1. Somatic sensation pain
Is protective mechanism
Occurs due to tissue damage
Cause the individual to react to remove the painful stimulus
For instance
Sitting for a long time
Ischemic pain
Weight shifting subconsciously
Spinal cord injury
If loose pain sense
Fail to feel pain-fails to shift
Tissue breakdown and desquamation of the skin at the areas of pressure

2. Physiology of pain Definition
An unpleasant sensory and emotional experience which we primarily associate with tissue damage or describe in terms of such damage, or both

3. Types & qualities of pain
First pain
a.k.a- sharp pain, pricking pain, acute pain, electric pain
Felt 0.1 sec after painful stimulus application
Not felt in most deeper tissues
Slow pain
a.k.a slow burning pain, throbing pain, chronic pain, nausea pain
occurs after 1 sec or more
Associated with tissue destruction
Leads to prolonged, unbearable suffering
Occurs skin, deep tissues and organs

4. Physiology of pain Pain receptors Free nerve endings
Location; superficial layers of skin, Internal tissues, Periosteum, arterial walls, joint surfaces etc
Stimuli that excite pain receptors
Mechanical – fast & slow pain
Thermal- fast & slow pain
Chemical-slow pain
Bradykinin
Serotonin
K+, acids, ach, proteolytic enzymes
PG & substance p (cause pain indirectly by enhancing the sensitivity of pain endings )

5. Physiology of pain Non adapting nature of pain receptors
Adapt very little, sometimes not at all
Importance of non adaptation
Allows the pain to keep the person appraised of a true damaging stimulation as long as it persist
Hyperlagesia
Increased sensitivity of pain receptors
RATE OF TISSUE DAMAGE AS A STIMULUS FOR PAIN
Temp. above 45 degrees centigrade Cause tissue damage
Elicits painful stimulus
Pain resulting from heat is closely correlated with the rate at which tissue damage is occurring

6. Physiology of pain Intensity of pain
Is closely correlated with the rate of tissue damage from causes such as heat, bacterial infection, tissue ischemia etc
Special importance of chemical painful stimulus
Bradykinin is responsible for causing pain following tissue damage
Mechanism of pain formation
Pain intensity
Correlates to local increase of K ions concentration & proteolytic enzymes that directly attack the nerves endings and excite pain by making the nerve membranes more permeable to ions
1. tissue ischemia
acumulation of large amounts of lactic acid in the tissues
Formed as a consequences of anaerobic metabolism (metabolism without oxygen)
Chemical agents formed
Bradykinin, proteolytic enzymes
Formed in the tissues due to cell damage
Stimulate pain nerve endings

7. Physiology of pain Mechanism of pain formation ctd 2. Muscle spasms
Basis for many clinical pain syndromes
Direct effect
Muscle spasms stimulates mechanosensitive pain receptors
Indirect
Compress blood vessels causing tissue ischemia
Increased metabolism in the muscle tissues
Release of chemical pain inducing substances

8. Physiology of pain Pain signals transmission in CNS Dual pathways
Fast sharp pain –pathway
Slow chronic pain –pathway
Peripheral pain fibers- Fast & slow fibers
Fast sharp pain signals
Elicited by mechanical or thermal stimuli
Transmitted in the peripheral nerves to the spinal cord
Small type A-delta fibers
Conduction velocity 6-30m/sec
Slow chronic type of pain
Eliciting stimuli- Chemical (commonest) and also Persisting mechanical & thermal stimuli
Fibers transmitting type C fibers
Conduction velocities 0.5 to 2m/sec

9. Physiology of pain Double pain sensation
Occurs when sudden painful stimulus gives a double pain sensation
It is common for a first sharp pain transmission to be followed by a slow pain transmission
Cause: existence of the double system of pain innervations
Sharp pain
Appraises the person of a damaging influence
Significance: make an individual to react immediately to remove himself /herself from the stimulus
Slow pain
Tends to become greater over time
Produces intolerable suffering of long continued pain
Makes the person keep trying to relieve the cause of pain

10. Physiology of pain Dual pathways in the cord & Brain stem
On entering the cord - Pain signals takes two pathways to the brain
1. Neospanothalamic tract for fast pain
First order neurons
Terminates at lamina I- (lamina marginalis) of the spinal cord dorsal horns to synapse with the second order neurons
Fibers fast type A delta
Mechanical and acute thermal pain
2nd order neurons
Cross immediately to the opposite side of the cord thru the anterior commissure
Turn upwards ,passing thru the brain into anterolateral columns
Termination
Reticular areas of the brainstem (few fibers)
Ventrobasal complex of the Thalamus -Most of the fibers-goes uninterrupted
3rd order neurons : terminates in Somatosensory cortex & Other basal areas of the brain

11. Physiology of pain Body localization fast pain by CNS
Exact localized compared to slow pain
Poor localization occurs only
When tactile receptors are stimulated (if information travels same tracts )
Yet when tactile receptors that excite DCML are simultaneously stimulated the localization can be nearly exact
Neurotransmitter substance
Glutamate is the substance secreted in the spinal cord at the type A delta nerve fiber endings
Acts only for a few milliseconds
2.Paleospinothalamic – slow chronic pathway
Pain transmitted from peripheral to spinal cord thru type C pain fibers as well as A delta fibers

12. Physiology of pain
Peripheral fibers terminate in the spinal cord lamina II & III of the dorsal horns (substantial gelatinosa)
Additional fibers enters lamina V
Then the fibers join fast pain pathway passing thru the anterior commissure to opposite side of the cord
Upward to brain in anterolateral pathway
Neurotransmitter
Substance P is the probable neurotransmitter of type C nerve endings
Released much more slowly
Builds up in conc. Over a period of seconds or even minutes
Double pain sensation-Following pin prick
Glutamate transmitter gives fast pain sensation
Substance P transmitter gives more lagging sensation
C fibers can also produce glutamate

13. Physiology of pain Projections of the paleospinothalamic pathway
Slow chronic pain signals terminates in
brain stem and thalamus
10-25 % pass to the thalamus
Most terminate in
Reticular nuclei (medulla, pons & mesencephalon)
Tectal area of mesencephalon (deep to the superior & inferior colliculi)
Periaqueductal gray –region surrounded the aqueduct of sylvius
Areas concerned with feeling the suffering types of pain

14. Physiology of pain From brain stem areas
Multiple short fiber neurons Relay pain signals upward
Thalamus (intralaminar & ventrolateral nuclei)
Hypothalamus (certain areas)
Other basal regions of the brain
Slow chronic pain
Poorly localized
Can only be localized to a major part of the body such as to one arm or leg
But not to a specific point on the arm or leg
Due to multisynaptic & diffuse connectivity of this pathway
Appreciation /conscious perception of pain
Pain perception is the principal function of the lower centers
Functions of Reticular formation, thalamus
Cerebral cortex
Apart from pain perception , Plays an important role in interpreting of pain quality

15. Physiology of pain dual pathway for pain transmission

16. Physiology of pain Overall brain excitability by Pain signals
Principal arousal system
Reticular areas of brainstem & intralaminar nuclei of the thalamus
Electrical stimulation leads to
strong arousal effect on nervous activity through out the entire brain
Thus pain signals – arouse overall brain excitability
It is almost impossible for a person to sleep when is in severe pain

17. Physiology of pain 2.Cauterize – experimental Pain management
1. Surgically
Interrupting pain pathways
Cut pain nervous pathway at any one point “CORDOTOMY”
Anterolateral sensory pathway cut in thoracic region deal with pain lower part of the body
Relieve pain in patients with severe intractable pain such as cancer
Failure
Uncrossed fibers
Sensitization of other pathways that normally are weak to be effectual e.g sparse pathways in the dorsal lateral
2.Cauterize – experimental
specific pain areas in the intralaminar nuclei in the thalamus

18. Physiology of pain 3. Pain suppression – the Analgesia system
Located in the brain and spinal cord
Brain suppress pain signals input to the nervous system
By activating pain control system- the analgesic system
3 major components
The periaqueductal grey & periventricular areas
mesencephalon & upper pons
Neurons of this areas sends signals to
The raphe magnus nucleus (upper medulla & lower pons) and nucleus paragigantocellular (lateral medulla)
From these nuclei, send signals down the
dorsal columns in the spinal cord to
A pain inhibitory complex located in dorsal horns of the spinal cord
Site of blocking the pain before it is relayed to the brain

19. Physiology of pain Electricle stimulation of either
periaqueduactal grey area or
raphe magnus nucleus
can suppress many strong pain signals entering by way of the dorsal spinal roots
Also stimulation of higher brain center areas such as
periventricular nuclei in the hypothalamus
Medial forebrain forebrain bundle in the hypothalamus
that excite periaqueductal grey thereby suppressing pain
Transmitters involved in analgesia system
Encephalin
Encephalin released by fibers originating in the periventricular & the periaqueductal grey on stimulation
Cause the dorsal horns spinal cord to release serotonin at their nerve endings
Serotonin

20. Physiology of pain
Serotonin cause local cord neurons to secrete encephalin as well
Which causes both presynaptic and postsynaptic inhibition of incoming type c and A delta pain fibers when they synapse at the dorsal horn
4. Brain opiate system
endorphins and encephalins
1. activation of the analgesia system by nervous signals entering the periaqueductal grey and periventricular areas OR
2.inactivation of pain pathway by morphine like drugs can almost totally suppress many pain signals entering thru the peripheral nerves

21. Physiology of pain Morphine like agents –mainly opiates
Acts at many other points in the analgesia system including the dorsal horns of the spinal cord
Opiates like substances
Beta endorphins (produced by hypothalamus & pituitary glands)
Met encephalin
Leu encephalin
Dynorphin
Also they are found in brain stem and spinal cord in the portion of analgesia system

22. Physiology of pain Others 1. simultaneously tactile sensory signals
Can inhibit pain transmission
stimulation of large type A beta sensory fibers from peripheral tactile receptors can depress transmission of pain signals from the same body area
Mechanism : local lateral inhibition in the spinal cord
2. psychogenic excitation of the central analgesia system
1& 2 forms the basis for pain relief by acupuncture
3. Treatment /suppression of pain by electrical stimulation
Clinical procedure
Stimulating electrodes are ..

23. Physiology of pain Placed on selected areas of skin
Implanted over the spinal cord-stimulate the dorsal sensory columns
Placed in Intralaminar nuclei of the thalamus
Periventricular or periaqueductal area of the diencephalon
The Patient can then personally control the degree of stimulation
Few minutes of stimulation can bring dramatic relief which can last for as long as 24 hours

24. Physiology of pain Referred pain
Is the feeling of pain in a part of the body that is fairly remote from tissue causing the pain
For instance
Pain in visceral organs referred to an area on the body surface

25. Physiology of pain Referred pain Mechanism
Branches of visceral pain fibers synapse in the spinal cord on the same second order neurons that receives pain signals from the skin
Thus a person has the feeling that sensation originate in the skin itself

26. Clinical abnormalities of pain
Hyperalgesia
Excessive excitability of pain nervous pathway
Cause
Primary hyperalgesia
Excessive sensitivity of sun burned skin which results from sensitization of the skin pain endings by local tissue products from the burn e.g histamine, PG
Secondary hyperalgesia
Facilitation of sensory transmission e.g lessions in the spinal cord or thalamus

27. Physiology of pain Herpes zoster (shingles)
Herpes virus infects a dorsal root ganglion
Causing severe pain in the dermatomal segment subserved by the ganglion
Pain is caused by the infection of the pain neuronal cells in the dorsal root ganglion by the virus

28. Physiology of temperature Thermal sensations
Thermal receptors and their excitation
Different gradations perceived
Cold and heat
From freezing cold to cold- to cool -to indifferent- to warm -to hot -to burning hot
Thermal gradations
Are discriminated by at least 3 types of receptors
Cold receptors
Warm receptors
Pain receptors
Pain receptors are stimulated only by extreme degree of heat or cold
Are there responsible (together with 1&2) for Freezing cold & burning hot sensation

29. Physiology of temperature
Cold and warm receptors
Located immediately under the skin
At discrete separated spots
There are 3 to 10 times as many cold spots as warm spots in the most areas of the body
cold spots per sq. cm
15-25 in the lips
3-5 in the fingers
4- in some broader body surface areas of the trunk

30. Physiology of temperature
Warm signals transmission
Type C nerve fibres
Velocities m/sec
Cold receptor
Is a special small type A delta myelinated nerve ending
Signal transmitted via type A delta fibres
Some transmitted in type C nerve fibres
Stimulation of thermal receptors
there are about 5 Sensation
Cold
Cool
Indiferent
Warm
Hot

31. Physiology of temperature
Four types of nerve fibers are present
They do respond differently at different levels of temperature
Pain fibers /cold pain fibers- stimulated by cold
Stimulated by Very cold temperature
Ceases stimulation when the skin becomes even colder to nearly freezing or does actually freeze
Impulses also cease when the temperature rises to + 10 to 15 degrees centigrade
A Cold fiber
Begin to be stimulated at temp + 10 to 15 degrees centigrade
Reach peak stimulation at 24 degrees centigrade and fade out slowly above 40 degrees centigrade
A Warm fiber
Begin to be stimulated at temp above 30 degrees centigrade
Fade out at 49 degrees centigrade

32. Physiology of temperature
iv. A pain fiber– stimulated by heat
Stimulated at 45 degrees centigrade
Also some of the cold fibers begin to be stimulated again due to damage to the cold endings by extreme heat
Therefore one determines the different gradations of thermal sensations by the relative degrees of stimulation of different types of endings
Burning hot and freezing cold feel almost alike___!

33. Physiology of temperature
Adaptation of thermal receptors
Cold receptors
Adapt to a great extent but never 100%
Sudden exposure to cold increase firing which fades with time
But does not stop completely after 30min
Thus its is evident that the thermal senses respond markedly to changes in temperature
In addition to being able to respond to steady states of temperature

34. Physiology of temperature
Mechanism of stimulation of thermal receptors
Thermal detection
Results from chemical stimulation of the endings as modified by temperature
Change of temperature is directly proportional to changes in the rate of cellular metabolism
Temperature alters the rate of intracellular chemical reactions more than 2fold for each 10 deg. cent.

35. Physiology of temperature
Spatial summation of thermal sensation
Due to small numbers of receptors
It is difficult to judge gradations of temperature when small skin areas are stimulated
Judgment of gradations of temperature in body surface is direct proportional to area stimulated
The smaller the area the poor the judgment
The bigger the area the better the judgment
For instance
Rapid changes in temperature as little as 0.1 deg cent. Can be detected if this change affect large entire surface of the body at the same time
Conversely
Changes 100 times as great will not be detected when the affected skin area is only 1 sq cm in size

36. Physiology of temperature
Transmission of thermal signals in the nervous system
Parallel with pain signals
On entry of spinal cord travels up/down wards a few segments
In the tract of lissauer
Then terminate in laminae I,II & III of the dorsal horns
Same for pain
Then enters long ascending thermal fibers that cross to the opposite anterolateral sensory tract

37. Physiology of temperature
Terminate in
Leticular area of the brain stem
Ventrobasal complex of the thalamus
Few thermal signals relayed to cerebral somatic sensory cortex from ventrobasal complex
Removal of entire cortical postcentral gyrus in humans reduces but does not abolish the ability to distinguish gradations of temperature