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The Tangled Mechanics of Pain in Complementary Medicine

By: Christopher K. Gaffney, Ph.D., FAAAP



Pain represents a complex psychophysiological phenomenon involving cognitive, neurochemical,
sensory, affective, emotional and motivational components that act in synergistic fashion to produce
varying degrees of intensity perception and reactions differing across individuals and
socioenvironmental conditions. The highly comorbid nature of symptomatic anxiety, somatic pain,
and insomnia is considered one of the most challenging illness constellations to treat in the U.S.
today.
1


As our scientific understanding of the pathophysiological mechanism(s) of painful disease has
evolved - so too has our ability to begin discerning the multitude of factors that can influence patients
experiences with pain (or the resultant consequences of it).
2
To that end, the evolution of the
biopsychosocial model in understanding chronic pain has broadened the perception of pain from a
narrow sensorineural perspective to one that recognizes the mutually interactive contributions of
biological, psychological, and environmental systems.
3


In this Chapter, we focus on how the use of complementary and alternative therapies in the
treatment of painful conditions (and their comorbidies) can offer practioners and patients an entirely
new realm of modalities in this complex disease process. Secondly, when possible, we will also
discuss how treatment with nutraceutical products can directly relate to the underlying
pathophysiology of the disease process. Lastly, we will discuss how various botanical extracts can be
safely and easily deployed by physicians towards providing optimal care.

How the psyche influences pain.

Anxiety, depression, insomnia, and functional impairment(s) are the most prevalent comorbidities
associated with chronic pain diagnoses in the United States.
4
Almost 50% of patients with chronic
pain report anxiety symptoms. One prospective study of 1,007
young adults found that a baseline history of migraine was
significantly associated with an increased risk (Odds Ratio =
12.8) of first-incidence panic disorder.
4
In contrast, depression
increased the risk of developing chronic musculoskeletal pain,
headache, and chest pain. In a community-based sample,
depression was associated with a fourfold increase in the
likelihood of seeking a physician consultation for a new
complaint of back pain.

To further complicate the interactive contributions of
psychological elements in treating patients with pain, recent
data has shown that approximately 60% of patients with
depression report pain symptoms at the time of diagnosis. Data
from the World Health Organization involving 14 countries on
five continents found that 69% of patients with depression
initially presented with only somatic symptoms.
5
Whats more, one-third to over half of patients
presenting to clinics specializing in the evaluation of chronic pain are suffering from a current major
depressive episode.

1
Tenenbaum J, Griffiths TL, Kemp C. (2006). Theory-based Bayesian models of inductive learning and reasoning. Trends in Cognitive
Sciences. 10(7): 309-318.
2
Julius D, Basbaum AI. (2001). Molecular mechanisms of nociception. Nature 413: 203-210.
3
Waddell G, McCullough JA, Kummel E, et al. (1989). Nonorganic physical signs in low back pain. Spine. 5:117-125
4
Fann JR, K. R. (2007). Physical Medicine & Rehabilitation. In JL Levensen, Essentials of Psychosomatic Medicine (pp. 405-450). Washington,
DC: American Psychiatric Press.
5
Clark, M. (2007). Pain. In JL Levensen, Essentials of Psychosomatic Medicine (pp. 451-490). Washington, DC: American Psychiatric Press.


Other researchers in the field of social psychology have been honing in on the specific constellation of
symptoms that are present in patients with chronic pain. There is empirical evidence that supports
Fishbein and Ajzens theory; that an increase in the anxiety expressed in chronic pain patients was
associated with corresponding increases in somatic preoccupation, dysfunctional thought processes,
and hypersensitivity to any physical symptoms.
6
In contrast, symptoms of affective distress and
depressive symptomatology were independently associated with increased pain, greater disability,
and more negative thoughts about pain.
4,7,8


While the number of people seeking care by physicians for chronic pain continually grows, first
treatment contact for comorbid conditions (such as anxiety and depression) is still typically delayed
more than 10 years after symptomatic onset.
4
Given the great strides in the delivery of care and
practice of medicine it is an unfortunate fact that although a veritable plethora of modalities exist to
aid in the treatment of patients with anxiety more often than not patients either go untreated
9
or
fail to adequately respond from traditional anxiolytic pharmacotherapy. Given the various obstacles
to delivering traditional care, it is not surprising to find that an estimated 43% of adults in the
United States use botanical medicine as either a primary (or adjuvant) treatment modality for
depression, anxiety, and pain.
10


While some have posited the theory that this modulating effect in pain perception occurs only after
demonstrable amounts of time there is little evidence to support this position. In fact, a growing
body of evidence had demonstrated the inverse to be far more likely. Dr. Kain (and colleagues) from
the Yale University School of Medicine sought out to decipher this very question. In addition, their
team also studied whether acute stress/anxiety could play a role in childrens perceptions of pain. In
their study of over 240 children undergoing elective tonsillectomy, they were able to utilize parental
assessments of anxiety before and after surgery as well as assess the utilization of post-surgical
opiate medication.
11
Not surprisingly, parental assessments of pain in their child showed that

anxious children experienced significantly more pain both during

their hospital stay and for the first
three days at home (follow-up evaluations were standardized for 14 days after hospital discharge).
Moreover, during the home recovery period, anxious children consumed, on average, significantly

more codeine and acetaminophen compared with the children who

were not anxious. Anxious
children also had a higher incidence

of emergence delirium compared with the children who were
not

anxious (9.7% vs 1.5%) and had a higher incidence of postoperative

anxiety and sleep
problems.
12


While there is no single biological model that can account for the synergistic effect that pain has on
both sleep and anxiety some interesting data might point to the biological underpinnings of these
relationships.
Quite simply, in certain brain regions, the neurobiology of pain and depression are almost
indistinguishable. The functional deficiencies that are observed in the monoamine,
gabanergic, glutaminergic, serotonergic, noradrenergic, or related neurochemcial
dysfunctions in affective disorder(s) could partially explain the clear linkages that exist
between pain and depression. In contrast to solely neurobiological actions the bodys
natural response to noxious stimuli results in the activation of the parasympathetic nervous
system (increasing the heart rate, speeding respiration, etc.).
13


6
Smith MT, Perlis ML, Smith MS, Giles DE, Carmody TP. (2000). Sleep quality and presleep arousal in chronic pain. J Beh Med. 23(1):1-13
7
Roth, R. (2000). Psychogenic Models of Chronic Pain. In M. J. Massie (Ed.), Review of Psychiatry - Pain: What Psychiatrists Need to Know.
(Vol. 19, pp. 89-131). Washington, DC: American Psychiatric Press.
8
Rudy, T., Kerns, R., & Turk, D. (1988). Chronic Pain and Depression: Toward a cognitive-behavioral mediation model. Pain (35), 129-140.
9
Sadock BJ, Sadock VA. (2003). Synopsis of Psychiatry. Philadelphia: Lippincott Williams & Wilkins.
10
Kessler RC, Soukup J, Davis RB, Foster DF, Wilkey SA, Van Rompay MI, et al. (2001) The use of complementary and alternative therapies
to treat anxiety and depression in the United States. American Journal of Psychiatry158: 28994.
11
Terry R, Niven C, Brodie E, Jones R, Prowse M. (2007) An exploration of the relationship between anxiety, expectations and memory for
post-operative pain. Acute Pain Management. 9(3): 135-143.
12
Kain Z, Mayer L, Caldwell-Andrews A, Karas D, McClain B. (2006) Preoperative Anxiety, Postoperative Pain and Behavioral Recovery in
Youths undergoing Surgery. Pediatrics 118(2): 651-658.
13
Temporal, M. (2005). Family medicine: Ambulatory Care & Prevention (4th Edition ed.). (M. Megel, & L. P. Schwiebert, Eds.) New York, NY:
The McGraw-Hill Companies.


Brousseau and colleagues discussed how positron emission tomography (PET) research has
revealed that emotional brain areas (e.g., limbic system, prefrontal cortex, hypothalamus,
etc.) have a direct role in pain perception.
14
Other data has shown that cells in the peri-
aqueductal gray area (PGA) of the midbrain receive input from the cortex as well as the
emotional brain areas. The cells receiving information in the PGA then relay information to
the rostral ventromedial medulla in the brain stem and spinal cord. Activation of this
pathway mediates the powerful suppression of pain that occurs during trauma, intense
stress, or excitement.
15

In 2004, Apkarian and his colleagues reported a significant decrease in brain volume of the
pre-frontal cortex in patients with chronic low back pain. Of note, a decrease in brain volume
of that magnitude was estimated to be similar to observations seen after 15 years of
aging.
20,16

Multiple studies have shown that cyclooxygenase (specifically COX-2) does not only act in the
periphery of the nervous sytem as one might expect, but also centrally (as it has been
observed in both the brain and the spinal cord).
10

Studies involving polysomnographic investigations (also conducted by Brousseau and
colleagues) indicated that even in a highly select group of non-pain/healthy subjects once a
noxious hypertonic solution was administered to subjects who were asleep, the pain
response triggered awakenings and shift in sleep stage over all sleep stages, including the less
responsive deep sleep and REM sleep.
10

However - some of the most exciting research in the study of the neurobiology of pain (and
its perceptions) in the anterior cingulated cortex (ACC). Specifically, noxious stimuli activate
the sensory areas of the brain; whilst concomitantly stimulating the ACC (a region of the
brain which is now believed to govern the emotional aspects of pain) and the amygdala
(where pain, fear, emotional drives are thought to reside).
o Trials are now underway at the Oregan Health and Science University to determine if
the ACC acts in concert with the amygdala to produce some the affective disturbances
that are seen in patients with chronic pain (such as depression, altered sleep, and
defense mechanisms like catastrophizing).
17


Therefore, while the complete picture as to the etiology of these alterations in the homeostatic
balance of the body are not yet complete; biologically based theoretical models continue to support
the assertion that there are enumerable factors which can influence not only the experience of pain
but the outcome that it can have on a patients functioning and life.




14
Brousseau MB, Manzini C, Thie N, Lavigne G. (2003) Understanding and Managing the Interaction between Sleep and Pain: An Update for
the Dentist. J Can Dent Assoc. 69(7): 437-442.
15
Porreca F, Price T. (2009, September/October). When Pain Lingers. (M. DiChristina, Ed.) Scientific American: Mind , pp. 34-50.
16
Apkarian AV, et al. (2004). Chronic Pain Patients Are Impaired on an Emotional Decision-Making Task. Pain 108:1-2(129-136).
17
Pain Catastrophizing as a Cause for Systemic Inflammation. (Last updated: 03/26/2009) retrieved from ClinicalTrials.gov (Clinical
Trials Identifier: NCT00823147). Electronic Source: http://clinicaltrials.gov/ct2/show/NCT00823147. Accessed: 09/07/2009 at
04:01AM. Sponsor: Oregon Health and Science University.