Pain is a sensation characterized by group of unpleasant perceptual and emotional experiences that trigger autonomic, psychological, and somatomotor responses. Pain sensation consists of two portions: (l) 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 that does not change dramatically from one point in time to another. Variations in pain sensation result from the differences in integration of action potentials from the pain receptors and the mechanisms by which pain receptors are stimulated.
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 the tactile receptors help localize the source of pain and monitor changes in the stimuli. Superficial pain is highly localized because of the simultaneous stimulation of pain receptors and mechanoreceptors in the skin. Deep or visceral pain is not highly localized because of the absence of numerous mechanoreceptors in the deeper structures, and its 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 association neurons in the posterior horn of the spinal cord. The association neurons have an inhibitory effect on the secondary neurons of the lateral spinothalamic tract. Thus pain action potentials traveling through the lateral spinothalamic tract can be suppressed by action potentials that originate in neurons of the dorsal column-medial lemniscal system. These neurons may act as a "gate" for pain action potentials transmitted in the lateral spinothalamic tract. Increased activity in the dorsal column-medial lemniscal system tends to close the gate, reducing pain action potentials transmitted in the lateral spinothalamic tract.
The gate-control theory may explain the physiological basis for the following methods that have been used to reduce the intensity of chronic pain: electrical stimulation of the dorsal column-medical lemniscal neurons, transutaneous electrical stimulation (applying a weak electrical stimulation to the skin), acupuncture, massage, and exercise. The frequency of action potentials that are transmitted in the dorsal column-medial lelmniscal 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 clinical management of chronic pain not associated with illness. Action potentials initiated by acupuncture procedures may also inhibit the action potentials in neurons that transmit pain action potentials upward in the spinal cord by influencing afferent cells of the posterior horn.
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 then internal organs are damaged or inflamed. This sensation usually occurs because both the area to which the pain is referred and the area where the actual damage occurs are innervated by neurons from the same spinal segment.
Many cutaneous afferent neurons and visceral afferent neurons that transmit pain action potentials converge on the same ascending neurons; however, 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 be a result of the fact that the number of receptors is much greater in the periphery 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 the painful stimulus. Heart attack victims often feel cutaneous pain radiating from the left shoulder down the arm.
Phantom pain occurs in people who have had appendages amputated. Frequently these people perceive pain, which can be intense, 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 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 very important in phantom pain results from the lack of touch, pressure and proprioceptive impulses from the amputate limb. Those action potentials suppress the transmission of pain action potentials in the pain pathways. When a limb is amputated, the inhibitory effect of sensory information, which is normally transmitted through the dorsal column-medial lemniscal system, on the ascending pain pathways is removed. As a consequence, the intensity of phantom pain may be increased. Another factor in phantom pain may be that the brain retains an image of the amputated body part and creates an impression that the part is still there.
Although pain is important in warning us of potentially injurious conditions, the pain itself can become a problem. Chronic pain, such as migraine headaches, localized facial pain, or back pain, can be very debilitating and 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 the victims are often unemployed or even housebound and socially isolate. 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 afferent 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 the level of perception, 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 actual intensify otherwise normal pain sensations. The depression, anxiety, and stress associated with chronic pain syndrome can also perpetuate the pain sensations. Treatment often requires a multidisciplinary approach, including such interventions as surgery and/or psychotherapy. Some suffers respond well to drug therapy, but some drugs, such as opiates, have a diminishing return and may become addictive.