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13 Articles in Volume 11, Issue #7
Fibromyalgia: Practical Approaches To Diagnosis and Treatment
Juvenile Fibromyalgia: Diagnostic Challenges and Treatment Options
Aqua Therapy Helpful in Treatment Of Systemic Lupus Erythematosus
Axial Neck Pain, Radiculopathy, and Myelopathy: Recognition and Treatment
Early Treatment of TMJ May Prevent Chronic Pain and Disability
Identifying Psychological Factors That Influence Surgical Outcomes
Managing Morton’s Entrapment
Premedicated Mask May Hold Promise for Migraine Patients
Mother With Low Back Pain
The Hip Replacement Patient
Evidence-based Medicine: Losing the Patient’s Voice?
What Is Going Wrong With Research?
Risk for Sedation and Car Accidents

The Hip Replacement Patient

Pain that transforms from peripheral to central pain can create treatment dilemmas for many pain practitioners. If not rapidly controlled, microglial cells may release excitatory amino acids, such as glutamate, nitric oxide, and proinflammatory cytokines, which damage central nervous system tissue.
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A 60-year-old woman underwent hip replacement surgery. The surgeon reported a good technical result, and x-rays showed good placement of the metal implant. After leaving the hospital, the patient experienced constant pain that was so severe she could not maintain her position as an executive in the financial industry. Over the course of the next 2 years, the patient underwent a number of failed pain treatments, including intralesional corticosteroid injections, acupuncture, prolotherapy, physical therapy, electromagnetic measures, nerve blocks, and topical lidocaine patch.

Laboratory findings included the following:

  • Erythrocyte sedimentation rate (ESR), 65 mm per hour (normal is <30 mm/h)
  • C-reactive protein (CRP), 3.20 mg/dL (normal is <0.80 mg/dL)
  • Slightly elevated early morning serum cortisol, 21 mcg/dL (normal is 5-18 mcg/dL)

Physical exam revealed no pain on pressure when applied around the hip joint. The patient had some hyperactive reflexes and cold extremities.

By now, most practitioners are aware of the discovery that peripheral pain may migrate to the central nervous system (CNS) and imprint itself into its memory.1-9 But does this discovery have practical ramifications for clinical practice? The answer is simply yes. Why? Treatments directed at peripheral pain will be ineffective if the pain has transformed itself into a central pain. Additionally, a diagnosis of central pain clearly has practical ramifications for prognosis.

Based on this new knowledge, every patient with chronic pain must be evaluated to determine if the pain is peripheral, central, or a combination of both. This article is a primer on how to recognize central pain transformation so that the pain practitioner can select better treatment options and educate patients about the consequences of this transformation.

How and Why Does Transformation Occur?
Any painful peripheral condition can, unfortunately, transform itself into central pain (Table 1, page 36). The transformation of postsurgical pain into central pain is one of the most studied conditions, as surgery is a traumatic event that damages many nerves. Injured nerves are believed to emit inflammatory stimulators, and possibly some electronic signals, that reach glial cells in the spinal cord and brain.3-9 Microglia, the smallest glial cells, comprise about 5% to 10% of all glial cells (the other 90% to 95% are astrocytes). Once activated by chemical stimuli, microglia change their morphology into amoeboid phagocytes.

The microglia instigate neuroinflammation that, like inflammation elsewhere in the body, is initially neuroprotective. Unfortunately, if the pain is not rapidly cured or controlled, microglial cells may produce too much inflammation.10-12 With excess neuroinflammation, microglial cells release excitatory amino acids, such as glutamate, nitric oxide, and proinflammatory cytokines. This process causes CNS cell death, apoptosis, and tissue atrophy.12 Cells attempt to heal or reform (neuroplasticity), but in this cellular transformation, the perception (also called memory or sensation) of pain is imprinted (also called encoded or embedded) in the cells of the brain.3-9

If the peripheral pain is not cured, it is believed that microglial cells remain activated, neuroinflammation continues, and brain tissue continues to shrink and atrophy. Numerous magnetic resonance imaging (MRI) studies have now demonstrated this loss of brain matter.13-17 When loss of brain tissue occurs, any number of brain functions may be altered, and some very deleterious impairments, such as dementia, may occur.

Predisposing Factors
In surgical patients, postoperative follow-up studies indicate that central pain may occur faster and with greater severity depending on preoperative pain, size of surgical cuts, and lack of pre- and postoperative analgesia.18-20 Any genetic neurologic disease or trait also may predispose to both occurrence and severity of central pain. Included here are depression, bipolar illness, attention-deficit disorder, post-traumatic stress disorder, dementia, addiction, and childhood sexual and physical abuse. When central pain occurs, it may worsen the underlying disease and require treatment of both conditions.21,22

Time Required for Central Transformation
As noted, the time it takes for peripheral pain to transform to central pain can be quite varied. With very traumatic events, such as head and neck injury, it can be almost immediate. Most cases appear to occur about 6 to 12 weeks postinjury. Some patients may have only peripheral pain for several years, but suddenly transformation may take place, perhaps precipitated by a new injury or illness. These patients give a history that their pain was mild, intermittent, and responded to simple measures, such as anti-inflammatory agents and topical treatments, until suddenly the pain became severe, constant, and unresponsive to the old, simple, stand-by measures.

Diagnosis of Central Pain
There are two major historical hallmarks of central pain. The first is that central pain is usually constant. Patients complain that it is present “24/7” and never goes away. Constancy is apparently due to permanent imprinting or encoding of the memory of pain in the brain’s cellular structures.

Peripheral pain, on the other hand, is not constant. It will be present some days or for some time with varying severity, but it is not constant. Peripheral pain ebbs and flows as it is part of an anatomic site that has variations in blood flow, lymph node drainage, and electrical conduction. The patient’s movement, activities, and temperature also influence peripheral pain.

The second hallmark of central pain is that patients respond poorly—or not at all—to treatments aimed at peripheral pain, including injection techniques, topical agents, electromagnetic measures, acupuncture, prolotherapy, and physical therapy. Practitioners should take careful note as to whether a patient responds poorly or not at all to these peripheral treatments. A poor or nonexistent response is a sign that transformation has occurred. On physical examination, the classic findings of swelling, redness, elevated temperature, or pain on pressure or slight movement, is not present. The patient can point to the site of the pain and describe the pain as severe, but applying pressure to that site does not make the pain better or worse.

In the early, developing phase of central pain, neuroinflammation and resulting abnormal cell reformation is believed to abolish a great number of inhibitory descending pathways in the brain and spinal cord.3,5 This may result in unchecked, descending electronic signals that may exhibit as allodynia, hyperalgesia, or burning sensation.

Last updated on: December 1, 2011
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