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9 Articles in Volume 15, Issue #3
Abuse-Deterrent Formulations
Ask The Expert: False-Positive Screen for Benzodiazepines
Clinical Diagnosis of Centralized Pain in the Age of ICD 10
Editor's Memo: The WHO Pain Treatment 3-Step Ladder
Letters to the Editor: Hormone Dosing, Adhesive Arachnoiditis
Pain in Women
PROMIS Pain-Related Measures: An Overview
Selective Interventional Spinal Techniques: Injections and Ablations
Transcranial Direct Current Stimulation (tDCS): What Pain Practitioners Need to Know

Clinical Diagnosis of Centralized Pain in the Age of ICD 10

Recommendations for a protocol for making a clinical diagnosis of centralized pain.
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This Consensus Task Force highly recommends that every chronic pain patient in every clinical setting be evaluated for pain centralization. The historical hallmarks of centralization are constant pain, sleep interference, and fatigue. The presence of pain centralization should be noted in a patient’s record and its clinical ramifications and prognosis communicated to all concerned parties.

Pain centralization is a pathologic state initiated by microglial overactivation, neuro-inflammation, metabolic disturbances, cellular destruction, and neuronal sensitization. It may severely impair patients and require specific treatment measures, so every chronic pain patient in every clinical setting should be evaluated for its presence.

This report provides a protocol to expeditiously make a clinical diagnosis of centralized pain using a rapid history and physical examination. Since centralization produces a large number of clinical manifestations, it is appropriate to label it central pain syndrome or chronic pain syndrome, which have International Classification of Diseases (ICD) 9 and ICD 10 code numbers.

Evolution of Pain

It has long been known that direct insult to the central nervous system (CNS)—trauma, infection, cerebral vascular accident, or disease, such as multiple sclerosis or Parkinson’s disease—can result in persistent pain.1 Pain that results from a direct brain insult has been called central pain for at least 5 decades.

Two relatively recent discoveries have expanded our understanding of pain that affects the CNS.2 One is that some disease processes, such as fibromyalgia, interstitial cystitis, and vulvodynia, are known to involve the CNS.3-5 The other is that a peripheral nerve injury or disease, such as phantom limb pain or some neuromas, can permanently implant pain sensation in the CNS.6-8

Regardless of how the CNS becomes involved with pain, it may become pathologically disturbed.9 The underlying mechanism is microglial cell overactivation, which produces neuro-inflammation, metabolic disturbances, cellular destruction, and neuronal sensitization (Figure 1).9-19 While centralization is the most common term used to denote this pathologic development, various other terms—neuropathic, persistent, intractable, and central sensitization—have been used to describe this condition.

Although there have been a plethora of basic science and imaging studies, reports, and descriptions of centralization, there is no consensus on how a practitioner should make a clinical diagnosis of centralization.9-19 To date, there is no specific laboratory test, so its presence must be clinically determined by history and physical examination. Consequently, Practical Pain Management convened a consensus task force to draft this report and provide a simple and rapid protocol to clinically diagnose the presence of pain centralization. This protocol can be used easily in any clinical setting, and it is a adjunctive screen that is compatible with the 1 to 10 pain scale.

Public Health Issue

Data and information collected to date are limited, but what data are available suggest that pain centralization is a major public health issue. The exact incidence and prevalence are unknown, but 2 recent epidemiologic studies indicate that a staggering number of Americans have centralized pain. A recent review of data from the 2010 National Health Survey found that about 20 million Americans have constant pain, which is one of the hallmark symptoms of centralized pain.20 Another national survey found that about 10 million people in the United States take opioid medications.21 Although the clinical need for opioids compared to non-opioid analgesics such as anti-inflammatories is unclear, it is likely that the need for regular opioid administration indicates the presence of centralization in many patients.

It is clear that centralized pain causes a high degree of suffering, mental and physical impairment, and an inability to care for oneself.22-29 But much about this condition remains a mystery and it is all too often unrecognized and untreated. A goal in developing this clinical protocol is to provide every practitioner in every clinical setting with the ability to rapidly diagnose the presence of centralized pain (Table 1). Only when practitioners across the nation begin making a clinical diagnosis will there be enough additional clarification and identification of the public health ramifications of centralized pain.

The Centralization Process

The process of centralization begins with an injury or disease that affects either brain tissue or peripheral nerves. In either case, microglial cells are activated in the CNS.30-35 These cells migrate and initiate neuroinflammation and the release of toxic substances, including glutamate, that sensitize neurons36 and cause cellular destruction. As a result, the brain tries to return itself to normal (neuroplasticity); in the process, the sensation of pain becomes implanted in CNS tissues.2,6,8,17 (Figure 2).

Studies show that patients with centralized pain produce serum and spinal fluid biomarkers of neuroinflammation.37-40 Magnetic resonance imaging (MRI) studies show that neuroinflammation is associated with loss of gray and white matter.19,41-43 Microglial overactivation, neuroinflammation, and neuronal sensitivity produce a typical set of signs and symptoms that make it possible to clinically recognize the patient who has centralized their pain.9 Typical symptoms include constant pain, insomnia, fatigue, depression, attention deficits, memory loss, and episodes of hyperalgesia and allodynia.

In addition, the autonomic, sympathetic nervous system becomes dysfunctional and overactive (dysautonomia) and produces the physical signs of hypertension, tachycardia, hyperhidrosis, hyperthermia, hyperreflexia, mydriasis, and vasoconstriction that may manifest as cold extremities and resemble Raynaud’s phenomenon.29 (Figure 3).

The hypothalamic-pituitary-adrenal axis is stimulated and several hormones may rise in the serum, including adrenocorticotropin, cortisol, and pregnenolone.44,45 Neuronal cells become overly sensitized and hyperalgesia may be present (central sensitization).32,36 Allodynia, apparently caused by a loss of inhibition of efferent electrical discharges from the CNS, also occurs.46-48 Skin biopsies may show a loss of small fibers, which apparently relates to this phenomenon.

Multiple studies describe the severe interruption of life and suffering of these patients.22-29 Psychologic and social impairment may be profound and include reclusivity, depression, and mental deficiencies, such as a loss of reading and mathematical abilities.49 Patients may be bedbound or housebound. There may be diminishment of hygiene, nutrition, and social interactions (Table 2).23-29

Last updated on: May 10, 2017
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Glial Cell Activation and Neuroinflammation: How They Cause Centralized Pain

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