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10 Articles in Volume 13, Issue #10
Poor Adherence to Opioid Pain Management Regimens
A Practical Approach to Discontinuing NSAID Therapy Prior to a Procedure
Opioid-induced Osteoporosis: Assessing Causes and Treatments
Persistent Acute Lower Back Pain: The Importance of Psychosocial Evaluation
Research Advance Of The Year
A Day of Consulting in Rural America
Ask the Expert: Should You Test For and Treat Opioid-induced Hypogonadism?
Ask the Expert: Do NSAIDs Cause More Deaths Than Opioids?
News Briefs
Letters to the Editor

Research Advance Of The Year

Editor's Memo from November/December 2013

As 2013 winds down, I want to recognize the year’s most significant research advance in practical pain management. This year’s award goes to the elucidation and understanding of the sequelae of head trauma. Prior to this year, most of us in clinical practice, including yours truly, regarded head trauma as a cause of an acute medical problem, such as subdural hematoma, or a cause of chronic or persistent headaches.1-3

Fueled by an increase in traumatic brain injuries (TBIs) seen among returning veterans of the Iraq and Afghanistan wars, as well as well publicized lawsuits brought against the National Football League for failure to prevent concussions, several first-class researchers have put together a new paradigm of head trauma, which has practical application in pain practice.4-13

Most of the recent research into the area has divided TBIs into 2 basic types:

  • Post-concussion syndrome (mild TBI and post-traumatic headache persisting >3 months after concussion)
  • Chronic traumatic encephalopathy (repeated head trauma leading to headache, confusion, and dementia)

The term post-concussion may conjure to mind a single traumatic blow to the head, caused by a fall, motor vehicle accident, or fight that caused a blackout or coma.9-11 The head injuries seen in soldiers returning from Afghanistan and Iraq wars, however, have caused researchers to broaden this notion of “concussion.” First, the person who sustains head trauma doesn’t have to pass out to sustain permanent injury.1,2,9-11 Second, the concept of “jarring” should be clinically considered a form of trauma or concussion. For example, the term “whiplash,” whether it occurs in a car accident, on a horse, or bungee jumping, can cause the same permanent, pathologic state as a black-out.9-11

The second category is caused by repetitive trauma such as seen in football players and boxers.5-8,12-13 You can likely throw into this category any person who has suffered repeated falls and jars. The repetitious head injury has a new name, chronic traumatic encephalopathy.5-8 Repeated head trauma causes a protein called tau to accumulate in brain tissue. It may lead to a form of dementia or mental impairment classically described as, “Punch Drunk Boxer,” or more euphemistically stated, “dementia pugilistica.”

Both chronic traumatic encephalopathy and post-concussion syndrome can produce a central pain state. While persistent headache is the most common pain manifestation, other pain patterns may ensue.7,9-12 The most common pain sites, other than the head, include neck, back, and upper trunk. In fact, it is common to have TBI patients give a pain description that is akin to fibromyalgia. Patients may describe their pain as “all over,” with areas of hyperalgesia and allodynia. Patients who are referred to pain practices may even be sent with the diagnosis of “fibromyalgia” or “myofascial pain syndrome.”

Three sequelae recently have been elucidated that are of direct and essential importance to the pain practitioner (Table 1). First, head trauma may be manifested clinically by changes in cognition, mood, and personality and behavior. The head trauma patient may develop the classic central pain state (“centralized” or “sensitized”), with depression, insomnia, and hyperarousal of the sympathetic nervous system (hypertension, tachycardia, mydriasis, hyperhidrosis, and hyperreflexia).1-3,10

Second, significant pituitary deficiencies (hypopituitarism) may develop as a result TBI, resulting in deficiencies of testosterone, progesterone, cortisol, thyroid, and estrogen—among others.13-16 In a study by Urban et al, one-third to one-half of patients with TBI had anterior pituitary hormone deficiencies, including growth hormone deficiency in 15% to 21%.15 In fact, symptoms of hypopituitarism and growth hormone deficiencies can mimic those of post-traumatic stress disorder, including fatigue, anxiety, depression, irritability, insomnia, sexual dysfunction, cognitive deficiencies, and decreased quality of life.16

Thirdly, an autoimmune, inflammatory disorder may result with arthro-pathies, neuropathies, and myopathies.17,18 It is now believed that the autoimmune, inflammatory response is caused by traumatic injury to the blood-brain barrier allowing brain tissue (surge of astrocytic protein S100B) to leak into the general circulation producing an antigenic response.17 Put simply, the blood-brain barrier isn’t just there to keep out foreign particles, but to keep antigenic brain tissue concealed and safely stored.

More Common Than Thought

Head trauma is apparently much more common than any of us had realized.19,20 One epidemiologic study reports that an astronomical 31.6% of children and teenagers have significant head trauma requiring medical attention before age 25 years.20 The usual causes are falls, motor vehicle accidents, and sports injuries. Of those adolescents who have TBI, about 25% have persistent pain 3 years after the event.20

Every patient who has neck, chest, or back pain of obscure origin must have a careful history for head trauma. Consider a traumatic event to be possibly significant, even if it occurred in childhood. There is a most practical message here. We must all take a more diligent history of head trauma among our chronic pain patients. It isn’t enough to simply know whether the patient was in an auto accident or fall. Did they hit their head or suffer a severe blast or jar? Once a history of head trauma is elicited, it’s proper to screen for and treat hormone deficiencies and autoimmune, inflammatory manifestations.

Forest Tennant, MD, DrPH

Last updated on: May 30, 2014
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