Thie cost of chronic, persistent pain cannot be fully measured, because it includes not only lost work time, or increased health care utilization, but also personal and quality-of-life issues, which have costs that cannot be calculated. Patients with chronic pain are often misunderstood and undertreated for the pain. As they seek relief for their pain, the health care system may view them as drug seeking rather than relief seeking. This may cause the chronic pain patient to present a social mask to the public that hides the full extent of the pain. Assessing pain in a patient who is trying to hide the effects of chronic pain is much more difficult and requires a comprehensive set of questions to obtain the needed information.
Most patients with chronic pain report pain that exists at some level throughout the day. The patients with low back pain may have episodes of pain in which the pain increases and then returns to a lower, more tolerable level. Along with the pain, patients can become anxious or depressed as the pain appears to be untreatable or as pain intensity increases. The uncertainty of the pain experience can lead patients to feel helpless and hopeless.
It is difficult to measure the cost of chronic pain. The best evaluation is that chronic pain costs are estimated to be $100 billion per year and are related to the following:
■ Welfare and disability costs
■ Losses in tax revenue
■ Lost productivity through both absenteeism and presentism (at work, but in pain)
Presentism alone is estimated to cost $61.2 billion per year (Stewart, Ricci, Chee, Morganstein, & Lipton, 2003). Most patients with chronic pain want to work but are limited by pain. Because these patients try to work but are less productive, it is a hidden cost that is hard to evaluate.
Pain that is long term can take a toll on money and employment, but it can also rob the patient of quality of life, disrupt sleep, and cause significant depression. Depression is a common occurrence in patients with chronic pain. The depression is more of a situational depression than a deep-seated clinical effect. If depression is a part of a patient's chronic pain, treatment with antidepressants is indicated. If the depression is allowed to go untreated, the patient may develop suicidal ideation. Unfortunately, the rate for suicide in chronic pain patients is twice the rate for the similar patient demographic without chronic pain (Tang & Crane, 2006).
Chronic pain can also result in sleep disturbances, which can rob the patients of needed rest and restorative sleep they need to help them cope with the stress of daily life with pain. Sleep disturbances are common and occurred in about 55% of patients in one study who reported restless/or light sleep after the onset of pain (Marin, Cyhan, & Miklos, 2006). The most common adverse effects of sleep disturbances that are reported by patients include the following:
■ Delayed onset of sleep
■ Daytime fatigue
■ Nonrestorative sleep
The personal costs for the older patient with chronic pain are very significant. Because prescribers are reluctant to provide high-level opi-oid medications to many older patients, for fear of unwanted side e ffects such as oversedation, constipation, and confusion, the pain will be untreated or undertreated (Bruckenthal & D'Arcy, 2007). Under-treated pain can lead to the following:
■ Depression, anxiety
■ Decreased socialization
■ Sleep disturbances
■ Impaired ambulation and functioning
■ Increased health care utilization and costs (Bruckenthal & D'Arcy, 2007)
Chronic pain can lead to poor self-esteem, financial ruin, and diminished quality of life. It affects the health status of the patient by suppressing natural killer cells, decreasing the body's ability to defend itself against tumor and virus-infected cells. Chronic pain not only reduces the quality of life but also can have an impact on life itself.
The mechanisms of pain transmission are different for acute pain and chronic pain. The onset of acute pain is sudden and can provoke a fight or flight type of response, with adrenaline release that will subside rapidly. Chronic pain, on the other hand, is long term, and over time, more complex and advanced pain-facilitating responses, such as the activation of N-methyl-D-aspartate (NMDA) receptors, take place. Many pharmaceutical companies aim the action of their medications at a specific sites in the pain transmission process. As one example, retaining serotonin at the synaptic junction can help reduce the amount of pain-facilitating substances available to create or continue the pain stimulus.
There are theories that have been advanced over the years about how pain is transmitted and what physiologic mechanisms are involved. One of the earliest theorists was René Descartes who felt that pain was a stimulus response mechanism. This concept was also called the labeled line theory. In this theory, pain was seen as a painful stimulus that traveled up to the brain, resulting in the body recognizing the sensation as pain. An example would be a stimulus, such as a burn or trauma, that would travel up to the brain, and the brain would recognize it as pain. The resulting response would be for the body to withdraw from the pain, such as removing the hand from a fire. This theory focuses primarily on the physical aspect of pain rather than including the emotional or psychological aspects of the pain experience.
Especially for patients with chronic pain, the psychological and emotional component of pain is an important aspect of the condition. Older theories, such as those espoused by Pavlov, considered pain to be a learned response that was affected by cultural and learned behaviors that could be offset by operant conditioning. Turk described pain as a multidimensional experience and proposes that the patient, not the health care practitioner, is really the specialist on the pain. This theory empowers the patient to become active participants in pain treatment and helps the patient diminish negative behaviors and increase positive reinforcing behaviors (American Society for Pain Management Nursing [ASPMN], 2010).
Perhaps the most well known theory of pain transmission is the Gate Control Theory developed by Melzack and Wall in 1965 (ASPMN, 2010). In this theory, the psychological and physiological aspects of pain transmission are combined. Simplistically, the Gate Control Theory states that a pain stimulus can be significant enough in intensity to "open" a neuronal gate that will allow the pain stimulus to proceed up the nervous system to create a sensation that can be identified as pain by the brain.
The actual steps in pain transmission according to the Gate Control Theory include the following:
■ A pain stimulus from the body periphery is carried by A-delta and C nerve fibers to the dorsal horn of the spinal cord.
■ The gate is located in the substantia gelatinosa in the dorsal horn of the spinal cord, and it can facilitate or inhibit, either promote or stop, the progression of the nerve impulse through the central nervous system.
■ If the painful stimulus is of sufficient intensity or persists, the pain is transmitted up through the limbic system to the cerebral cortex.
■ In the cerebral cortex, the stimulus is recognized as pain and the efferent neural path is activated to provide a response to the pain. (Adapted from ASPMN, 2010)
As science has investigated and furthered the knowledge of this pain transmission theory, several other concepts have emerged:
■ The central control processes and central intensity process located in the brain and limbic system help to translate the understanding of the sensation and can modulate the section of the descending pain pathways.
■ When pain stimuli entering the nervous system reach critical levels, the T-cell system is activated, which creates a link between the brain and body that connects the subjective and objective experience of pain.
■ By increasing the sensation of pain, peripheral nerve sensitization can be caused through continued nerve stimulation producing a state of hyperexcitability because of alternation in the sodium ion channels. Continued pain stimulation can be increased as inflammatory response persists.
■ Wind-up and neuroplasticity can also occur. Wind-up is a phenomenon that develops when, as the result of continued moderate to severe pain, the NMDA receptors are activated. These receptors serve to process the pain faster and with more intensity, creating a pain intensity that is greater than expected for the stimulus. The pain response is greatly enhanced when wind-up has occurred. Central sensitization can occur as a result of wind-up, which allows normal tissue to become extremely sensitive to pressure in areas that are not identified as painful.
Neuroplasticity is the result of moderate to severe pain that lasts for more than 24 hours and occurs in the spinal area of the nervous system. With neuroplasticity, pain fiber growth is stimulated and the pain inhibition system is damaged, resulting in more intense pain that is widespread, lessening the ability of the body to stop the pain.
Peripheral sensitization can occur as a result of neuroplasticity. This creates a condition in which nonpainful touch and pressure become painful (ASPMN, 2010).
As we study and begin to understand the process and theory of pain transmission, more information about the process is discovered. As science expands its understanding of the pathophysiology of pain, more information will lead to a better understanding of the transmission process.
How is pain really felt? The concept of nociception can help us determine just how pain moves through the nervous system, and it can also provide us with ideas about how we can interfere with pain facilitation and about pain inhibition. Nociception is defined as the perception of pain by sensory pain receptors called nociceptors located in the periphery. In the theory of nociception, there are four stages, or levels, of pain transmission.
1. Transduction. A noxious stimuli converts energy into a nerve impulse, which is detected by sensory receptors called nociceptors.
2. Transmission. The neural pain signal moves from the periphery to the spinal cord and brain.
3. Perception. The pain impulse is transmitted to the higher areas of the brain, where it is identified as pain.
4. Modulation-facilitating and inhibitory input. Input from the brain either inhibits or facilitates the sensory transmission at the level of the spinal cord. Forms the brain modulates or influences the sensory transmission at the level of the spinal cord. (Berry, Covington, Dahl, Katz, & Miaskowski, 2006; D'Arcy, 2007)
The transmission of pain is basically the passing along of a pain stimulus from the peripheral nervous system into the central nervous system, where it is translated and recognized as pain. The afferent nerve fibers are the means of moving the stimulus along the neuronal pathways.
Nociception can come from visceral organs, where pain is identified as "crampy" or "gnawing," or it can be somatic, from skin, muscles, bones, and joints, where pain is identified as "sharp." There are several different types of receptors that can trigger a pain response:
■ Mechanoreceptors—activated by pressure
■ Thermal receptors—activated by heat or cold
■ Chemoreceptors—activated by chemicals, such as inflammatory substances (ASPMN, 2010)
Pain can first be experienced by free nerve endings or nociceptors located in the periphery of the body. As a person cuts a hand or fractures an extremity, the pain stimulus is first perceived in the nerves closest to the injury. In order for a pain stimulus to be created, the sodium ions on the nerve fiber must depolarize, and this causes the pain stimulus to be initiated and passed along the neural circuitry. There are two main types of nerves that transmit pain impulses or stimuli:
■ A-delta fibers are large nerve fibers covered in myelin that can transmit a nerve impulse rapidly. The pain transmitted on an A-delta fiber is easily localized and the patients may describe the pain as sharp or stabbing.
■ C fibers are smaller and unmyelinated, and the pain impulse is conducted at a much slower rate. Pain that is produced by C fibers is identified by patients as achy or burning in nature (ASPMN, 2010).
Two primary substances can help facilitate the transmission of pain from the periphery. Substance P is a neurotransmitter secreted by the free nerve endings of C fibers whose function is to speed the transmission of the pain impulse. Bradykinin is a second type of neurotransmitter whose function is to participate in the inflammatory response and hyperalgesia (ASPMN, 2010). Nociception can stimulate both A-delta and C fibers for pain transmission.
Other substances that participate in the facilitation of pain include the following:
■ Histamine is a substance released from mast cells produced in response to tissue trauma.
■ Serotonin can be released from platelets and is produced in response to tissue trauma.
■ COX products (prostaglandin E2 and thromboxane E ) act to sensitize and excite C fibers causing hyperexcitability.
■ Cytokines (interleukins and tumor necrosis factor) can sensitize C fiber terminals and participate in the inflammatory and infection process involving mast cells.
■ Calcitonin gene-related peptide (CGRP) is located at C fiber nerve endings and produces local cutaneous vasodilatation, plasma extravasation, and skin sensitization in collaboration with substance P production (ASPMN, 2010).
Once transduction takes place, the nerve impulse is passed through a synaptic junction from the peripheral nervous system to the central nervous system. This synaptic junction has various functions and secretes various substances. Some medications, for example pregabalin, act at the synaptic junction by blocking calcium channels. This in turn can reduce the amount of neuronal firing and decrease the passage of pain stimuli. The synapse is between the peripheral neuron into the central nervous system via the dorsal root ganglion.
As the pain stimulus is passed from the peripheral nervous system into the central nervous system, the signal passes through the dorsal root ganglion to a synaptic junction in the substantia gelatinosa located in the dorsal horn of the spinal cord. As the stimulus pushing the pain impulse forward overcomes any opposing or inhibiting forces, the "gate" is opened, allowing the pain impulse to proceed up the spinal cord to the limbic system and brain.
Thie opening of the gate is controlled by a summing of all the forces involved in the conduction of the pain impulse. If the facilitating forces, neural excitability, and pain-facilitating substances, such as substance P, predominate, the pain impulse is passed on. If pain inhibiting forces predominate, the signal is blocked and the gate does not open. If by chance the pain impulse is perceived as potentially life threatening, a reflex arc across the spinal cord will fire, causing an immediate response to protect the affected area (e.g., touching a hot surface causes the body to react by removing the hand from the hot surface). This event can take place before any central processing of the neural signal.
Centrally active pain-facilitating and inhibitory substances include the following:
■ Glutamate—responsible for communication between the peripheral and central nervous systems. Also plays a role in activating the NMDA receptors
■ Dynorphin—an endogenous opioid
■ Beta-endorphin—an endogenous opioid
■ Gamma-aminobutyric acid (GABA) (ASPMN, 2010)
Also performing an inhibitory role are the opioid receptors located both presynaptically and postsynaptically that are available for binding opioid substances, such as morphine, and producing analgesia. Although there are opioid receptors located at other sites in the body, those that are located inside the spinal cord have the most information available about how they function.
As the pain impulse passes through the dorsal horn, it passes across the spine to the lateral spinothalamic tracts, which then allow the pain impulse to proceed up to the thalamus and limbic system, activating the emotions and memories associated with pain, and then to the cerebral cortex, where the pain impulse or stimulus is recognized as pain. Although this process seems complicated, the body can conduct a pain impulse in only milliseconds.
Within the limbic system, two pain substances, norepinephrine and serotonin, are active. Current drug therapies, such as tricyclic antidepressants and selective serotonin reuptake inhibitors (SSRIs), are aimed at this process and use the substances to reduce the amount of serotonin available to activate neuronal firing at synaptic junctions. The synaptic junctions have such varied functions that they not only are important for producing pain but are also critical sites for reducing pain by controlling the production of pain-facilitating substances and actions.
Once the pain stimulus reaches the cerebral cortex, the afferent pathway is completed. At that time, the efferent nerve fibers are used to pass the neuronal response identified as pain back to the periphery or affected area. Descending nerve fibers from the locus ceruleus and pe-riaqueductal gray matter are activated, and the pain stimulus is passed back down the efferent pathway, where a response to the pain stimulus, such as moving the affected area away from the pain, is produced.
All patients with chronic pain should be assessed for depression and sleep disturbances when they are seen by their regular health care provider. Treating these conditions will help decrease the effects of pain that the patient is experiencing.
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