Aα Proprio, somatic Motor yes 12–20
Aβ Touch, pressure yes
5–12
Aγ Motor muscle spindle Yes
3–6
Aδ Pain, cold, touch Yes
2–5
B Preganglionic autonomic Yes
3
C Pain, temperature,No
0.4–1.2
70–120
30–70
15–30
12–30
3–15
0.5–2
PAIN STARTS
Pain receptors (nociceptors)
 The sensation of pain then travels from the
periphery to the spinal cord along A-delta and C
fibers
 Lissauer’s tract
 synapse on second order neurons in substantia
gelatinosa in dorsal horn (second order neuron)

Spino thalamic tract
 (Neo and paleo)
 crossing via the anterior white commissure
before ascending contralaterally.
 Before reaching the brain, the spinothalamic
tract splits into
 lateral neospinothalamic tract and
 medial paleospinothalamic tract


Neo - posterolateral nucleus of the thalamus

Paleo spinothalamic neurons carry information
from C fibers and terminate throughout the
brain stem, a tenth of them in the thalamus
and the rest in the medulla, pons and
periaqueductal grey matter
OTHER SECOND ORDER NEURONS
Spino mesencephalic
 Midbrain – behavioural responses to pain


Spino reticular
Alerting and arousal motivational aspects -pain
 Pontine and medullary reticular formation


Third order neurons from thalamus to cortex

anterior cingulate cortex (emotional aspect )

Somatosensory cortex
SIMPLE NEUROANATOMY OF PAIN
DESCENDING INFLUENCE
DESCENDING INFLUENCE

In 1858 Bernard found that spinal afferents
can be modified by supraspinally organized
systems.

Three and three
Brain ,thalamus and brainstem
 PAG, LC, NRM
 Serotonin , noradrenaline and opioids

Additional
 GABA , glutamate and acetyl choline

COX ET AL
Medial forebrain
 Lateral hypothalamus


Electrical stimulation attenuated foot pain
ESSENTIAL NUCLEI
Periaqueductal grey
 PAG – extensive connections


Opioids
NUCLEUS LOCUS CERULEUS
Pons
 Projection to hippocampus ,spinal cord and
cortex
 Noradrenergic system

NUCLEUS RAPHE MAGNUS
Medulla
 Serotonin – originally


But now multiple , glutamate and opioids
PAIN FACTS – SUMMARY
DEFINITION
 CLASSIFICATION
 THEORIES
 PATHWAYS
 DESCENDING CONTROL

OH !! PAINFUL LECTURE ENDS ??
Thank you all