Part II

Physiology of chronic pain
After a lifetime of experiencing pain, and over a year of studying, contemplating, and reading about pain, I am afraid that I can speak of all that is involved in this phenomenon about as well as a baby can make babbling sounds in an attempt to speak its native language. The historically held specificity theory of pain is straightforward: a noxious stimulus evokes a threshold potential in a nociceptor, or pain cell, which then sends the signal of pain to the brain by way of the spinal cord. The signal is processed in the pain center, and voila, the organism is enlightened with a perception of pain! The organism is now equipped to react accordingly.
In real life, pain cannot be understood this simply. Elements of one’s surrounding environment, state of mind, level of physiological arousal, and history of injury are just a few examples of how the experience of pain can be affected. Imagine that on a sunny afternoon you are playing an intense game of Ultimate Frisbee and you are guarding an opponent who is on the offensive team. While you are intent on keeping the Frisbee away from her, you watch the disk sail straight for your head. In your excitement for keeping it away from the enemy, you barely notice the impact. The next morning you see the tender, bulging welt on your forehead and you can only faintly remember the heroic maneuvers that resulted in this mark. Now consider an instance when you are walking outside with one of your friends on a cold and dreary evening. You are deeply engaged in an important conversation when a Frisbee flies out of the periphery and smacks you in the forehead. The rest of the evening, you are plagued with a splitting headache, and you do not stop whining about the bump on your head for a week. The injury is the same in both situations, but the perception of the pain in each is dramatically different. The intervening variables that affect the perception of pain in these two situations are fairly obvious, but what exactly lies at the root of such a difference? The former examples are illuminating enough to realize that there is much more to pain than the specificity theory can explain.
Yet, it is important to have a basic knowledge of the physiology behind pain in order to understand how hypnosis might be effective in providing relief. In their work, The Challenge of Pain, Ronald Melzack and Patrick Wall continually discourage the reader from holding a simplistic theory of pain sensation and perception. They write, “…we have learned to recognize that chronic pain rarely has not a single cause but is instead the result of multiple, interacting causes (1983).” This theme of complexity resonates through their entire work and becomes amplified throughout the vast, global research body addressing pain. From the seemingly endless investigations into complex second-messenger and signaling mechanisms which cause an overwhelmingly and insufficiently understood array of effects at the cellular level (Purves, 2004) to the theorizing about overarching, cognitive psychological constructs, understanding the mechanisms of pain becomes less and less simplistic with each new day of scientific progress.
Loeser and Melzack (1999) explain that there are four components of pain. The first is known as “nociception,” or the detection of tissue damage that is transmitted as a nerve impulse by nociceptors to the central nervous system. The second component is the perception of pain which is often the result of injury. However perception of pain is not necessarily preceded by nociception, as is the case with many patients who suffer from chronic pain. Additionally, some amputees experience excruciating phantom limb pain despite the obvious lack of pain--sensing cells that were once on the missing limb. The third component of pain is the negative, affective response which is known as “suffering”. This occurs in conjunction with a threat to one’s physiological or psychological state of balance due to the pain. Finally pain behaviors constitute the fourth aspect of pain. These can be described as any behavior demonstrated as a response to the injurious stimulus. While example of the Frisbee injury involves these four components of pain, it only covers two of the three types of pain specified by Loeser and Melzack. In this instance, transient, or the short-lived pain intended to warn, occurs as the Frisbee hits your head. Such acute pain is the result of tissue damage and continues as the body heals—the pain from the nasty bruise on your forehead would be classified as acute pain. Although such commonplace instances of pain are helpful in providing an overall understanding of the subject, they represent a limited view of how complex the problem of pain, especially chronic pain can be.
In the 1960s Melzack and Wall began developing the gate-control theory of pain answer to the commonly held and overly simplistic specificity theory of pain. “Basically,” they explain, “the theory proposes that a neural mechanism in the dorsal horns of the spinal cord acts like a gate which can increase or decrease the flow of nerve impulses from peripheral fibres to the central nervous system. Somatic input is therefore subjected to the modulating influence of the gate before it evokes pain perception and response (1982).” In other words, in this model of pain, inhibitory and excitatory impulses from an array of neurons, of variable axon width and degrees of myelination, stemming from the injured site summate in the dorsal horns of the spinal cord. The neurons that converge at this theoretical gate proceed not only from the site of injury, but also from efferent pathways running from the brain. Upon reaching or exceeding a threshold, the neurons in the dorsal horn activate the chain of events, called the “action system,” concurrent with tissue damage. Aware of how complex cases of pain can be, Melzack and Wall (1982) are careful to describe this system as follows: “Pain, as we have seen, does not consist of a single ring of the appropriate central bell, but is an ongoing process comprising a sequence of responses by the action system, beginning with a series of reflex responses and continuing with complex strategies to terminate the pain.” It is through this understanding of pain signal propagation that there can be theoretical room for the modulation of the signal in any number of ways before it becomes a perception of pain.
It is now widely understood that discriminative pain information, “location, intensity, and quality,” ascends to the brain by way of the anterolateral system (Fig. 1) (Purves, 2004). This pathway begins in the dorsal horns of the spinal cord (at Melzack and Wall’s pain gate) and projects to brain structures that are involved in pain sensation such as the thalamus and the primary somatic sensory cortex. The affective-motivational pain pathway sends pain signals along a similar route as the anterolateral system. However, the affective-motivational pain pathway targets structures such as the reticular formation, amygdala, and hypothalamus which are involved in evoking an aversive perception of the pain. Additionally, it is known that structures in the brain such as the somatic sensory cortex, amygdala, hypothalamus, and other mid to lower brain ganglia can send modulatory signals to the afferent pain pathways (Purves, 9.7, Fig. 2?).
Over the last half century, the gate-control theory of pain served its purpose very well. Melzack and Wall (1982) write:
The major impact of the gate-control theory, initially, was to free the field of pain from the straitjacket of specificity theory...Psychologists suddenly found a model which placed psychological observations and techniques in the mainstream of pain research. Physiologists began to explore regions of the spinal cord and brain that were previously held to play no role in pain and discovered complex mechanisms and relationships that were hitherto unsuspected. The transmission of pain signals to the brain was no longer restricted to a single pathway and it became possible to speculate on the functional relations among different ascending and descending systems.
The authors of Neuroscience confirm the success of the gate theory, stating that it “stimulated a great deal of work on pain modulation and has emphasized the importance of synaptic interactions within the dorsal horn for modulating the perception of pain intensity. (Purves, 2004)” Even a standard anatomy and physiology book pays homage to the theory: “it fostered a generation of valuable research (Marieb, 2004).”
Despite the fecundity of the gate control theory Melzack is perhaps the first to agree that recent discoveries, birthed out of the very climate of pain research brought about by this theory, warrant yet another reviion of our pain model. Melzack courageously writes, “…as historians of science have pointed out, good theories are instrumental in producing facts that eventually require a new theory to incorporate them. And this is what has happened (Melzack, 2005).” From this statement, Melzack continues to propose his “neuromatrix” theory of pain which attempts to incorporate the knowledge we now have regarding the workings of the brain while keeping in mind the gate theory and what we already understand about pain processing in the periphery and spinal cord.
We understand that patients, such as amputees, can perceive pain despite the absence of a stimulus where the pain is “felt”. It therefore follows that there is a mechanism in the brain itself that can independently account for the perception of pain. The neuromatrix theory suggests that the circuitry of our brain is such that our brains have an individual electrochemical pattern that arises from a network of circularly interconnected brain structures. Melzack (2004)