Giving Severe and Chronic Pain a Name: Maldynia
Research over the past decade clearly shows that severe or chronic pain leads to abnormal changes in the brain and spinal cord. Central neurologic mechanisms may prolong the experience of pain, even after the inciting factor resolves. Researchers and clinicians give a variety of names to this phenomenon—neuropathic pain, neuroinflammatory pain, central sensitization, centrally enhanced pain, centrally mediated pain, embedded pain memory, sympathetic-mediated pain, neural plasticity, and brain reorganization. Some of these mechanisms can exert both negative and positive effects on the experience of pain.
Our understanding of the science, however, is incomplete. Because we do not yet know how the subjective experience of pain is organized in the brain, we cannot fully understand how it is “reorganized.” Similarly, we can only speculate how sensitivity to pain is increased or decreased by neural mechanisms. The words we use as symbols for this phenomenon, “neuro-talk,” imply we know more than we do. How is the pain practitioner to make sense of what is known, to keep what is unknown clearly in view, and to use that understanding in the care of real people in pain?
This commentary attempts to answer some of the questions posed by Forest Tennant, MD, DrPH, in a recent issue of Practical Pain Management.1 If chronic pain is subjective and not necessarily dependent on a stimulus, how can we accurately assess its affect on the brain and spinal cord? How can we best apply our current understanding to the benefit of patients seen in clinical practice? What can be done to increase understanding of chronic pain as a neuro-
biologic function of the body–brain, without arbitrarily separating peripheral from central mechanisms? As research continues into the interaction between pain and the brain, which terms will correctly describe this phenomenon, and does nomenclature affect the relationship between patient and clinician?
Experience of Pain Is Subjective
I begin by declaring my assumptions. I assume that pain is subjective. The objective measurable substrate or precursor of the subjective experience of pain is nociception. There is evidence to support the definition of nociception as the process of transduction, transmission, and partial encoding of a stimulus that causes or mimics tissue damage. The science of neural representation of nociception began with Penfield’s somatotopic mapping of sensory stimuli,2 however, cortical localization of a sensory stimulus is a superficial indicator of the representation (brain organization) of nociception. The chemical, electrical, and structural events within and among cells (neurons, glia, and possibly connective tissue) that result in the experience of pain are under study, but the understanding of them currently is limited.
A corollary to the assumption that the experience of pain is subjective is that pain cannot be measured. Pain, like all subjective experience, has no contents. It is about something, and that something is the process and neural representation of nociception, but it has no substance, nothing to measure or to observe—no contents. Pain is an experience, not an emotion. Surprise, fear, grief, or anger that are evoked by pain are emotions, pain is not. Pain, therefore, is a state of consciousness, a subjective experience.
Theory of Pain
My theory regarding pain as a subjective experience is a variation of the ideas put forth by Wolf Singer, Rodolfo Llinas, and Henry Markram, among others.3-6 Although this theory lacks scientific validation, no one has yet to propose a reasonable, alternative theory of how consciousness happens, that is, not one that has any practical value for the pain practitioner. I propose that subjectivity, particularly the experience of pain, is the synchronous oscillation of bioelectrical activity in widely distributed circuits, networks, and systems of the body–brain. Some may view this hypothesis as abstract, but a coherent theory of how subjectivity occurs is necessary if the practitioner is to make sense of the anomalies so often seen in the clinical presentation of severe and chronic pain.
Maldynia Is the Illness
In this commentary, as in the clinical experience of most pain practitioners, we are dealing with severe or chronic pain that causes distress and disability. Therefore, I will use the proper term for such a “painful” experience: maldynia. Eudynia, good pain, and maldynia, bad pain, are terms coined by Philip Lippe to distinguish the subjective experience of pain from the nociception of a “painful” stimulus.7 Neuro-
scientist and neuroethicist James Giordano argues that clinicians treat the illness of chronic and severe pain; that is, they treat maldynia, not simply pain.8,9 However, the province of pain practice includes the treatment of pain in an effort to prevent eudynia from evolving into maldynia. Simply put, the pain of a wrist fracture (eudynia) indicates whether treatment has been sufficient or if there are impending complications. If eudynia is ignored, maldynia is likely to follow. What might have been a self-limited condition becomes chronic illness. In short, eudynia is instructive and corrective; maldynia is distressing and disabling.
Mistaken Ideas About Pain
The notion that the reign of pain starts mainly near the brain10 is false because the experience of pain is entirely in the brain; more precisely, in the functionally indivisible body–brain. The Cartesian notion that mind and body are separate substances is passé; but it is intuitively seductive to think there must be a functional separation between the physical body and the subjective mind. This dogged dualism is perpetuated when we think of the body–brain functioning like a computer.
If the nervous system worked like a computer, then the pain when I strike my thumb with a hammer would be transduced in the sensory organs of my thumb, transmitted to the spinal cord, then to the thalamus, and on to my perceptual cortex. From there, the pain signal would branch out to the cognitive and affective apparatus of the brain. This describes a linear process, that is only when the signal finally stimulates certain structures is it experienced as pain. In a linear process, the relative intensity of the signal, frequency, or distribution determines whether the sensory or the affective experience of the pain dominates my consciousness. Were that true, you could measure the pain by the electrical activity of the place where the pain experience occurs. This can’t be done and a linear model of pain does not support the subjective experience of maldynia. I submit that the “brain organization” of pain, or of any subjective experience, doesn’t happen as a linear process.
Instead, an oscillatory model of maldynia presents the image of a distributed, resonating network of circuits, each of which is oscillating to maintain its perceptual, associative, or motivational contents. One theory of short-term memory holds that local cortical oscillation persists momentarily and fades if not reinforced by wider oscillatory activity. If the local oscillation resonates widely to include hippocampal or cerebellar circuits (among others), the perceptual contents may be transferred into long-term memory. Theories of the organization of memory are incomplete.