Download Somatic sensation pain

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
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
Types & qualities of pain
First pain
1.
• 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
2.
• a.k.a slow burning pain, throbing pain, chronic pain, nausea
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pain
occurs after 1 sec or more
Associated with tissue destruction
Leads to prolonged, unbearable suffering
Occurs skin, deep tissues and organs
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
1. Mechanical – fast & slow pain
2. Thermal- fast & slow pain
3. Chemical-slow pain
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Bradykinin
Serotonin
K+, acids, ach, proteolytic enzymes
PG & substance p (cause pain indirectly by enhancing the
sensitivity of pain endings )
Physiology of pain
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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
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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
Physiology of pain
• Intensity of pain
• Is closely correlated with the rate of tissue damage from causes such as
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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
Physiology of pain
• Mechanism of pain formation ctd
2. Muscle spasms
• Basis for many clinical pain syndromes
a. Direct effect
• Muscle spasms stimulates mechanosensitive pain
receptors
b. Indirect
• Compress blood vessels causing tissue ischemia
• Increased metabolism in the muscle tissues
• Release of chemical pain inducing substances
Physiology of pain
• Pain signals transmission in CNS
• Dual pathways
i.
Fast sharp pain –pathway
ii.
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
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
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
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
Physiology of pain
• Peripheral fibers terminate in the spinal cord lamina II &
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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
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C fibers can also produce glutamate
Physiology of pain
• Projections of the paleospinothalamic pathway
• Slow chronic pain signals terminates in
• brain stem and thalamus
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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
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
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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
Physiology of pain
dual pathway for pain transmission
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
Physiology of pain
• 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
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Relieve pain in patients with severe intractable pain such as cancer
• Failure
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Uncrossed fibers
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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
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
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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
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
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that excite periaqueductal grey thereby suppressing pain
• Transmitters involved in analgesia system
• Encephalin
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Encephalin released by fibers originating in the periventricular & the
periaqueductal grey on stimulation
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Cause the dorsal horns spinal cord to release serotonin at their nerve
endings
• Serotonin
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
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
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 ..
Physiology of pain
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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
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
Physiology of pain
 Referred pain
 Mechanism
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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
Clinical abnormalities of pain
 Hyperalgesia
 Excessive excitability of pain nervous pathway
 Cause
1. Primary hyperalgesia
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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
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Facilitation of sensory transmission e.g lessions in the spinal
cord or thalamus
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