Many neuropathic pain states have traditionally been thought of as having a primary peripheral etiology. Recent investigation, however, using functional neuroimaging techniques, demonstrates that many neuropathic and other chronic pain conditions may have a large centralized component (central vs. peripheral model). These conditions include chronic low back pain (CLBP), fibromyalgia, irritable bowel syndrome, and Complex Regional Pain Syndrome (CRPS)/Reflex Sympathetic Dystrophy (RSD). (Mackey and Maeda 2004)
Inflammation can play a significant role in both nociceptive and neuropathic pain. Inflammation occurs when cells and tissue are damaged and release chemical mediators, commonly referred to as “the inflammatory soup,” that not only induce an inflammatory response but also sensitize nociceptors and other somatosensory components of the nervous system. Peripheral sensitization occurs when inflammatory mediators cause a reduction in the threshold required for nociceptor activation. A similar short-term central sensitization can occur in which there is an increase in neuronal excitability and responsiveness in the dorsal horn. In central sensitization, chemical mediators for inflammation can also upregulate the expression of genes that alter synaptic transmission.
Because of neuronal plasticity, current research is showing that protracted central sensitization (neuronal hyperexcitability) can result in long-term changes that may be important in the transition from acute to chronic pain and the development of chronic pain syndromes. Patients with these syndromes generally have severe and persistent pain that is disproportionate to the tissue injury.
Models are the conceptual framework for physicians, patients, families, healthcare facilities, carriers, and compensation systems for understanding pain. Models help to establish parameters for reasonable outcomes and acceptable standards of care. Several different models of pain have developed over time, each with insights and limitations.
Acute vs. Chronic Pain Model
In many situations, acute pain serves as a highly adaptive and beneficial experience. Fundamentally, it serves as a warning of actual or impending tissue damage. Acute musculoskeletal pain is a common example in the injured worker and is often a signal of real or impending tissue damage.
Most acute pain is self-limited or responds to short term administration of analgesics and conservative therapies. However, continued activation of nociceptors with poor pain control can lead to peripheral and central sensitization, a risk factor for persistent pain leading to a neuropathic pain state with prolonged disability, delayed return to baseline function, and delayed return to work.
Chronic pain can be distinguished from acute pain by more than just the time course. Whereas acute pain serves as a warning signal, chronic pain has no known survival benefit. Chronic pain is persistent and relentless, serving no obvious purpose for the individual. Evidence suggests that generation and subsequent maintenance of chronic pain, as opposed to acute pain, involves changes in central pain processing mediated through mechanisms of neural plasticity and ultimately leading to hyper-excitability of central structures in the spinal cord and brain. To complicate matters, unremitting pain may be associated with depression or anxiety.
As a practical matter, it is noted that “[t]he distinction between acute and chronic pain is somewhat arbitrary” and “[c]hronicity may be reached from one to six months postinjury”, ACOEM recognizes that the most clinically useful definition might be “chronic pain persists beyond the usual course of healing of an acute disease or beyond a reasonable time for an injury to heal”. (ACOEM Medical Treatment Guidelines Chapter 6 page 108). Therefore, it is a clinical decision to recognize chronicity or persistence of pain when 1) the condition is not improving over time, 2) fails to improve with treatments directed to the specific injured body part (see Clinical Topics section of the MTUS), 3) or in the absence of a specifically correctable anatomic lesion (see Clinical Topics section of the MTUS). Often it takes a number of months for the clinician to recognize when pain becomes chronic.
Illness Behavior Model
As previously stated pain is a subjective experience, influenced and modulated by cognitive, emotional, and environmental elements. Psychosocial factors can affect the perception and expression of pain. These might include a tendency toward anxiety, depression, somatization, fear avoidance, emotional lability, catastrophizing, job dissatisfaction and embellishment.
Further, while frank malingering is rare, secondary gain factors, such as disability income and avoidance of perceived unpleasant tasks can impact the overall clinical presentation. Taken together, psychosocial factors may play a larger role in eventual patient outcome than obvious somatic factors as determined by the nature and extent of the original injury. Efforts directed solely to the management of possible pain generators without addressing psychosocial factors may result in a suboptimal outcome.
Biomedical vs. Biopsychosocial Model The traditional biomedical model “assumes disease to be fully accounted for by deviations from the norm of measurable biological (somatic) variables” (Engel 1977). Thus there is always a direct causal relationship between a specific pathophysiologic process and the presence and extent of a particular symptom. While this model has served the medical community well in the treatment and cure of certain diseases (e.g. infectious diseases), it has generally failed in the treatment of chronic illness including persistent pain. For example, for decades there has been an approach to identify the “pain generator” and remove it by cutting it out or blocking it.
In 1977 Engel proposed an alternative, the biopsychosocial model, which focuses greater attention on the patient, rather than presumed pathophysiology. The biopsychosocial model approaches pain and disability as a complex interplay of biological, psychological and social factors. These psychosocial factors can be easily assessed.
The following chart contrasts these two pain models (Hanson and Gerber 1993).
Most appropriate for acute pain conditions
More useful for those with chronic pain conditions
Emphasizes peripheral nociception
Recognizes the role that central mechanisms play in modulating peripheral nociception or generating the experience of pain in the absence of nociception
Focus on physical disease mechanisms
Recognizes the importance of illness behavior including cognitive and emotional responses to pain
Multidimensional systems approach to understanding and treating pain
Reliance on medical management approaches
Utilization of self-management approaches
Linton, when discussing the psychosocial risk factors involved in the creation of chronic back and neck pain, noted that “there is strong evidence that psychosocial variables are strongly linked to the transition from acute to chronic pain disability.” He stated “there is strong evidence that psychosocial variables generally have more impact than biomedical or biomechanical factors on back pain disability.” Thus, when clinical progress is insufficient, the clinician should always be prepared to address confounding psychosocial variables, in a coordinated, multidisciplinary manner.