Pain :: Physiological Consideration

Pain is a universal human experience and the most common reason people seek medical care. Pain tells us something is wrong, that tissue in our body has been damaged, and we need to do something to change the situation. Because pain is such a strong motivator for action, it is considered one of the body's most important protective mechanisms.

Definition of Pain:

Random House Webster's Dictionary defines pain as "bodily, mental or emotional suffering, as due to injury or illness." The International Association for the Study of Pain defines pain as a "sensory and emotional experience associated with tissue damage or described in terms of such damage." Pain, however, is much more than a physical sensation caused by a specific stimulus. It is a complex mechanism with physical, emotional, and cognitive components. It is subjective, and highly individual. Pain cannot be objectively measured in the same way as, for example, the chemical content of urine or the oxygen content level of blood. Only the person who is suffering knows how the experience feels. For these reasons, McCaffery defined pain as "whatever the experiencing person says it is and whenever he says it does (1979)." The American Pain Society goes further by stating that it is "not the responsibility of clients to prove they are in pain; it is the nurse's responsibility to accept the clients report of pain (2005)."

Physiology of Pain:

Pain Theories:

A number of theories have been formulated to explain noxious perception. One of the earliest idea proposed by, Descartes that a straight line channel of pain exists from skin to brain. During the 19th century, Von Frey theorized that pain pathways move from specialized receptors in body tissues to a pain center in the brain. The focus of this theory, known as the specificity theory, is specialized peripheral receptors rather than a central mechanism of pain in the brain. However, although receptors are specialized, a focus on peripheral receptors does not explain how an amputee can feel pain in the amputated limb (a phenomenon known as phantom limb pain) when the peripheral receptors no longer exist. According to the pattern theory of pain proposed in the late 19th century, pain is the result of stimulation of certain nerve impulses that form a pattern and are then combined and dumped into the spinal cord as a lump sum of pain, a process called "central summation." This theory can better account for the phantom limb phenomenon, because the focus is on what occurs in the brain rather than on peripheral receptors. However, the theory does not account for other factors in pain perception, such as the effect of placebos on pain. In 1965, Melzack and Wall published the well-known gate control theory of pain.

Fig: Gate control theory of pain

According to this theory, a mechanism in the brain acts as a gate to increase or decrease the flow of nerve impulses from the peripheral fibers to the CNS. An "open" gate allows the flow of nerve impulses, and the brain can perceive pain. A "closed" gate does not allow flow of nerve impulses, decreasing the perception of pain (Figure 1). Although the gate control theory has been widely accepted since the 1970s, it leaves unanswered questions, including chronic pain issues, sex-based differences, stress effects, and the effects of previous pain experiences. In 1999, Melzack and Wall presented a newer theory of pain, consistent with the idea of gate control, that addresses some of these unanswered questions. This "new and improved" theory, the neuromatrix theory, says that each person has a genetically built-in network of neurons called the "body-self neuromatrix." Just as each person is unique in physical appearance, each person's matrix of neurons is unique and is affected by all facets of the person's physical, psychological, and cognitive makeup, as well as his or her experience. Thus, the pain experience does not reflect a simple one-to-one relationship between tissue damage and pain.

Pain Pathway:

Nociceptors, or pain receptors, are free nerve endings that respond to painful stimuli. Nociceptors are found throughout all tissues except the brain, and they transmit information to the brain. They are stimulated by biological, electrical, thermal, mechanical, and chemical stimuli. Pain perception occurs when these stimuli are transmitted to the spinal cord and then to the central areas of the brain. Pain impulses travel to the dorsal horn of the spine, where they synapse with dorsal horn neurons in the substantia gelatinosa and then ascend to the brain. The basic sensation of pain occurs at the thalamus. It continues to the limbic system (emotional center) and the cerebral cortex, where pain is perceived and interpreted. Two types of fibers are involved in pain transmission. The large A delta fibers produce sharp well-defined pain, called "fast pain" or "first pain," typically stimulated by a cut, an electrical shock, or a physical blow. Transmission through the A fibers is so fast that the body's reflexes can actually respond faster than the pain stimulus, resulting in retraction of the affected body part even before the person perceives the pain. After this first pain, the smaller C fibers transmit dull burning or aching sensations, known as "second pain." The C fibers transmit pain more slowly than the A fibers do because the C fibers are smaller and lack a myelin sheath. The C fibers are the ones that produce constant pain. According to the gate control theory, stimulation of the fibers that transmit nonpainful stimuli can block pain impulses at the gate in the dorsal horn. For example, if touch receptors (A beta fibers) are stimulated, they dominate and close the gate. This ability to block pain impulses is the reason a person is prone to immediately grab and massage the foot when he or she stubs a toe. The touch blocks the transmission and duration of pain impulses. This capacity has implications for the use of touch and massage for some patients in pain.

Regulators of Pain:

Chemical substances that modulate the transmission of pain are released into the extracellular tissue when tissue damage occurs. They activate the pain receptors by irritating nerve endings. These chemical mediators include histamine, substance P, bradykinin, acetylcholine, leukotrienes, and prostaglandins. The mediators can produce other reactions at the site of injury, such as vasoconstriction, vasodilatation, or altered capillary permeability. For example, prostaglandins induce inflammation and potentiate other inflammatory mediators. Aspirin, nonsteroidal anti-inflammatory medications, and the new COX-2 inhibitors block cyclooxygenase 2, the enzyme needed for prostaglandin synthesis, thus reducing pain. Consequently, these medications are often prescribed for painful conditions due to inflammation. The body also has a built-in chemical mechanism to manage pain. Fibers in the dorsal horn, brain stem, and peripheral tissues release neuromodulators, known as endogenous opioids, that inhibit the action of neurons that transmit pain impulses. β -Endorphins and dynorphins are the types of natural opioid like substances released, and they are responsible for pain relief. Endorphins are the modulators that allow an athlete to continue an athletic event after sustaining an injury. Endorphin levels vary from person to person, so different persons experience different levels of pain. This endogenous opioid mechanism may play an important role in the placebo effect. A placebo is an inactive substance or treatment used for comparison with "real" treatment in controlled studies to determine the efficacy of the treatment under study. Despite the lack of any intrinsic value, placebos can and do produce an analgesic response in many persons. Placebo analgesia can affect nociceptive mechanisms in the cortex of the brain and descending pathways of the spinal cord. Matre et al20 found that expectations about pain and analgesia can modify pain perception by altering pain mechanisms in the spinal cord. For example, psychological factors such as the threat of pain and expectations about analgesia modify spinal pain transmission, thereby modifying pain.

Factors that influence Pain:

The perception of pain is influenced by physiologic, psychological, and cultural factors, all of which must be considered by caregivers of persons in pain.

Physiologic Factors

Age affects the way people respond to pain. It influences both the development and decline of the nervous system. Aging affects the whole body, exposing the older adult to painful degenerative disorders such as osteoarthritis, painful secondary injuries such as skin abrasions and fractures, and painful surgical procedures such as cataract and hip replacement. Age also affects the way nurses and families respond to a complaint of pain. For example, a nurse may be more sympathetic toward a toddler than an adolescent or a young adult. Table-1 gives a brief overview of the perception of pain relative to age.

FATIGUE

Fatigue decreases coping abilities and heightens the perception of pain. When people are exhausted from physical activity, stress, and lack of sleep, their perception of pain is heightened. Thus, rest from physical, emotional, and social demands as well as sleep are important measures that reduce pain.

GENETIC MAKEUP

Recent research suggests that sensitivity to and tolerance for pain may a genetically linked trait (Ruda et al., 2000). This factor does not negate the need for adequate pain management of all clients.

MEMORY

Memory of painful experiences, especially experiences that occur when a child was very young, may increase sensitivity and decrease tolerance to pain. This may be due to anticipation and fear of a specific painful event, such as repeated immunization injections. Sensitivity to pain is increased when there is nonspecific memory of a painful event, such as newborn circumcision without anesthesia. Fortunately, modern medicine no longer condones such draconian practices.

STRESS RESPONSE

Research has shown that severe, unrelieved pain can cause an overwhelming stress response in both pre-term and full term infants which can lead to serious complications and even death (Pasero, 2004).

NEUROLOGIC FUNCTION

Any factor that interrupts or interferes with normal pain transmission affects the awareness and response of clients to pain and places them at risk for injury. Analgesics, sedatives, and alcohol depress the functioning of the central nervous system and some diseases (such as leprosy, or Hansen's disease) damage peripheral nerves, decrease sensitivity to touch and pain, and render affected individuals more vulnerable to injury.

Psychological Factors

FEAR AND ANXIETY

The relationship between pain and anxiety is complex and difficult to manage. Fear tends to increase the perception of pain and pain increases feelings of fear. This connection occurs in the brain because painful stimuli activate portions of the limbic system believed to control emotional reactions. People who are seriously injured or critically ill often experience both pain and heightened levels of anxiety due to their helplessness and lack of control. Nurses need to address both pain and anxiety, using all appropriate measures to relieve suffering.

COPING

People manage pain and other stressors of life in different ways. Some see themselves as self-sufficient, internally controlled, and independent. As a result, they may deny or be slow to admit they are in pain. Others may see themselves as insufficient, externally controlled, and dependent on others to treat their pain. No matter what coping style a person may have, it is the responsibility of nurses to relieve pain. Self-sufficient, internally controlled people may do better with client-controlled analgesia, whereas dependent, externally controlled individuals may prefer nurse-administered analgesia. In the interest of alleviating pain, people in both categories may need to modify their coping style.

Cultural Factors

Cultural beliefs and values affect the way people respond to pain. As children they learn what is and what is not acceptable behavior when in pain. In some cultures, any expression of pain is considered cowardly and shameful. In others, noisy demonstrations of pain are expected and acceptable. The meaning of pain itself may be markedly different in different cultures. Some ethnic groups see pain as a punishment for wrongdoing. Others see pain as a test of faith, and still others view pain as a challenge to be overcome. Recent immigrants to America are more likely to view pain from the perspective of their place of birth. Regardless of language, religion, or situation, nurses respect every individual and strive to alleviate pain and suffering.

Classification of Pain:

Pain can be categorized according to several variables, including its duration (acute, convalescent, chronic), its pathophysiologic mechanisms (physiologic, nociceptive, neuropathic), and its clinical context (eg, postsurgical, malignancy related, neuropathic, degenerative).

Acute Pain is usually a self-limited issue due to specific illness, inflammation, injury, or surgery. It is of short duration, typically resolving as healing progresses. It may be accompanied by vital sign changes such as tachypnea, tachycardia, hypertension, or diaphoresis. The patient may display obvious signs of discomfort. Acute pain may serve a physical warning or protective role that alters one to injury, and may mitigate further injury or insult. Assertive management of acute pain may thwart the development of a chronic pain syndrome.

Chronic pain is a persistent ( 3-6 months) problem that may be constant or intermittent, lasting long after healing has occurred and an illness, injury, or wound has resolved. It may last for months or years, rarely abating on its own. It may be associated with cancer or chronic nonmalignant illness such as arthritis, spine pathology, headaches, or neuropathy; or, it may become its own source of distress with no obvious underlying cause. It serves no protective function and is not accompanied by vital sign changes, and the sufferer may show no obvious signs of distress. However, it may be accompanied by social withdrawal and isolation, chronic fatigue, dysomnia, anxiety and depression, and impaired cognitive and physical function.

With regard to a more recent classification, pain states may be characterized as physiologic, inflammatory (nociceptive), or neuropathic.

Physiologic pain defines rapidly perceived nontraumatic discomfort of very short duration. Physiologic pain alerts the individual to the presence of a potentially injurious environmental stimulus, such as a hot object, and initiates withdrawal reflexes that prevent or minimize tissue injury.

Nociceptive pain is defined as noxious perception resulting from cellular damage following surgical, traumatic, or disease-related injuries. Nociceptive pain has also been termed inflammatory because peripheral inflammation and inflammatory mediators play major roles in its initiation and development.

In general, the intensity of nociceptive pain is proportional to the magnitude of tissue damage and release of inflammatory mediators.

Somatic nociceptive pain is well localized and generally follows a dermatomal pattern. It is usually described as sharp, crushing, or tearing in character. Visceral nociceptive pain defines discomfort associated with peritoneal irritation as well as dilation of smooth muscle surrounding viscus or tubular passages. It is generally poorly localized and nondermatomal and is described as cramping or colicky. Moderate to severe visceral pain is observed in patients presenting with bowel or ureteral obstructions, as well as peritonitis and appendicitis. Visceral pain radiating in a somatic dermatomal pattern is described as referred pain. Referred pain may be explained by convergence of noxious input from visceral afferents activating second-order cells that are normally responsive to somatic sensation. Because of convergence, pain emanating from deep visceral structures may be perceived as well-delineated somatic discomfort at sites either adjacent to or distant from internal sites of irritation or injury. The process of neural sensitization and the clinical term hyperalgesia describe an exacerbation of acute nociceptive pain, as well as discomfort in response to sensations that normally would not be perceived as painful. These changes, termed hyperpathia and allodynia, although common following severe or extensive injuries, are most pronounced in patients developing persistent and neuropathic pain. Hyperalgesia can be classified into primary and secondary forms. Primary Hyperalgesia reflects sensitization of peripheral nociceptors and is characterized by exaggerated responses to thermal stimulation at or in regions immediately adjacent to the site of injury. Secondary hyperalgesia involves sensitization within the spinal cord and central nervous system (CNS) and includes increased reactivity to mechanical stimulation and spread of the hyperalgesic area. Enhanced pain sensitivity extends to uninjured regions several dermatomes above and below the initial site of injury.

Neuropathic pain is defined by the International Association for the Study of Pain as "pain initiated or caused by a pathologic lesion or dysfunction" in peripheral nerves and CNS. Some authorities have suggested that any chronic pain state associated with structural remodeling or "plasticity" changes should be characterized as neuropathic.1 Disease states associated with classic neuropathic symptoms include infection (eg, herpes zoster), metabolic derangements (eg, diabetic neuropathy), toxicity (eg, chemotherapy), and Wallerian degeneration secondary to trauma or nerve compression. Neuropathic pain is usually constant and described as burning, electrical, lancinating, and shooting.

A common characteristic of neuropathic pain is the paradoxical coexistence of sensory deficits in the setting of increased noxious sensation. By convention, symptoms related to peripheral lesions are termed neuropathic , whereas symptoms related to spinal cord injuries are termed myelopathic . Causalgia or chronic regional pain syndrome describes pain following injury to sensory nerves, whereas discomfort associated with injury or abnormal activity of sympathetic fibers is termed reflex sympathetic dystrophy or chronic regional pain syndrome.

Cancer pain often has intermingled nociceptive and neuropathic aspects. It usually is due to direct effects of tumor, but may be a long-lasting aftereffect of treatment such as neuropathy after chemotherapy, radiation treatment, or surgery. Cancer patients often suffer from collateral pain that is unrelated to their malignancy, and patients will have a varying mix of pains at different times. Pain may herald the onset of cancer, may wax and wane during the course of the disease and its treatment, may signal recurrence or spread of disease, and may worsen with progression of disease. Cancer survivors may have chronic pain as a lingering and bothersome reminder of their experience.

Total pain is what the patient actually perceives and expresses, and is a complex interaction of physical pains, underlying psychosocial problems, and existential or spiritual distress. The complexity of the pain experience means that there are multiple ways to intervene that require effective teamwork.

Trigger Points of Pain:

Trigger points are discrete, focal, hyperirritable spots located in a taut band of skeletal muscle. Both acute trauma and repetitive microtrauma may lead to the development of stress on muscle fibers and the formation of painful trigger points. These trigger points are located on the muscles used to maintain body posture, such as those in the neck and shoulders, among others. Trigger points may manifest as tension headache, tinnitus, temporomandibular joint pain and lumber pain. Palpation of a hypersensitive nodule of muscle fiber is an essential criterion to identify trigger points of pain.

Fig: Trigger point Front Side

Fig: Tigger Point Back side

Conclusion: A review of pain physiology is essential to fully understand the pain and its management. To provide the best possible care for patients experiencing pain, physicians must understand the physiology, the different types of pain and their varied manifestations, the diversity of patient's responses, and The choice of therapeutic measure.