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13 Articles in Volume 11, Issue #5
Case Study: Patient With Fibromyalgia And Sleep Apnea
Current Treatments for Phantom Limb Pain
Doctor Shopping
Effective Protocol for the Management of Plantar Fasciitis
Giving Severe and Chronic Pain a Name: Maldynia
Is the New Pain Vocabulary Helping Patient Care?
Medications for Chronic Pain—Other Agents
New Technique Combines Electrical Currents and Local Anesthetic for Pain Management
Pain Management Dilemmas of Sickle Cell Disease
Sleep Apnea in Patients With Fibromyalgia: A Growing Concern
The Essential FDA/PDR Indications and Warnings For Opioid Prescribing
The Role of the Clinician In Determining Disability and Pain
Why Does Acute Postoperative Pain Become Chronic and Can It Be Prevented?

Giving Severe and Chronic Pain a Name: Maldynia

I submit that the “brain organization” of pain, or of any subjective experience, doesn’t happen as a linear process.

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.

When the synchronous oscillation includes areas of the brainstem, hypothalamus, and limbic forebrain, these parts of the motivational apparatus (responsible for the initiation of behavior, but not necessarily in awareness) evoke functions of attentional focus, homeostasis, and emotional biomarkers; the experience of which are symptoms of maldynia. These latter functions are commonly called the affective domains of pain, as opposed to the sensory or cognitive domains. The distinction may seem obvious; but it is artificial and deceptive. It is a residue of thinking about maldynia in a linear model.

Parsing the Neuro-talk

I’ve listed nine terms commonly used to describe maldynia below and defined and critiqued each in the context of the present discussion.

Neuropathic pain

Definition: Denotes pain that results from stimulation of the transmission apparatus rather than stimulation of the peripheral sense organ.

Critique: To classify pain that originates proximal to the sense organ as “neuropathic” and describe pain that originates from the peripheral sense organ as “nociceptive” confuses the definition of nociception as the transduction, transmission, and partial encoding of a stimulus. The scope of “neuropathic pain” is suitable for a very limited number of neuropathies, such as post-herpetic neuralgia and diabetic peripheral neuropathy.

Neuroinflammatory pain

Definition: Indicates a pain mechanism in which nociception, and perhaps experience, is enhanced or increased by immune mechanisms, including cytokine production, receptor sensitization, and glial activation, among others.

Critique: Neuroinflammatory pain includes neuropathic pain, but has a much broader scope. Neuroinflammation is one of the protective and reparative systems of normal homeostasis and response to injury. Its role in maldynia is now under intense study. In a recent issue of Practical Pain Management, Mark Cooper and I summarized a workshop on the subject of glial activation and neuroinflammation.11 Neuroinflammation is an important component of the neural substrate of maldynia—not the only component, but a central one. Neuroimmune impairments, particularly prolonged or non-reparative glial activation may well be responsible for many of the neurotransmitter, receptor, and peptide hormone abnormalities associated with maldynia.

Central sensitization and centrally enhanced pain

Definition: These terms denote the experience of a painful stimulus that is increased or enhanced by mechanisms in the spinal cord or brain.

Critique: The separation between peripheral and central mechanisms is unclear. Do they exclude the dorsal root ganglion or autonomic nervous system? This terminology mistakenly implies the existence of a normative pain experience for any given nociception. This false assumption is associated with a judgmental approach.

Centrally mediated pain

Definition: The mechanism of the pain experience is modified or regulated centrally, not solely by the peripheral transduction of the stimulus. Centrally mediated pain also might describe the phenomenon denoted by embedded pain memory.

Critique: Central mediation, or facilitation, may increase or diminish the experience of pain. The phrase is not specific to the neurobiological mechanism by which it happens.

Embedded pain memory

Definition: Denotes the experience of pain as if there were nociception, even though the stimulus is absent and remote.

Critique: Clinicians use this term as partial explanation for phenomena like phantom limb pain. It is consistent with the nonlinear oscillatory model of how maldynia happens and suggests that the experience of somatotopic maps related to an injury, as if stimulated by sense organs, combines or literally resonates with memory functions related to the experience of pain.

Sympathetic-mediated pain

Definition: A special type of maldynia that occurs in complex regional pain syndrome (CRPS).

Critique: Signs and symptoms of CRPS easily lead to the conclusion that abnormal sympathetic nervous system (SNS) mechanisms are responsible for maldynia. Good science does not support this. There are gaps in the chain of evidence to support the conclusion that the SNS is the primary agent.

Neural plasticity

Definition: The capacity of neurologic tissue to change both form and function in response to injury, healing, and the substrates of both eudynia and maldynia.

Critique: The science of neural plasticity is extensive and complex; yet, for all that is known, the body of knowledge is distressingly superficial. At best, neural plasticity accounts for the wonderful capacity to recover from injuries such as stroke or surgery; at worst, for the terrible propensity of eudynia to evolve into maldynia. “Neural plasticity” evokes images of structural changes such as neuronal branching (a linear model). The oscillatory model suggests that alterations in patterns of synchronous oscillation also can result in the same functional changes attributed to neural plasticity.

Brain reorganization

Definition: When applied to the experience of pain, brain reorganization describes the process by which the pattern of brain activation changes when eudynia evolves into maldynia and a transduced and transmitted stimulus activates different functional areas of the brain.

Critique: Brain reorganization and neural plasticity are related. The post-stroke brain is thought to be capable of functional reorganization by virtue of plastic changes in form and function of neural tissue. Most of this is characterized by branching of surviving neurons to replicate lost patterns of motor control. How do these findings apply to the person in pain? Evidence suggests that there is focal brain volume loss through the course of maldynia and that there is volume recovery as pain remits. There is also evidence of activation of different cortical brain regions that differentiate eudynia from maldynia. It is scientifically unsafe to extrapolate the imaging studies of stroke victims further. Yet, we know that there is dendritic and axonal branching in CRPS and other types of maldynia. The detailed effects of such phenomena on the transmission and experience of painful stimuli remain obscure. We can only speculate how such events evoke the “as if” experience of pain that defies anatomic determination as in phantom limb syndrome and CRPS.

Brain reorganization in an oscillatory model

The science is incomplete, but consider again the oscillatory model of how subjective experience happens, particularly with regard to pain. The experience of pain (in awareness) oscillates at about 40 Hz. In other words, the massively interconnected, distributed network of neuronal or local field activity is capable of shifting to incorporate or exclude circuits, networks, or systems as it moves through the global neuronal workspace. This shifting movement can happen with each beat of the oscillation (40 times per second). In theory, perceptual, associative, or motivational events that occur out of awareness are capable of reorganization at much faster rates. Such speeds might be detected by micro-array electroencephalography (EEG), but it is too fast to be understood by functional magnetic resonance imaging (fMRI). Persistent states of maldynia, with relatively stable oscillatory patterns, will appear on fMRI, but most of the component parts will be filtered out as “background” or “noise” in favor of a few dominant regions.

Letting Go of a Linear Model

A linear model of subjective experience leads us to think that if we could find brain regions associated with maldynia, we could target them with therapeutic technologies. The fMRI seduces us into thinking that there is a place where chronic or severe pain happens. Such thinking is partially correct, especially when considering peripheral pain generation. It offers reasonable justification for interventional pain management. The initial phases of nociception—transduction and transmission—are linear. The neurons course, interconnect, and branch in linear chains. But that ends with the encoding and neural representation of the stimulus that is the substrate for the experience of the painful event.

Thinking of brain reorganization in maldynia within an oscillatory model of subjective experience allows us to make a different sort of sense of research findings. A good example is the work of Christopher deCharms, Sean Mackey, and colleagues at Stanford University.12 In their research, patients with low back pain were taught to control the activation of specific brain regions using real-time fMRI. In so doing, subjects were able to control their pain. They were not altering the nociception, only the experience of it. According to my theory, they were reorganizing the pattern of oscillation (activation) away from the regions associated with maldynia. If we think of neural plasticity in terms of the shifting of iterative oscillation, it makes more sense than to think of it only in terms of cellular and intercellular morphology and electrical or chemical biology that comprise a linear model of pain experience.

Critics might propose that “maldynia” has no mechanistic value, but that is probably as it should be. All existing mechanistic expressions lack specificity. Even the term “brain reorganization,” as a mechanism of maldynia, is limited because we don’t know how either eudynia or maldynia is organized in the brain at first instance.

One might also argue that any term that does not include the word “pain” is not intuitively understandable when the clinician is treating a patient whose chief complaint is pain. I propose that the principal role of the practitioner is to trust and understand the patient’s narrative of illness. The patient’s story of suffering is the context that gives the practitioner’s identification of the pain generator and thus, the diagnosis of the condition, meaning, and purpose. Often the pain generator of maldynia is obscure or remote. It is then the role of the practitioner to minimize suffering and to help the patient develop coping strategies by which to adapt to the experience of pain.

Identifying Maldynia

Although maldynia is a subjective experience, it has characteristics that permit the practitioner to identify it and understand its nature. Maldynia may not always have a definable pain generator and it may be caused by a medical condition. Even when there is a specific pain generator, treatment may not resolve the maldynia.

The pain that is maldynia is often out of proportion to the original trauma. I consider CRPS to be the quintessential “maldynic” condition. The signs and symptoms of CRPS are typical of conditions associated with immune impairments and inflammation, such as fibromyalgia, multiple sclerosis, rheumatoid arthritis, interstitial cystitis, inflammatory bowel disease, and some forms of neuralgia. Maldynia is characterized by allodynia and hyperalgesia of various sorts. There may be dysvascular effects or swelling, along with sensory and motor impairments that do not follow a predictable anatomic distribution. Motion disorders, when present, do not follow the patterns of common or anatomically-specific lesions. Patients who suffer maldynia often are anxious, depressed, or both. They display common impairments of intense grief, fear, and anger. In addition, they are manipulative, prone to bargaining, and often express irrational notions of agency in the cause and course of their maldynia.

Clinicians tend to mistrust patients with maldynia and may classify them as malingerers. A patient may be mistakenly labeled as “crazy” when he or she fails to respond to treatment. The patient may be misdiagnosed with somatization disorder or conversion reaction. When labels have therapeutic value, they are useful. When they are applied without therapeutic value, or, specifically to exclude it, they are pre-judicial. Practitioners who cleave only to the signs of impairment that can be measured and who disregard and demean the subjective experience of the patient are performing a disservice.

The practitioner can help the patient who suffers from maldynia by documenting the subjective narrative and the sequence of events that make that narrative understandable and trustworthy. Furthermore, the practitioner can document the subjective symptoms and the objective signs in the context of maldynia, not according to the linear determination of anatomic pathways. Finally, the practitioner positions the medical record as a means of understanding the patient as a whole, not just as an injured extremity, a disease, or an anatomical deformity. The oscillatory model of pain underscores how the experience of maldynia is more than the sum of its parts.

The practitioner must trust each patient to express and reveal the narrative of suffering that resulted in the disabling predicament of maldynia. Only then can clinician and patient parse out its causes, contexts, and effects. With hope and encouragement, patients with maldynia can learn to cope with—and even overcome—their debilitating illness.

 

Last updated on: November 30, 2011
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