Physiology of Pain, Characteristic of pain, Basic consideration of nervous system, Pain receptor, Mechanism of pain causation, Theories of pain, Pathways of pain, Pain Receptors
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Understanding Pain Physiology
1. PHYSIOLOGY OF PAIN
DR. DHARATI PATEL
DEPARTMENT OF PEDODONTICS AND PREVENTIVE
DENTISTRY
Perhaps the capacity of the human brain falls short of the
ability to understand its own complexity
-Thibodeau
2. Content
Introduction
Definition
Historical aspect
Characteristic of pain
Basic consideration of nervous system
Pain receptor
Mechanism of pain causation
Theories of pain
Pathways of pain
References
3.
4. Introduction
Pain is an unpleasant sensory action
Seriously impairs the lives of millions of people around the world
Described in many ways by patient
5. Pain is
Subjective
Protective
and it is modified by developmental, behavioural, personality
and cultural factors
It is a symptom
Associated signs are crying, sweating, increased heart
rate, blood pressure, behavioral changes etc.
6. Produced by real or potential injury to the body
localized to the area stimulated but the experience involves the
whole being.
Pain also imply that the same painful experience may evoke
widely different degrees of suffering in different persons, and
even in the same person under different circumstances.
It is expressed in terms of damage done by the injury
7. In 1984, Bonica reported that nearly 1/3rd of the population in
industrialized nations suffer to some extent from chronic pain.
This results in loss of billions annually in health care services, loss
of work, decreased productivity and disability compensation
The clinical management of pain is the primary concern of health
professionals around the world.
8. Benefits of pain
Pain is a protective mechanism for the body, it occurs whenever any
tissues are being damaged, and it causes the individual to react to
remove the pain stimulus
Gives warning signal – creates awareness of injury
Prevents further damage – causing reflex withdrawal of the body
Forces the person to rest or to minimize the activities thus enabling
the rapid healing of injurious part
9. Definition
• Poin/Poena – punishment
Pain
• “An unpleasant sensory or emotional experience associated with
actual or potential tissue damage, described in terms of such
damage“
International Association for the Study of Pain
(1979)
American Pain Society[APS]2003
• Pain is whatever the experiencing person says it is, existing
whenever he/she says it does
Margo Mc Caffey (1999)
10. Cancer Web
(2011)
• An unpleasant sensation induced by noxious
stimuli and generally received by specialized
nerve endings.
Bell
• The subject’s conscious perception of
modulated nociceptive impulses that generate
an unpleasant sensory and emotional
experiences associated with actual or potential
tissue damage or described in terms of such
damage.
Monheim’s
• An unpleasant emotional experience usually
initiated by noxious stimulus and transmitted
over a specialized neural network to CNS
where it is interpreted as such damage.
12. Inducing pain
ALGOGENIC
Pain that occurs without noxious stimulation at the site of pain
ALLODYNIA
absence to pain perception
ANALGESIA
Absence of all sensation
ANESTHESIA
Unpleasant sensation with or without stimulus
DYSESTHESIA
Diminished response to noxious stimulus
HYPOALGESIA
Increased pain from a stimulus that normally provokes pain
HYPERALGESIA
Reduced cutaneous sensation
HYPOASTHESIA
Increased response to mild stimulus
HYPERASTHESIA
An abnormal sensation perceived without an apparent stimulus
PARASTHESIA
13. Pain in disturbance of a nerve
NEURALGIA
The mechanism that provides for the reception and conversion of noxious
and or potentially noxious stimuli into neural impulses and the
transmission of such impulses by A-delta and C-fibers to the CNS where
they are modulated and acted on.
NOCICEPTION
an afferent neural pathway that mediates pain
NOCICEPTIVE
PATHWAY
a sensory receptor preferentially sensitive to noxious or
potentially noxious stimuli.
NOCICEPTOR
Increased responsiveness of nociceptive neurons to their normal
input
SENSITIZATION
pain that is felt in a tooth
ODONTALGIA
14. Historical aspect
Homer pain was due to arrows shot by the gods
Aristotle a “passion of the soul” that somehow resulted from
intensification of other sensory experience
Plato pain and pleasure arose from within the body i.e. pain is an
emotional experience more than a localized body disturbance
Bible anguish of the soul
Freud symptoms such as pain could develop as a solution to
emotional conflicts
15. 1664 AD - Descartes introduced the concept of pain
pathway.
Recent years – Specialization of nociceptive pathways
have been identified.
16. Incidence of pain
According to Cohen – It was found that 21.8% of adult in the
United States experience orofacial pain symptoms within 6
months of study.
The most common pain was toothache, which was estimated
to have occurred in 12.3% of the population
18. Threshold and Intensity
If the intensity of the stimulus is below the threshold (sub-
threshold) pain is not felt. As the intensity increases more and
more, pain is felt more and more according to the Weber-
Fechner’s law.
This law ensures that while our body can perceive pain due to
low intensity stimulus, a severe crushing injury will not cause
death due to pain sensation, yet as stimulus increases, sense of
perception also increases.
19. Adaptation
Pain receptors show no adaptation and so the pain continues as
long as receptors continue to be stimulated.
Localization of pain
Pain sensation is somewhat poorly localized. However superficial
pain is comparatively better localized than deep pain.
Rate of damage
damage = intensity of pain
If the rate of tissue injury (extent of damage per unit time) is
high, intensity of pain is also high.
21. The human being is a phenomenal organism with the
complexity far beyond the imagination of the best
scientific minds
Because of its complexity, a master control system, the
“Nervous system” …coordinate all the activities.
In order to manage the patients pain problem
understanding the normal function of the nervous system is
necessary
26. Neuron
It is a structural and functional unit of nervous system
Called as “ nerve cell”
It is different from other cells in the body in 2 ways:
1. It has processes called as axon & dendrites
2. Does not have centrosome- cannot differentiate
27. Classification
1.Depending upon the number of poles
Unipolar
Bipolar
Multipolar
2. Depending on function
Motor
Sensory
3. Depending on length
Golgi type I
Golgi type II
33. 1. Nerve cell body
Known as soma or perikaryon
Irregular in shape
Consists of cytoplasm known as- neuroplasm
Covered by cell membrane
Cytoplasm contains large nucleus, nissl bodies, neurofibrils,
mitochondria and golgi apparatus
2. Dendrite
Branched process of neuron
It contains nissl granules and neurofibrils
Conductive in nature- transmits impulses towards cell body
34. 3. Axon
Arise from nerve cell body
Extends for a long distance away from cell body
35. Internal structure
It has a long central core of cytoplasm – axoplasm
Axoplasm covered by tubular membrane-axolemma
Axoplasm+ axolemma = axis cylinder of nerve fibre
Mylein sheath
Axons insulated by myelin sheath
Does not form a continuous sheath and is absent at intervals- node
of Ranvier
Segment of nerve fibre between the nodes – internode
Responsible for faster nerve conduction where the impulse jumps
from one node to other
Acts as an insulator
36. Neurilemma
Surrounding the myelin sheath there is thin membrane –
neurilemma/ sheath of Schwann
Contains – Schwann cells
The cells have flat & elongated nuclei
37. Classification of nerve-fibers
1. Depending on structure
Myelinated
Nonmyelinated
2. Depending on distribution
Somatic
Visceral
3. Depending on origin
Cranial
Spinal
4. Depending on function
Motor
sensory
38. 5. Depending on secretion of neurotransmitter
Adrenergic
Cholinergic
39. Depending on diameter and conduction
Type A fibers
Alpha fibers: size - 13 to 20 µm, velocity - 70 to 120 m/ s.
Beta fibers: size – 6 to 13 µm, velocity – 40 to 70 m/s.
Gamma fibers: size – 3 to 8 µm, velocity – 15 to 40 m/s.
Delta fibers: size – 1 to 5 µm, velocity – 5 to 15 m/s.
Type B fibres
Size- 1 to 2 µm, 3-10 m/s.
Type C fibers
Size – 0.5 to 1 µm, velocity – 0.5 to 2 m/s.
44. Sensory Receptors :
Input to the nervous system is provided by sensory receptors that
detect such sensory stimuli such as touch, sound, pain, cold and
warmth.
All the stimuli capable of evoking pain are noxious because they are
associated with actual or potential tissue injury.
Sherrington postulated the existence of sensory receptors that sensed
noxious agents and called nociceptors.
Perception of pain
44
nociception
45. Pain Receptors:
Pain Receptors Are Free Nerve Endings.
Widespread in the superficial layers of the skin, periosteum, the
arterial walls, the joint surfaces, and the falx and tentorium in the
cranial vault.
Most other deep tissues are only sparsely supplied with pain
endings.
45
47. Fields has described that the subjective experience of pain arises by
four distinct processes
Transduction
Transmission
Modulation
Perception
48. A pain sensation to reach the cortex from the nosiceptors it requires
three neuron sets.
NOCICEPTORS
BRAIN STEM SPINAL CORD
THALAMUS
CEREBRAL CORTEX
Spinal nerve
Cranial nerve
B
B
C
C
A A
A - 1st order neuron
B - 2nd order
C - 3rd order.
51. All or none phenomenon:
The action potential either happens completely or it doesn’t happen at all.
Coding for stimulus intensity:
Once generated all action potentials are independent of the stimulus
strength, and all action potentials are alike. Strong stimuli cause nerve impulses
to be generated more often in a given interval of time than do weak stimuli.
Thus stimulus intensity is coded for by the number of impulses generated per
sec- i.e. by frequency of impulse transmission.
52. Absolute and Relative refractory period:
When a patch of neuron membrane is generating an action potential and it’s Na
voltage gates are open, the neuron is incapable of responding to another
stimulus no matter how strong it may be Absolute refractory period.
Relative refractory period is the interval following the absolute refractory
period when the Na gates are closed, and the K gates are open, and
repolarization is occurring. During this time the axons threshold for impulse
generation is substantially elevated. A threshold stimulus is unable to trigger an
action potential, but an exceptionally strong stimulus can reopen the Na gates
and allow another impulse to be generated.
53. Synapse Or Synaptic Junction:
It is a unique junction that mediates the transfer of information from one
neuron to the next, or neuron to an effector cell.
Types
1. Electrical
2. Chemical
54. Neuronal Sensitization:
When the excitatory neurotransmitters are released in the synaptic cleft, the
post synaptic neuron is excited and an impulse is started and carried down the
axon. If the excitatory neurochemicals remain in the region of the synapse, the
neuron can be depolarized quicker with the next release of neurotransmitter.
This process is called sensitization. This could be the cause for hyperalgesic
state in inflammatory tissues.
56. It is often assumed that pain is a warning that damage has
occurred. But this is not strictly true.
Because pain may occur when there is no obvious disease as in
primary neuralgias and many diseases does not cause pain, at
least in the early stages.
So these are various theories being put forward on how nerve
impulses give rise to sensation of pain.
56
57. INTENSITY THEORY
According to this view, pain is produced when any sensory nerve
is stimulated beyond a certain level.
In other words pain is supposed to be a non-specific sensation
and depends only on high intensity stimulation.
But the trigeminal system provides an example against this
theory. In case of trigeminal neuralgia the patient can suffer
excruciating pain from a stimulus no greater than a gentle touch
provided it is applied to a trigger zone.
Although, the intensity theory is not accepted, it remains true
to say that intensity of stimulation is a factor in causing pain.
57
58. Specificity Theory (Johannes Muller, 1842)
According to this view, pain is a specific modality equivalent to vision and
hearing etc.
Just as there are Meissner corpuscles for the sensation of touch, Ruffini end
organs supposedly for warmth and Krause end organs supposedly for cold, so
also pain is mediated by free nerve endings.
Certain psychophysical studies have been regarded as supporting specificity
theory. Specialization is known to exist in nervous system and there are well
known tracts.
But concept of specific nerve ending is no long tenable. The Krause and
Ruffini endings are absent from the dermis of about all hairy skin, so it is
certain that these structures cannot be receptors for cold and warmth.
58
59. Protopathic and Epicritic theory:
Head and Rivers (1908) postulated the existence of two
cutaneous sensory nerves extending from the periphery to the
CNS.
The protopathic system is primitive, yielding diffuse impression
of pain, including extremes of temperature and is upgraded.
The epicritic system is concerned with tough discrimination and
small changes in temperature and is phylogenetically a more
recent acquisition.
59
60. Pattern theory (Goldscheider, 1894):
This theory states that pain sensation depends upon
spatio – temporal pattern of nerve impulses reaching
the brain.
According to Woddell (1962) warmth, cold and pain
are words used to describe reproducible spatio –
temporal pattern, or codes of neural activity evoked
from skin by changes in environment.
The precise pattern of nerve impulse entering the
CNS will be different for different regions and will
vary from person to person because of normal
anatomical variations. 60
61. Gate Control Theory
This theory proposed by Melzack and Wall in 1965 and recently
re-evaluated is receiving considerable attention.
This theory of pain takes into account the relative in put of
neural impulses along large and small fibers, the small nerve
fibers reach the dorsal horn of spinal cord and relay impulses
to further cells which transmit them to higher levels.
The large nerve fibers have collateral branches, which carry
impulses to substantia gelatinosa where they stimulate
secondary neurons.
61
62. The substantia gelatinosa cells terminate on the smaller nerve
fibers just as the latter are about to synapse, thus reducing
activity, the result is, ongoing activity is reduced or stopped –gate is
closed.
The theory also proposes that large diameter fiber input has ability
to modulate synaptic transmission of small diameter fibers within
the dorsal horn.
Large diameter fibers transmit signals that are initiated by
pressure, vibration and temperature; small diameter fibers transmit
painful sensations.
Activation of large fiber system inhibits small fiber synaptic
transmission, which closes the gate to central progression of
impulse carried by small fibers.
62
67. Sensory pathways for transmitting
somatic signals into CNS
Somatic segment Spinal cord Brain
1. The dorsal columm-medial lemniscal system or
2. The anterolateral system.
Partially at the level of the thalamus.
68. Dorsal column-medial lemniscal system
Composed of large, myelinated nerve fibers
At velocities of 30-110m/sec.
Has a high degree of spatial orientation.
Rapidly and with temporal and spatial fidelity.
Touch, vibrating, position from the joints, pressure.
69. Anterolateral pathway
Composed of smaller myelinated fibers.
At velocities ranging from a few meter per second up to 40m/sec.
Less spatial orientation.
Does not need transmitted rapidly or with great spatial fidelity.
Ability to transmit the broad spectrum of sensory modalities-
Pain, warmth, cold, and crude tactile sensations.
70. Anatomy:
Originate mainly in: dorsal lamina I, IV, V and VI.
Upper terminals mainly two folds:
Reticular nuclei of the brain stem
The ventrobasal complex and the intralaminar nuclei.
Small fraction : Ventrobasal complex of thalamus.
Most of : Reticular nuclei Intralaminar nuclei Further proceed.
71. Dual pathways for pain
Free nerve endings
Use two separate pathways.
1. Fast pain pathway
2. Slow pain pathway
72. Neospinothelmic tract for fast
pain:
Elicited by either mechanical or thermal pain
stimuli
By small type AꝽ
At velocities between 6 to 30 m/sec.
Terminate mainly in lamina I.
Can be localized much more exactly.
Glutamate is neurotransmitter at the type AꝽ
pain nerve fiber.
73. • A few fibers: reticular areas of brain
stems.
• Most of : Ventrobasal complex.
• Can be localized much more exactly.
• Glutamate is neurotransmitter at
the type AꝽ pain nerve fiber.
74. Paleospinothalmic pathway for
slow pain
Elicited by chemical types of pain stimuli.
Sometimes by thermal or mechanical.
By type C fibers.
Although transmit signals from AꝽ fibers also.
At velocities between 0.5 and 2m/sec.
Terminate in laminae II and III together called substantia
gelatinosa then through short fiber neurons entering to
lamina V.
75. Type C secrete glutamate and substance P.
Glutamate act instantaneously and last for few milliseconds.
Substance P released slowly, building up in concentration over a period
of seconds or even minutes.
Localization is poor.
Localized to major part but not specific point.
synaptic , diffuse connectivity.
76. • Slow pathway terminates mostly into the brainstem only.
• 1/10 to ¼ pass : Thalamus.
• Most of terminate:
1. Reticular nuclei of medulla, pons, mesencephalon
2. Tectal area of mesencephalon deep to the sup. and inf. colliculi.
3. The periaqueductal gray region.
• This region is important.
77. Surgical interruption
Severe and intractable pain: pain nervous pathway can be
cut at any one of several points.
Lower part of body: cordotomy for few week to a few
months.
Cordotomy not always successful.
Second, cauterize specific pain areas.
79. 1. Bell`s ‘Orofacial pain’, 5th edition, Jeffrey P. Okeson.
2. Text book of Medical Physiology, 2nd edition, Chaudhari.
3. Text book of Medical Physiology, 10th edition, Arther C Gyton.
4. Dental Clinics of North America 1978: 22 (1); 1-61.
5. Text book of ‘Oral medicine’- 10th edition, Burkett’s.
6. Gray's Anatomy – 38th Edition, Churchill Eivingstone.
7. Understanding “Medical physiology”- 3rd edition, R L Bijlani.
8. Core Topics in Pain – Anita Holdcroft, Sian Jagger.
79
80. 80
9. Pain – Wikipedia, the free encyclopedia
10. Rolf-Detlef Treede. Neurophysiological studies of pain pathways in
peripheral and central nervous system disorders. J Neurol (2003) 250 : 1152–
1161.
11. Ascending Sensory Pathways, Chapter 10.
12. Pain pathway & Medications – Painexplained.ca, The Canadian Pain Society.