Subscription is FREE for qualified healthcare professionals in the US.
12 Articles in Volume 12, Issue #3
Alternative Medicine in Chronic Migraine: What Clinicians Need to Know
Classic Central Pain Syndromes: Review of Neurologic Causes of Pain
Effective Treatments for Neuropathic Pain
Electric Current and Local Anesthetic Combination Successfully Treats Pain Associated With Diabetic Neuropathy
HCG and Diabetic Neuropathy
Migraine Treatment From A to Z
Opioid-induced Constipation: Causes and Treatments
Pain Management of Diabetic Neuropathy
Partnering With Parents
PPM Editorial Board Discusses Mental Deterioration in Pain Patients
The Critical Necessity to Diagnose Pain That Is Centralized
Unique Use of Near-Infrared Light Source to Treat Pain

The Critical Necessity to Diagnose Pain That Is Centralized

Once physicians understand how centralized pain develops from a peripheral site, it is incumbent upon practitioners to make a clinical diagnosis of centralized pain.
Page 1 of 2

Centralized pain is fast emerging as a critical factor in therapeutic, diagnostic, and medical-legal issues. Knowledge about centralized pain has rapidly spread into the public, and the supporting organizations and institutions around medical practice. It is now highly recommended that every chronic pain patient be evaluated for the presence of centralized pain. If present, a diagnosis of “centralized pain” should be given in addition to whatever primary diagnosis is given. For example, a primary diagnosis of “lumbar spine degeneration” would carry a secondary diagnosis of “centralized pain.”

How Centralized Pain Develops
If a peripheral injury doesn’t heal and completely resolve its acute pain, inflammatory mediators from the injury site and possibly electronic signals enter the spinal cord and central nervous system (CNS) (Figure 1, page 56). Microglial cells activate and produce neuroinflammation. Neuron hyperexcitability, known as “central sensitization,” occurs. Glutamate and other excitatory amino acids are released in the inflammatory process causing tissue destruction in the CNS. In this process, memory of the pain somehow becomes permanently imprinted. The inflamed, hyperexcited tissue in the CNS causes excess efferent electronic signals manifested by allodynia and hyperalgesia. Excess sympathetic discharge occurs and hypothalamic-pituitary stimulation increases adrenal hormone production. Centralized pain, with its underlying neuroinflammation and hyperexcitable manifestations, displays a characteristic clinical profile, which can be assumed and diagnosed by history and physical.

Characteristic Clinical Profile
The hallmark of centralized pain is that patients report their pain to be “constant,” which usually has been so since their injury or surgery; patients feel its presence “24/7” (Table 1). It never goes away unless the patient is asleep. Although terms such as “persistent,” “chronic,” or “intractable” may be applied to a patient for any number of medical or legal reasons, the key point is that pain is constant. If pain is intermittent or episodic it is likely peripheral in nature. Just know that the memory of pain is imprinted or imbedded in the CNS and remains ever present in centralized pain.

The inflamed, hyperexcitable CNS puts out excess electronic signals through its efferent and sympathetic systems giving rise to tachycardia, hypertension, and periodic bouts of allodynia (pain to light touch) and hyperalgesia (excess pain on pressure). Patients may complain of episodes of burning, crawling, or stabbing. Insomnia is always present and probably related to the hyperexcitable CNS. Excess sympathetic discharge is manifested by vasoconstriction (cold hands and feet), mydriasis (dilated pupil), hyperhydrosis, tachycardia, hypertension, and hyperreflexia. Patients historically report poor or zero response to peripheral pain treatments such as local anesthetics, cortisone injections, acupuncture, and electromagnetic measures.

Laboratory Testing
If the history and physical suggests the possibility of “centralized pain,” the common inflammatory markers, erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP) should be tested. These are non-specific markers of inflammation, including neuroinflammation. If these markers are elevated, it likely means there is CNS inflammation and ongoing tissue destruction. In addition to these two simple inflammatory markers, it is advisable to do some basic hormonal testing such as a serum cortisol and pregnenolone test. Centralized pain causes overstimulation of the hypothalamus and pituitary that initiates a hormonal cascade producing elevated serum pregnenolone and cortisol. If centralized pain goes uncontrolled for an excessive time period, adrenal hormones including cortisol and pregnenolone may be suppressed and show low serum levels. In summary, abnormal inflammatory markers and/or hormone serum levels are strong biologic evidence that centralized pain is present. More important is if you believe centralized pain is present, laboratory testing is warranted.

A Tip on Diagnosing Centralized Pain
The diagnosis of “centralized pain” is strictly a clinical diagnosis. Even though magnetic resonance imaging (MRIs) may show brain atrophy and laboratory testing may show elevated inflammatory markers or hormone abnormalities, they are only contributing components to the diagnosis.

In addition to the clinical characteristics listed in Table 1, I like to do the following as a simple test. I apply 5% lidocaine over the painful, peripheral area and apply heat, massage, infrared, or radiowave over the lidocaine for 5 minutes. If the patient gets no relief, I assume there is little or no active, inflammatory peripheral pain site, and the pain must, therefore, be central.

Listed here, not necessarily in order of importance, are benefits of clinically diagnosing centralized pain and entering it into the patient’s record (Table 2).

Opioid Treatment
Since the hallmark of centralized pain is constancy, opioids—including a high-dose opioid regimen—may be necessary to control pain. The FDA’s approved labels for long-acting opioids are only to be used “when around-the-clock dosing is indicated.” This label can be found for each agent in the Physician’s Desk Reference (PDR). Constant pain is the primary indication for “around-the-clock” dosing. High or ultra-high opioid dosages may be necessary to control centralized pain and its attendant complications including hormonal abnormalities, inflammation, insomnia, and excess sympathetic discharge (ie, tachycardia). The major point is that a diagnosis of centralized pain is now essentially a necessity to warrant long-acting opioids for around-the-clock dosing.

Recognition of Pseudoaddiction
The hyperexcitable and inflamed CNS of centralized pain may cause patients to desperately seek pharmacologic relief. Patients with centralized pain often describe an intolerable, dysphoric, suffering state that may drive them to great lengths in seeking pharmaceutical relief with an opioid, benzodiazepine, or alcohol. With our new understanding of centralized pain, every patient who appears to be drug seeking should be evaluated for centralized pain. For example, the following case report is illustrative.

Last updated on: May 1, 2012