Biopsychosocial Model of Pain and Patient-Centered Pain Management

Biopsychosocial Model of Pain and Patient-Centered Pain Management

Angela Starkweather

Definition and Epidemiology of Pain

Pain has been described throughout time as a symptom, similar to fatigue or depression, that is capable of overwhelming a person’s normal capacity to cope and function, in which case it can become a health condition in and of itself. The International Association for the Study of Pain (1994) defines pain as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage” (p. 1). This definition describes pain as a complex phenomenon with multiple components that impact a person’s psychosocial and physical functioning. Another clinical definition of pain, which was proposed by McCaffery (1968), states, “Pain is whatever the experiencing person says it is, existing whenever he says it does” (p. 8). This definition is accepted worldwide and reinforces that pain is a highly personal and subjective experience, a reason that all accepted guidelines consider the patient’s report to be the most reliable indicator of pain. Although both definitions refer to the individual’s report of pain, some people are unable to communicate because of developmental or cognitive status, disability, disease, or mechanical obstruction. In these situations, we must rely on behavioral cues, facial expressions, or other modalities to identify pain.

Pain is one of the most common reasons for seeking medical care across all age groups and is often a presenting symptom of an underlying injury or pathology (National Institutes of Health, 2016). It can serve as an indicator of disease severity, an index of prognosis, and a determinant of health. The prevalence of chronic pain in the general population of U.S. adults has been shown to exceed 48% in some studies, with low back and neck pain, osteoarthritis, and headache being the most common (National Academies, 2011). Reportedly 25.3 million American adults suffer from daily pain and 14.4 million experience severe pain (Nahin, 2015). It is currently estimated that pain costs Americans $635 billion annually for direct and indirect care, and lost productivity (National Academies, 2011).

One in four children have episodes of chronic pain that last 3 months or longer (King et al., 2011; Korterink, Diederen, Benninga, & Tabbers, 2015). Similar to adult
populations, the prevalence of chronic pain is higher in girls compared with boys and increases with age (pubertal development). The median prevalence of idiopathic pain in community-based samples of children ranges from 11% to 38%, with the most common chronic pain conditions being reported in up to 51% for headache, 41.2% for abdominal pain, up to 40% for musculoskeletal pain, and 24% for low back pain (Brun Sundblad, Saartok, & Engström, 2007; Korterink et al., 2015; McBeth & Jones, 2007). Chronic pain is associated with significant psychosocial and physical burden for children and families and ranks among the costliest health conditions in the United States, at an estimated $19.5 billion per year (Groenewald, Essner, Wright, Fesinmeyer, & Palermo, 2014). Effective multimodal treatment for pain in children entails efforts to reduce pain severity, non interference with daily activities, and preservation of physical, psychological, social, and role functions. A major goal is to prevent immediate and future disability because there is convincing evidence that childhood pain predisposes an individual for pain chronicity and development of comorbid pain disorders in adulthood (Walker, Dengler-Crish, Rippel, & Bruehl, 2010).

Nociception and Pain

The physiologic systems that result in pain developed, from an evolutionary standpoint, as a protective mechanism to alert the individual of actual or potential tissue injury, and it typically resolves with the normal phases of healing. When pain continues beyond normal healing and becomes chronic, it no longer serves any useful purpose and is referred to as pathologic pain. Although the physiologic mechanisms that contribute to the transition from acute to chronic pain are not completely understood at this time, there are several lines of evidence suggesting that the severity, impact, and resolution of pain may be influenced by genetics. First we will discuss the physiology of pain as a protective factor and then possible alterations that can lead to chronic pain.

The cells that are capable of transducing and transmitting noxious pain signals are known as nociceptors, and they are found in the skin, muscle, connective tissue, circulatory system, and the viscera of the abdomen, pelvis, and thorax. Nociceptors are free nerve endings that transduce noxious stimuli, which can be mechanical, thermal, or chemical, into neuronal action potentials that are transmitted centrally to the spinal cord and brain. Stimulation of nociceptors can be the result of direct nerve damage, exposure to noxious stimuli at a specific threshold, and the release of chemicals at the site of injury. During tissue injury, a host of inflammatory mediators are activated to travel to the site of injury. Inflammatory mediators, as well as chemical mediators released in response to the injury (K+, H+, lactate, histamine, serotonin, bradykinins, and prostaglandins), alter the membrane
potential of nociceptors, thereby facilitating depolarization and generation of action potentials.

The mechanisms that lead to the perception of nociceptive pain are described as transduction, transmission, perception, and modulation (Figure 1-1). This normal response of the somatosensory system to noxious stimuli is the process known as nociception. When the brain receives and interprets the information as an unpleasant painful sensation, it is known as nociceptive pain (Haines, 2012). This exquisite network of cells, fibers, and nociceptive pathways can result in pain only when the brain is capable of receiving and interpreting stimuli. However, the activity of the nociceptive system does not always result in the experience of pain; thus, pain and nociception are not synonymous. The brain has a powerful influence on how we perceive sensory information and may filter or block pain information from awareness or change our perception of the sensory information (Pasero & Portenoy, 2011). This is an important concept for some of the pharmacologic and nonpharmacologic therapies used to manage pain, such as distraction, guided imagery, or cognitive behavioral therapy (CBT).

Figure 1-1. Processes of pain signaling.


Tissue damage results in the release of chemical mediators from damaged cells that activate nociceptors. These chemical mediators include prostaglandins, bradykinin, serotonin, substance P, and histamine (Starkweather & Pair, 2013). When the chemical mediators attach to the membrane of the nociceptor, it can result in the opening of sodium channels, which activate the nociceptor and cause the generation of an action potential, an electrical impulse.


The action potential subsequently moves from the site of nociceptor activation along specialized afferent nerve fibers that carry pain impulses, known as A-delta and C fibers, to the spinal cord. A-delta fibers are thinly myelinated sensory fibers that send pain impulses faster than unmyelinated C fibers. Because of the myelin covering the A-delta fibers, they are capable of transmitting sharp, stabbing pain sensations, whereas C fibers transmit aching, burning-type pain sensations. Substance P and other neurotransmitters allow the action potential to proceed across the cleft to the dorsal horn of the spinal cord, where it ascends the spinothalamic tract to the thalamus and midbrain.


Fibers from the thalamus send the nociceptive message to the somatosensory cortex, frontal and parietal lobes as well as the limbic system, where pain is perceived and interpreted on the basis of past experience, beliefs, attitudes, and meaning.


Activation of the midbrain results in the release of substances such as endorphins, enkephalins, serotonin, and dynorphin from neurons that descend to the lower areas of the brain and spinal cord, stimulating the release of endogenous opioids that inhibit transmission of pain impulses at the dorsal horn.

Once the pain signal is transmitted to the cell bodies of pain neurons in the dorsal root ganglion, they enter the dorsal horn of the spinal cord by way of the posterior nerve roots, where the A-delta and C fibers synapse with interneurons, anterior motor neurons, and sympathetic preganglionic neurons. A specific area of the spinal cord (referred to as laminae II and III regions) known as the substantia gelatinosa houses multiple synaptic connections among the primary sensory afferent neurons, interneurons, and anterolateral ascending fibers (Figure 1-2). This region is important because pain signal transmission can be modulated by CNS activity or release of endogenous substances. Lamina V of the spinal cord receives somatic input from mechanical, thermal, and chemical receptors, besides visceral receptors, which is thought to explain the potential for referred pain, when pain from a visceral organ is perceived at the body surface.

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Apr 16, 2020 | Posted by in NURSING | Comments Off on Biopsychosocial Model of Pain and Patient-Centered Pain Management
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