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).
- Throbbing (beating).
- Colicky (abdominal). / - Pricking.
- Burning.
- Aching (deep). / - Continuous.
- Intermittent. / - Localized.
- Referred.
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.
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.
* 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 ventral nucleus of thalamus (PLVNT).
* Third order neuron:
- It arises from the thalamus, passes to sensory area of cerebral cortex “somatic sensory area I” for pain localization. / - It terminates in the reticular formation of the brain stem and non-specific thalamic nuclei, which discharge diffusely to all areas of cerebral cortex, forming reticular activating system.
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:
- 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 / Emotional reactionsComplicated withdrawal reflexes to remove the body or a part of the body from the painful stimulus. / - Crying, anxiety and nausea.
- Acceleration of the heart.
- 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.
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.
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 morphine-like actions were discovered in the brain, called enkephalins and endorphins.
Enkephalins / Endorphins- They are found mainly in brain areas associated with pain control (4 areas).
- There are two types; met-enkephalin and Leu-enkephalin. / - They are found in high concentration in the in the hypothalamus and pituitary glands.
- The most potent type is β-endorphin.
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.
* 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.
- 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 pain0 / No pain
1 / Mild pain
2 / Discomforting pain
3 / Distressing pain
4 / Horrible pain
5 / Exacerbating pain
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