pain

1. PAIN – SOME FACTS
Dr. S. Parthasarathy
MD., DA., DNB, MD (Acu), Dip. Diab. DCA, Dip. Software
statistics

2. DEFINITION
 An unpleasant sensory and emotional
experience associated with actual or
potential tissue damage, or described in
terms of such damage.
 ISSP definition

3. 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

4. MARGO MCCAFFREY
 Whatever the patient says hurts.

5. 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

6. 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

7. ANALGESIA
 Patient has no pain
 But the noxious stimulus is there
 Anaesthesia – all sensory modalities gone
 While analgesia – only pain

8. 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

9. 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

10. 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

11. ALGOGENS
 Histamines, substance P, potassium, and
prostaglandins, bradykinin, 5 HT are
examples of algogenic substances
 Produced or injected – nociception

12. HYPERALGESIA-
SHIFT OF THE STIMULUS PAIN RESPONSE
CURVE TO THE LEFT
 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
stimulus
P
A
I
n

13. PRIMARY SECONDARY
 Starts within
minutes
 Area of injury
 Sensitive to heat
and mechanical
 Peripheral
sensitization
 Delayed onset
 Wider area
 Only thermal
 Central role

14. PRIMARY HYPERALGESIA – MECHANISMS
 Expansion of receptive field of nociceptor
 Sensitization of nociceptor
 Loss of central inhibition
 Increased CAMP levels
 Activation of protein kinase C

15. SECONDARY HYPERALGESIA
 Antidromic release of algogens
 Dorsal horn neurons – sensitive
 WDR neurons – plastic changes
 Sometimes irreversible
 Post op pain - !!!

16. SENSITIZATION
 shift of the
stimulus - nerve
fibre response
curve to the left
stimulus
F
I
B
r
e
s

17. 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

18. CLASSIFY PAIN

19. TYPES OF PAIN
 Nociceptive
 Somatic
 Visceral
 Nonnociceptive
 Peripheral
 Central
 Psychogenic

20. NOCICEPTIVE – SOMATIC
 Dull or sharp
 Localized
 Increased with movement
 Eg. Tooth ache

21. SKIN, MUSCLE, BONE, JOINT ETC….

22. VISCERAL NOCICEPTION
autonomic sensations
including nausea,
vomiting, and
diaphoresis.
There are often
cutaneous referral
sites

23. NEUROPATHIC
 burning, electrical, and numbing
 Intervening normal
 Sudden
 Post herpetic, trigeminal,
glossopharyngeal

24. 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.

25. DEJERINE ROUSSY SYNDROME
 severe, persistent, paroxysmal, often
intolerable, pains on the hemiplegic side, not
yielding to any analgesic treatment

26. THEORIES HAVE BEEN PROPOSED-
NEUROPATHIC 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

27. 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.

28. PSYCHOGENIC PAIN
 No nociception
 No neuropathic mechanism
 But some evidence of psychologic symptoms
to meet criteria for somatoform pain disorder,
depression,
 Usually chronic

29. WHY DO WE NEED TO CLASSIFY PAIN ??
 Origin of pain
 Treatment modalities
 Prognosis

30. 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

31. OTHER CLASSIFICATIONS
 Etiology
 Arthritic
 Cancer
 Site
 Appendix
 Mastitits

32. 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

33. 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

34. SPECIFICITY THEORY
 when someone pulls
the rope to ring the
bell, the bell rings in
the tower.
 Proved not correct

35. 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.

36. 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

37. 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

38. THE GATE OPENS AND CLOSES

39. 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

40. 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.

41.  How is pain perceived ??

43. TYPES OF FIBRES MYELIN – DIA MM VELOCITY MM/S
Aα Proprio, somatic Motor yes 12–20 70–
120
Aβ Touch, pressure yes 5–12 30–
70
Aγ Motor muscle spindle Yes 3–6 15–
30
Aδ Pain, cold, touch Yes 2–5 12–
30
B Preganglionic autonomic Yes 3 3–
15

44. 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)

45.  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

46.  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

47. OTHER SECOND ORDER NEURONS
 Spino mesencephalic
 Midbrain – behavioural responses to pain
 Spino reticular
 Alerting and arousal motivational aspects
-pain
 Pontine and medullary reticular formation

48.  Third order neurons from thalamus to cortex
 anterior cingulate cortex (emotional aspect
)
 Somatosensory cortex

49. SIMPLE NEUROANATOMY OF PAIN

50. DESCENDING INFLUENCE

51. DESCENDING INFLUENCE
 In 1858 Bernard found that spinal afferents
can be modified by supraspinally organized
systems.
 Three and three

52.  Brain ,thalamus and brainstem
 PAG, LC, NRM
 Serotonin , noradrenaline and opioids
 Additional
 GABA , glutamate and acetyl choline

53. COX ET AL
 Medial forebrain
 Lateral hypothalamus
 Electrical stimulation attenuated foot pain

54. ESSENTIAL NUCLEI
 Periaqueductal grey
 PAG – extensive connections
 Opioids

55. NUCLEUS LOCUS CERULEUS
 Pons
 Projection to hippocampus ,spinal cord and
cortex
 Noradrenergic system

56. NUCLEUS RAPHE MAGNUS
 Medulla
 Serotonin – originally
 But now multiple , glutamate and opioids

57. PAIN FACTS – SUMMARY
 DEFINITION
 CLASSIFICATION
 THEORIES
 PATHWAYS
 DESCENDING CONTROL

58. OH !! PAINFUL LECTURE ENDS ??
Thank you all