Download 9a-Pain Sensation

Pain sensation
Pain sensation is a protective mechanism for the body, which is
produced whenever there is tissue damage. It is a purely subjective
sensation, initiating important reflexes, the aim of which is to remove the
painful stimulus.
Terminology used to describe pain:
Intensity
Quality
Frequency
Distribution
- Stabbing (sharp).
- Pricking.
- Continuous.
- Localized.
- Throbbing (beating).
- Burning.
- Intermittent.
- Referred.
- Colicky (abdominal).
- Aching (deep).
Pain receptors:
They are in the form of free never endings, widely distributed all
over the body. They are excited by the following agents:
- Chemo-sensitive pain receptors: Histamine, bradykinin and serotonin.
- Thermo-sensitive pain receptors: Excessive heat.
- Mechano-sensitive pain receptors: Mechanical stress.
Mechanism of stimulation:
Pain receptors are stimulated when there is tissue damage:
- Tissue damage releases proteolytic enzymes.
- The proteolytic enzymes immediately split bradykinin and similar
polypeptides from the globulins in the interstitial fluid.
- Bradykinin and similar polypeptides stimulate pain receptors.
It was found that injection of minute amount of bradykinin in the
skin produces severe pain.
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Cutaneous pain:
This type of pain is perceived as a result of stimulation of pain
receptors in the skin. Pain receptors are slowly-adapting receptors, which
continuously inform the CNS about tissue damage.
Pathway for cutaneous pain sensation:
Cutaneous pain is conducted from pain receptors along two types
of afferent fibers:
- Thin-myelinated Aδ fibers: Having a diameter of 1 - 5 microns and
conduction velocity of 5 - 15 meters / second.
- Non-myelinated C fibers: Having a diameter of less than 1 micron and a
conduction velocity of 0.5 meter / second.
Thus, when a sudden injurious stimulus is applied to the skin, a
double pain sensation is perceived:
* Fast pricking pain: It can be localized within 10 - 20 cm of the
stimulated area, being conducted along Aδ fibers. It informs the person
rapidly of the damaging stimulus and starts important reflexes to avoid
such stimulus.
* Slow burning pain: It is very grossly spread to a major part of the body,
being conducted along C fibers. This type of pain tends to become more
and more vigorous by time, causing the unpleasant intolerable suffering
of pain.
These two types of pain can be dissociated from each other by:
- Moderate compression of the nerve trunk: It will destroy Aδ fibers
leaving C fibers, so the fast pricking pain is lost, while the burning pain
remains.
- Low concentration of local anesthesia: It will block C fibers only, so
the pricking pain is felt while the burning pain is lost.
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* First order neuron:
Pain fibers enter the spinal cord along lateral division of the
posterior root then ascend for 2 – 3 segments in Lissauer's tract to end
around the cells in substantia gelatinosa of Rolando (SGR).
* Second order neuron:
It arises from cells in the SGR, crosses the midline in front of
central canal and passes upward in the opposite side in the lateral
spinothalamic tract. In the brain stem, pain fibers separate into:
Pricking pain pathway
Burning pain pathway
- It terminates in the posterolateral
- It terminates in the reticular formation
ventral nucleus of thalamus (PLVNT).
of the brain stem and non-specific
* Third order neuron:
thalamic
- It arises from the thalamus, passes to
diffusely to all areas of cerebral cortex,
sensory area of cerebral cortex “somatic
forming reticular activating system.
nuclei,
which
discharge
sensory area I” for pain localization.
Function of thalamus and cerebral cortex in perception of pain:
Perception of pain can take place at the level of thalamus, since
complete removal of somatic sensory areas of cerebral cortex does not
abolish the perception of pain. Lesions in the sensory areas of cerebral
cortex lead to severe pain.
Pain relief:
* Cordotomy: The intractable pain (e.g. cancer) can be relieved by
sectioning of anterolateral quadrant of the cord (of opposite side of upper
thoracic area, if the pain is in the lower half of the body). This procedure
is not always successful because:
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- Pain from upper half of the body does not cross to the opposite side of
the spinal cord.
- Pain returns after few months and becomes more severe.
* Spinal cord stimulation:
Shealy (1967) devised dorsal column
stimulator (50 % success rate). Now, it is done epidurally.
* Physiotherapy:
It may utilize one or more of the following theories:
- Block pain gate.
- Stimulation of the descending pain suppression system.
- Endogenous opiate mechanisms.
- Physiological block of the nociceptive input.
- Removal of the painful stimulus.
- Placebo effect.
Reaction to pain:
The threshold for pain is the same for all individuals but they differ
only in their reactions to pain.
Reflex motor reactions
Complicated
withdrawal
reflexes
Emotional reactions
to - Crying, anxiety and nausea.
remove the body or a part of the body - Acceleration of the heart.
from the painful stimulus.
- Rise of the arterial blood pressure.
The reaction to pain depends upon the degree of spread of pain
impulses in brain stem, hypothalamus and various brain areas.
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Pain control systems in the brain and spinal cord
Electrical stimulation in the several spinal cord and brain areas can
reduce or block pain signals (stimulus-produced analgesia):
- Periventricular area of diencephalon (adjacent to the third ventricle).
- Periaquaductal grey area of the brain stem.
- Midline Raphe nuclei of the brain stem.
- Medial forebrain bundle.
The possible underlying mechanisms may be:
Stimulation of these areas may lead to:
* Excitation of tracts which pass in the spinal cord to end in the dorsal
horns, mainly in laminae I, II and III (stations for afferent pain fibres).
So, this stimulation will block or suppress pain transmission.
* Inhibition of pain transmission in the pain pathways, particularly in:
- Reticular nuclei in the brain stem.
- Intra-laminar nuclei of the thalamus.
Gate control theory of pain:
Melzack and Wall (1965) reported that conduction of pain
impulses in the spinal cord can be inhibited by:
- Stimulation of large sensory fibres from peripheral mechanoreceptor
(e.g. TENS).
- Corticofugal fibers from the brain to the spinal cord.
The sites of synapses for pain sensation can be considered as gates
for the ascending pain impulses:
- Spinal gate at the neurons of SGR.
- Brain stem gate at the neurons of reticular formation.
- Thalamic gate at the neurons of thalamus.
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It was found that:
* Stimulation of large sensory fibers: It produces presynaptic inhibition
for pain fibers before they synapse with neurons of SGR. In other words,
pain fibers are constantly balanced against tactile signals, each of them is
capable of inhibiting the other. So, the excessive tactile stimulation can
suppress pain transmission.
* Corticofugal fibers: It was explained before.
Brain's opiate system: (enkephalins and endorphins)
Recently, two closely related types of compounds with morphinelike actions were discovered in the brain, called enkephalins and
endorphins.
Enkephalins
Endorphins
- They are found mainly in brain areas
- They are found in high concentration in the
associated with pain control (4 areas).
hypothalamus and pituitary glands.
- There are two types; met-enkephalin
- The most potent type is β-endorphin.
and Leu-enkephalin.
Therefore, it is suggested that both compounds function as
excitatory transmitter substances which activate portions of the brain's
analgesic system.
Referred pain:
Visceral pain is usually referred to the body surface. Such pain is
not felt in the diseased viscus but in the body surface somatic structures
supplied by the same posterior roots as the diseased viscus.
The mechanism of the referred pain will be as follows:
* Pain impulses from the diseased viscus converge on the same cells in
the SGR, which receive pain impulses from a particular skin dermatome.
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in the
* Cells of SGR will discharge impulses along the lateral spinothalamic
tract to the sensory area of the cerebral cortex.
* Sensory area of the cerebral cortex is accustomed to receive pain
sensation from the skin, therefore pain impulses from the diseased viscus
is projected to the skin area, which is called the “dominant area”. This is
called the “convergence-projection theory”.
Some disturbances in sensation:
* Hyperalgesia:
It means hypersensitivity to pain, which may be:
- Primary: It is due to hypersensitivity of pain receptors (burnt skin).
- Secondary: It is due to facilitation of pain transmission.
* Herpes zoster:
It is due to viral infection of the dorsal root ganglion, causing
severe pain in the dermatomal segment supplied by this ganglion.
* Thalamic syndrome:
It is due occlusion of the posterolateral branch of the posterior
cerebral artery, which supplies the posterolateral ventral nucleus of
thalamus (PLVNT). The PLVNT degenerates, while the anteromedial
nuclei remain intact, leading to:
- Loss of all sensation from the opposite side of the body.
- Sensory ataxia (loss of kinesthetic sense).
- Sensation begins to return but always painful.
* Syringomyelia:
It is characterized by cavity formation in the grey matter around
the central canal of spinal cord, leading to interruption of the crossing
fibers for pain, temperature and crude touch sensations.
- There will be loss of these sensations of the opposite side of the body
below the level of lesion.
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- If the lesion affects the cervical enlargement, a jacket distribution of
loss of pain, temperature and crude touch sensation occurs.
- Fine touch sensation is intact, as it is carried along the dorsal column
tracts.
* Brown-Sequard syndrome:
There will be damage of one side of the spinal cord, leading to the
following sensory changes below the level of lesion:
- Loss of pain, temperature and crude touch sensations on the opposite
side of the body.
- Loss of fine touch, kinesthesia, vibration and discrimination of weight
sensations on the same side of the body.
Melzack scale of pain:
Grade
Type of pain
0
No pain
1
Mild pain
2
Discomforting pain
3
Distressing pain
4
Horrible pain
5
Exacerbating pain
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