History of Pain: The Nature of Pain
Our thinking regarding the nature of pain has shifted over the past four centuries from the linear dualistic concepts of Descartes to the Gate Control Theory of Pain, a more global model that includes affective components of pain.1,2 The evolution of scientific research has helped us appreciate that the pain experience is more complex and highly multifaceted from the subjective to the specific. This article will discuss the nature of pain with some general assumptions based on our current understanding and then move to more specific considerations.
Subjective Nature of Pain
After 30 years of experience working with pain patients, it is obvious to me that the pain experience is subjective by nature. The pain experience can change on a moment’s notice, depending on the external demands imposed on our nervous system. So why is it so difficult to accept the subjective nature of pain?
One explanation is that the nature of science has been based on the empirical search for cause-and-effect relationships and the scientific community is uncomfortable with subjective data. Today’s neuroscientists, for example, search for more specific intracellular mechanisms to explain the pain experience. Professionally, I use subjective impressions to formulate my clinical impressions and treatment plans.
Second, the individual nature of the pain experience is highly variable. As we know, no two patients are the same even though they can be matched on numerous physical, social, and psychological factors. Because the pain experience is so individualized, this raises additional challenges for the physician treating pain patients.
Third, pain is a perceptual experience, which involves multiple integrated systems that act in a coordinated fashion. The pain experience as a perceptual process was mentioned throughout the 19th and 20th centuries, culminating with the work of Livingston, and Melzack and Wall.3,4 When I was a faculty member in the anesthesiology department at Oregon Health & Science University (OHSU), I attempted to impress upon our anesthesia residents that to be effective in working with chronic pain patients you needed to treat the patient’s perception of their pain. Further, it is important to consider that perception has thresholds, which can be explained by modifications in the periphery after injury or inflammation.
Loeser’s Model of Pain
In the August issue of Practical Pain Management, I introduced the Melzack and Casey model of pain that was published in 1968 (Figure 1).5 I still use it today to formulate my clinical impressions and treatment plans. Now, I would like to introduce another more contemporary model of pain by John Loeser (Figure 2).6 In Loeser’s model, nociception is at the center—which is physiological in nature and similar to the sensory component of the Melzack and Casey model. This model is based on overlying circles that are actually linear in nature. It starts with a physiological stimulus (nociceptive) that leads to pain (sensory) and results in suffering (affective). Finally, the outer circle represents pain or antalgic behaviors.
The main difference between the two models is that the Melzack and Casey model is circular in nature and all of the components are interdependent. The Loeser model, by contrast, is linear in nature. Accumulating research suggests that our nervous system is highly integrated, interdependent, and reciprocal in nature.
Definition of Pain
Next, we need to consider how we define pain. There are a number of definitions of pain as represented by various pain organizations. The definition that predominates research is promulgated by the International Association for the Study of Pain (IASP): “An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.”7 IASP also added that pain is a subjective experience. It is associated with our perception of the event and influenced by our past experiences. It is important to note that this definition is not a dualistic, either sensory or emotional experience, but a combination of both, as reflected in the Gate Control Theory of Pain.
Acute vs Chronic
We now need to consider how acute pain is differentiated from chronic pain. In other words, what is a normal response to an event such as trauma or surgery as compared with abnormal persistent pain that continues beyond an expected timeframe. The expected timeframe is a hotly debated topic, but, generally, it is felt that pain persisting longer than 3 to 6 months (outside the expected timeframe of recovery) is considered chronic. There are many in the field, including pain physicians, researchers, and pain psychologists, that feel that the passage of time is somewhat of an arbitrary and artificial benchmark. John J. Bonica, MD, suggested that chronic pain be defined as pain that persists longer than 1 month beyond the normal healing period or that is associated with a pathological process that causes continuous or recurrent pain over months or years.8 According to Serge Marchand, PhD, an expert in pain mechanisms, the distinction between acute and chronic pain is essential, because acute pain plays a protective role and acts as an alarm. Further, acute pain enables us to recognize that there is a problem. Conversely, chronic pain does not play a protective role if it persists long after the triggering event is resolved.9
How Pain Works
As we move toward more specific considerations regarding the nature of pain, some basics about the nervous system should be reviewed. The history of pain provides valuable background on the evolution of thinking regarding the neurophysiology of pain.1,2 As noted, Charles Sherrington (1857-1952) was the first to introduce the term nociception (activity of receptors and nerve fibers caused by potentially harmful stimulation of the body).10 Today, we know that for painful stimulation to reach consciousness, it has to be influenced by mechanisms within the central nervous system (CNS). This influence can increase or decrease the nociceptive stimulus. Further, we need to understand the process of the painful stimulus as it travels from the periphery to the higher centers in the brain.
From nociceptive stimulation to perception, it is now known that a whole series of endogenous mechanisms influence our experience of pain. These excitatory and inhibitory mechanisms may increase or reduce the nociceptive signal that translates into more or less intense pain.9
So how does this process begin? To answer this question we need to introduce the term transduction: the process by which the energy of a stimulus is transformed into an electrical response. How does the energy of a stimulus transfer into an electrical response? According to current thinking, the nociceptor has more than one transduction mechanism that result from direct excitation or through receptor cells. Continuous painful stimulation results in sensitizing the CNS, which contributes to the pain experience.9 There are three categories of pain fibers as described in Table 1.