Pain as an unpleasant emotional experience usually initiated by a noxious stimulus and transmitted over a specialized neural network to the central nervous system where it is interpreted as such

1. PRESENTED BY-
Dr.Himanshu Gorawat
Dental surgeon

2. Definition-
 Pain as an unpleasant emotional experience usually
initiated by a noxious stimulus and transmitted over a
specialized neural network to the central nervous system
where it is interpreted as such .

3. Types of pain-
 According to pain intensity-
1. Mild pain-controlled by the use of simple analgesics.
2. Moderate pain-controlled with narcotic analgesic.
3. Severe pain.

4.  According to temporal relationship and duration-
1. Intermittent- short duration.
2. Continuous- longer duration.
3. Protracted- last for several days.
4. Intractable-pain does not response to therapy.
5. Recurrent- two or more similar episode of pain.
6. Remission- pain free- interval b/w recurring episode.
7. Periodic- pain that is characterized by regularly recurring
episode.

5.  According to qualities of pain-
1. Steady pain- unpleasant sensation.
2. Paroxysmal pain- sudden attack.
3. Bright pain-stimulating quality
4. Dull pain- it has got depressing quality.
5. Itching- warm and burning quality.
6. Pricking- sharp intermittent character of short and intense,
electric shock like
7. Stinging- more continuous & of higher intensity &quality.
8. Burning- gives a feeling of warmth or heat.
9. Throbbing- pulsatile pain is timed to cardiac systole.
10.Aching-most frequently used unless the pain is
overshadowed by one of the other characteristic sensation

6.  According to onset-
1. Spontaneous- pain occurs w/o being provoked
2. Induced- some provocation cause the painful sensation.
3. Triggered- when evoked response is out of proportion to
the stimulus.

7.  According to pain localization-
1. Localized- exact location.
2. Diffuse- less well defined and variable anatomically.
3. Radiating- rapidly changing pain.
4. Lancinating - a momentary cutting exacerbation
5. Spreading- gradually changing pain
6. Enlarging- pain progressively involves adjacent anatomical
area.
7. Migrating- changes from one location to another.

8. Pain theories-
Specificity theory- this classical description was provided by Descartes in 1644 when
he conceived of the pain system as a straight-through channel from the skin to the
brain.
 The concept changed little until the nineteenth century when Muller postulated the
theory of information transmission only by way of the sensory nerves.
 In the late nineteenth century, von Frey developed the concept of specific
cutaneous receptors of the mediation of touch, heat, cold & pain . Free nerve ending
were implicated as pain receptors. A pain center was though to exist within the
brain ,which was responsible for all overt manifestations of the unpleasant
experience .
 this theory responsible for development of several surgical approaches to the
management of chronic pain by cutting straight – through tracts.

9.  Pattern theory- in 1894 goldschider was the first to propose
that stimulus intensity and central summation are the critical
determinants of pain. The theory suggested that particular patterns of
nerve impulses that evoke pain are produced by the summation of
sensory input within the dorsal horn of the spinal column. Pain results
when the total output of the cells exceeds a critical level. For eg.-
touch plus pressure plus heat might add up in such a manner that pain
was the modality experienced.

10.  Central summation theory- Livingstone suggested a
specific neural mechanism in which intense pathologic
stimulation of the body, setup a reverberating circuit in
spinal internuncial pools that can be triggered by non –
noxious stimuli leading to abnormal volleys that can be
interpreted centrally as pain.

11.  Sensory interaction theory- it is stated by noordenbos
and it states the large fiber-pain inhibitory and small fiber
pain contributory concepts with the two systems being in
balance with one another a decrease in the ratio of large to
small fiber activity results in central summation and an
increase in pain.

12.  Gate control theory- psychologist ronald melzack & the anatomist Patrick wall
proposed the gate control theory for pain in 1965 to explain the pain suppression.
According to them the pain fibers are blocked by gate mechanism located at the
posterior gray horn of spinal cord. “If the gate is opened pain is felt .if the gate is
closed pain is suppressed”
Mechanism of gate control at spinal level-
1. When pain is stimulus is applied on any part of body , beside pain receptors of
other sensations such as touch are also stimulated.
2. When all these impulses reach the spinal cord through posterior nerve root , the
fiber of touch sensation (posterior column fibers) send collaterals to the neurons of
pain pathway , i.e. cells of marginal nucleus and substantia gelatinosa.
3. Impulses of touch sensation passing through these collaterals inhibit the release of
glutamate & substance p from the pain fibers
4. This close the gate & pain transmission is blocked.

13.  Role of brain in gate control mechanism-
according to melzack & wall brain also plays some important role in gate control system of the
spinal cord as follows-
1. It the gate in spinal cord are not closed pain signals reach thalamus through lateral
spinothalamic tract
2. These signals are processed in thalamus & sent to sensory cortex
3. Perception of pain occurs in cortical level in context of the person’s emotional status and
previous experiences
4. Person respond to the pain based on integration of all these information in the brain ,Thus
the brain determines the severity and extent of pain.
5. to minimize the severity &extent of pain , brain send message back to spinal cord to close
the gate by releasing pain relievers such as opiate peptides
6. Now the pain stimulus is blocked and the person feels less pain.
 Significance- thus gating of pain at spinal level is similar to presynaptic inhibition it forms
the basis for relief of pain through rubbing, massage tech. application of ice pack
acupuncture &electrical analgesia. All these tech. relieve pain by stimulating the release of
endogenous pain relievers (opioid peptides) which close the gate & block the pain signals.

15.  Peripheral nerves- pain impulse are believed to be conducted into the central the
CNS by two types of nerve fibers, which are classified by the size & speed at which
they conduct the impulse.
1. A delta fibers- large myelinated fibers . Diameter- 3 to 20 micra . Conduct fast or
first pain at a rate up to 100 meters per second .
2. C fibers- small unmyelinated nerve fibers from .05 to 1 micron , conduct slow or
second pain at the rate of 0.5 to 2 metes per second .
a nerve fiber that forms an afferent nerve is a separate pathway by which impulse
are transmitted into the CNS .each pathway is a separate unit unto itself. These
single units that form a nerve trunk maybe stimulated individually or in varying
numbers until all the individual fibers are affected.

16. Substantia gelationsa- facilitation & inhibition occur within the dorsal horn of the
spinal cord and nucleus of 5th cranial nerve. Dorsal horn divide into six laminae
based on synaptic connections of afferent neurons. The Substantia gelationsa,
consisting of laminae II & III, is of particular interest since it represents a unique
system that appears to have modulating effects on input. Gate control theory
proposes that –
 Large diameter fiber transmit impulse as a greater rate of speed they transmit signal
that are initiated by pressure , vibration, temperature.
 small diameter fiber transmit impulse noxious or painful sensations.

17. The dental pulp-
 Dentinal sensitivity is a result of direct stimulation of sensory nerve ending in the
dentin. Nerves exist in the mineralized part of the dentin, although several
physiological studies indicate that the nerves are located in the most pulpal portion
of the dentin and none are present in the periphery . Clinical experience has shown
that most sensitive area of tissue is near the DEJ.
 Odontoblast are sensory cells through their processes in the dentinal tubules,
odontoblasts & transfer stimuli to nerve endings in the pulp.
 Dentinal sensitivity is a result of mechanical stimulation of free nerve endings in
the pulp caused by rapid fluid flow in the dentinal tubules when the dentin is
stimulated.
the degree of pain noted is the rate of change of fluid flow and not the maximum
flow rate produced. Though not yet universally accepted the hydrodynamic theory
does explain how an impulse may be initiated by environmental change without
direct contact with the receptor being made.

19. Pain receptors-
 Many investigators have shown that various chemical consistently produce pain following
injection or application . Among these “algesic” or pain producing substances are hypertonic
saline , potassium chloride , acetylchopeptide bradykinin is very potent and elicits the kind
of pain that mimicked the clinically experienced sensation. These finding led to the
conclusion that sensory nerve ending that mediate pain are actually chemoreceptor. It is
currently believed that there are both mechanoreceptive & chemoreceptor nociceptors.
Different algesic may act independently of each other . The chemical transmitters in
nociceptive , thin , myelinated or nonmylinated fibers may include substance P & glutamate .
Criteria that must be met for a substance to be classified as a chemical pain mediator include:
1. General accessibility and activation as a consequence of injury , infection , or mechanical
tissue damage.
2. Suppression of mediator formation resulting in prevention of pain fiber activation.
3. Easy formation from labile precursors , release formation sensitive storage sites, and short
half life.
4. Pain caused by exogenous application onto nociceptors.

20.  Soon after injury the vasoactive amines (5-hydroxytryptsmine,histamine and bradykinin ) are
released. In addition to pain , they cause hyperemia & swelling. They are mediators of
inflammation & are important in the induction of inflammatory pain. Basophils , platelets
and mast cells are the main sources of the amines. Other cells appear to release bradykinin
on deformation of its formation . The blood clotting system acts as the activator.
kallikreinogen bradykininogen
Activating factors
(of the coagulation system) activating
kallikrein
bradykinin
deactivation by
plasma kininases
inactive fragments
“Formation & degradation of bradykinin”

21.  Cellular injury leads to the formation of kallikrein , a protease, that liberates kinins from
their precursors. Degradation of bradykinin by plasma &lymph kininass occurs rapidly.
Because of their potency , the kinins are strongly implicated in inflammatory pain. No
known kinin antagonists exist.
 Bradykinin also releases prostaglandins , which form a complex group of fatty acids. They
are not stored in cells but are generated from phospholipids precursors in the cell membrane
in response to noxious stimuli. PG themselves do not cause pain except in very high doses.
The main contribution of PG is to sensitize the nociceptors to the effects of bradykinin,
thereby accentuating its action.
 Drugs such as aspirin , indomethacin and other minor analgesic agents block the
cyclooxygenase reaction by inactivating the enzyme , thereby preventing the biosynthesis of
PG the principal site of action of aspirin like drugs is probably does not produce analgesia.
the anti in inflammatory effects of glucocortioids are the basis of their efficacy in the
treatment of inflammatory pain.

22. Cell membranes
(phospholipids)
Phospholipase A2 steroidal anti –inflammatory
Agents inhibit
Arachidonic acid
Cyclo-oxygenase drugs such as aspirin
&indomethacin inhibit
Cyclic endoperoxides
prostacyclin prostaglandin
syntheses syntheses
prostacyclin PGE2 PGF2
PGI2
“FORMATION OF PROTHAGLANDINS AND SITES OF ACTION OF ANTIINFLAMMTORY STEROID AND ASPIRIN - LIKE ANALGESICS”

24. sensation
somatic sensations special sensations
Epicritic sensations protopathic sensations deep sensations vision, hearing, taste , smell
Tactile sensations
Tactile Localization pressure sensation
Tactile Discrimination pain sensation
Temp. sensations with Temp. sensations with vibratory sensation
Finer range(25˚c to 40˚c ) wider range( below 25˚c & visceral sensation
above 40˚c) kinesthetic sensation
conscious subconscious
kinesthetic sensation kinesthetic sensation
classification of sensations-

25. Trigeminal nerve first received by both mylinted &nonmylinted fibers
Conducted impulse along the afferent fibers of ophthalmic,
Maxillary &mandible branches in semilunar or gasserian ganglion
Impulse mediated by sensory root of nerve into the Pons
Sensory root either ends directly in the main sensory nucleus
Or
Bifurcates into Ascending and descending Ascending fiber convey general tactile sensibility and descending
fiber convey pain & temperature
Pain impulse descend from Pons by the spinal tract fibers of the trigeminal nerve through the medulla down
to about the level of the second cervical segment the ophthalmic, Maxillary & mandible branches
terminate in the nucleus in that order.
 Axons of secondary neurons emerge from the spinal nucleus , cross the midline and join to the fiber of
mesencephalic nucleate form the trigeminal lemniscus or spinothalamic tracts of fifth nerve continue
upward and terminate in the poster ventral nucleus of the thalamus. Some fibers of the lateral
spinothalamic tract cause a general stimulation of reticular formation that increases the pt. awareness of
and reaction to pain.

27. Control of pain-
1. Removing the cause-environmental change in tissue would be eliminated.
2. Blocking the pathway of painful impulses- most widely use in dentistry by this
method a suitable drug possessing local analgesic properties, is injected into the
tissue in proximity to the nerve or nerves involved. LA prevent depolarization of
the nerve fibers at the area of absorption .
3. Raising the pain threshold-in this method pain control the cause of the original
stimulus may still be present the neuroanatomical pathways are intact and able to
conduct impulses. in other word pain perception is unaffected but pain reaction is
decreased. Drugs such as aspirin are effectively only in relief of mild discomfort.
4. Preventing pain reaction by cortical depression-eliminating pain by cortical
depression is within the scope of general anesthesia and general anesthetic agent.
5. Using psychosomatic methods- this method affects both pain perception and pain
reaction and depends for its effectiveness on putting the patient in the proper frame
of mind. It is amazing what can be accomplished without the use of drugs when the
patient’s faith and confidence are gained

28. Applied physiology-
 Analgesia- means loss of pain sensation
 Hyperalgesia – the increased sensitivity to pain sensation.
 Paralgesia - abnormal pain sensation is called paralgesia.