PAIN

Pain is a sensation characterized by a group of unpleasant and complex perceptual and emotional experiences that trigger autonomic, psychologic, and somatic motor responses.

Pain sensation has two components:

(1)?? rapidly conducted action potentials carried by large-diameter, myelinated axons, resulting in sharp, well-localized, pricking, or cutting pain, followed by (2) more slowly propagated action potentials, carried by smaller, less heavily myelinated axons, resulting in diffuse burning or aching pain. Research indicates that pain receptors have very uniform sensitivity, which does not change dramatically from one instant to another. Variations in pain sensation result from the mechanisms by which pain receptors are stimulated, differences in the integration of action potentials from the pain receptors, and complex interactions in the cerebral cortex, cingulate gyrus, and thalamus, where the emotional component of pain is registered.

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Neurons in the cerebral cortex respond to pain stimuli selectively based on prior experience and context. Stress, for example, can reduce pain perception. Although the dorsal-column/medial- lemniscal system contains no pain fibers, tactile and mechanoreceptors are often activated by the same stimuli that affect pain receptors. Action potentials from tactile receptors provide information that allows the pain sensation to be localized. Superficial pain is highly localized, in part, because of the simultaneous stimulation of pain receptors and mechanoreceptors in the skin. Deep or visceral pain is not highly localized (diffuse) because of fewer mechanoreceptors in the deeper structures, and it is normally perceived as a diffuse pain. Dorsal-column/medial-lemniscal system neurons are involved in what is called the gate-control theory of pain control. Primary neurons of the dorsal-column/medial-lemniscal system send out collateral branches that synapse with interneurons in the posterior horn of the spinal cord. These interneurons have an inhibitory effect on secondary neurons of the spinothalamic tract. Thus, pain action potentials traveling through the spinothalamic tract can be suppressed by action potentials that originate in neurons of the dorsal-column/medial-lemniscal system. The arrangement may act as a “gate” for pain action potentials transmitted in the spinothalamic tract. Increased activity in the dorsal-column/medial-lemniscal system tends to close the gate, thereby reducing pain action potentials transmitted in the spinothalamic tract.

Descending pathways from the cerebral cortex or other brain regions can also regulate this “gate.” The gate-control theory may explain the physiologic basis for the following methods that have been used to reduce the intensity of chronic pain: electric stimulation of the dorsal-column/medial-lemniscal neurons, transcutaneous electric stimulation (applying a weak electric stimulus to the skin), acupuncture, massage, and exercise. The frequency of action potentials that are transmitted in the dorsal-column/medial-lemniscal system is increased when the skin is rubbed vigorously and when the limbs are moved and may explain why vigorously rubbing a large area around a source of pricking pain tends to reduce the intensity of the painful sensation.

Exercise normally decreases the sensation of pain, and exercise programs are important components in the management of chronic pain not associated with illness. Action potentials initiated by acupuncture procedures may act through a gating mechanism in which inhibition of action potentials in neurons that transmit pain action potentials upward in the spinal cord is influenced by activity in sensory cells that send collateral branches to the posterior horn. Analgesics act in much the same way as gate control. Some analgesics block the transmission of nociception in the spinal cord from primary neurons to neurons of the ascending pathways. Other analgesics function at the level of the cerebral cortex to modulate pain.

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?Referred Pain

?Referred pain is a painful sensation in a region of the body that is not the source of the pain stimulus. Most commonly, referred pain is sensed in the skin or other superficial structures when internal organs are damaged or inflamed.

This sensation usually occurs because both the area of skin to which the pain is referred and the visceral area that is damaged are innervated by neurons that project to the same area of the cerebral cortex. The brain cannot distinguish between the two sources of painful stimuli, and the painful sensation is referred to the most superficial structures innervated by the converging neurons. This referral may occur because the number of receptors is much greater in superficial structures than in deep structures and the brain is more “accustomed” to dealing with superficial stimuli. Referred pain is clinically useful in diagnosing the actual cause of a painful stimulus. Heart attack victims often feel cutaneous pain radiating from the left shoulder down the arm.

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Phantom Pain

?Phantom pain occurs in people who have had appendages amputated or a structure such as a tooth removed. Many of these people perceive pain, which can be intense, or other sensations, in the amputated structure as if it were still in place. If a neuron pathway that transmits action potentials is stimulated at any point along that pathway, action potentials are initiated and propagated toward the CNS. Integration results in the perception of pain that is projected to the site of the sensory receptors, even if those sensory receptors are no longer present. A similar phenomenon can be easily demonstrated by bumping the ulnar nerve as it crosses the elbow (the funny bone). A sensation of pain is often felt in the fourth and fifth digits, even though the neurons were stimulated at the elbow. A factor that may be important in phantom pain is the lack of touch, pressure, and proprioceptive impulses from the amputated limb. Those action potentials suppress the transmission of pain action potentials in the pain pathways, as explained by the gate-control theory of pain. When a limb is amputated, the inhibitory effect of sensory information is removed. As a consequence, the intensity of phantom pain may be increased. Another factor in phantom pain may be that the cerebral cortex retains an image of the amputated body part.

Chronic Pain

Chronic pain is long-lasting. Some chronic pain has a known cause, such as tissue damage, as in the case of arthritis. Other chronic pain cannot be associated with tissue damage and has no known cause. Pain is important in warning us of potentially injurious conditions because pain receptors are stimulated when tissues are injured. Pain itself, however, can become a problem. Chronic pain, such as migraine headaches, localized facial pain, or back pain, can be very debilitating, and pain loses its value of providing information about the condition of the body. People suffering from chronic pain often feel helpless and hopeless, and they may become dependent on drugs. The pain can interfere with vocational pursuits, and many victims are unemployed or even housebound and socially isolated. They are easily frustrated or angered, and they suffer symptoms of major depression. These qualities are associated with what is called chronic pain syndrome. Over 2 million people in the United States at any given time suffer chronic pain sufficient to impair activity. Chronic pain may originate with acute pain associated with an injury or may develop for no apparent reason. How sensory signals are processed in the thalamus and cerebrum may determine if the input is evaluated as only a discomfort, a minor pain, or a severe pain and how much distress is associated with the sensation. The brain actively regulates the amount of pain information that gets through to the level of perception, thereby suppressing much of the input. If this dampening system becomes less functional, pain perception may increase. Other nervous system factors, such as a loss of some sensory modalities from an area, or habituation of pain transmission, which may remain even after the stimulus is removed, may actually intensify otherwise normal pain sensations. Treatment often requires a multidisciplinary approach, including such interventions as surgery or psychotherapy. Some sufferers respond well to drug therapy, but some drugs, such as opiates, have a diminishing effect and may become addictive.

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Sensitization In Chronic Pain

Tissue damage within an area of injury, such as the skin, can cause an increase in the sensitivity of nerve endings in the area of damage, a condition called peripheral sensitization. One class of pain receptors is not activated by traditional noxious stimuli but is recruited only when tissues become inflamed. These receptors, once activated, add to the total barrage of sensory signals to the brain and intensify the sensation of pain. The CNS may also respond to tissue damage by decreasing its threshold and increasing its sensitivity to pain. This condition is called central sensitization. Central sensitization apparently results from a specific subset of receptors that is only recruited during repetitive neuron firing, such as when intense pain sensations are experienced. These receptors maintain a hyper-excitable state in the CNS cells. This chronic, hyper-excitable state can result in persistent, chronic pain states. This information concerning peripheral and central sensitization and the knowledge that sensitization involves neuronal and chemical receptors not normally involved in sensation may lead to the discovery of new drugs for treating chronic pain. Rather than searching for new analgesics, which may decrease a broad range of sensations, an opportunity is now available to develop a new class of drugs, the “anti-hyper-analgesics,” which may block sensitization without diminishing other sensations, including normal pain.