Department of Family Medicine, University of Michigan, Ann Arbor jillsch@med.umich.edu
The authors reported no potential conflict of interest relevant to this article.
Fibromyalgia, osteoarthritis, and low back pain require multimodal, evidence-based treatment plans. Tailoring those plans to the underlying mechanisms of pain is key.
› Recommend cognitive behavioral therapy for most patients suffering from chronic pain. A
› Recommend movement and exercise therapies for all patients with chronic pain. A
› Prescribe anti-inflammatory medications for patients with peripheral nociceptive pain and centrally-acting agents, such as tricyclic antidepressants, serotonin norepinephrine reuptake inhibitors, and alpha 2 delta ligands, for patients with centralized pain. A
Strength of recommendation (SOR)
A Good-quality patient-oriented evidence B Inconsistent or limited-quality patient-oriented evidence C Consensus, usual practice, opinion, disease-oriented evidence, case series
References
CASE 1 › Lola A is a 28-year-old woman with a history of muscular aches and joint pain throughout her body, fatigue, and mental fogginess. She has been seen by a rheumatologist and has been given a diagnosis of fibromyalgia, but just moved to your town and is establishing care. She is feeling desperate because her pain has worsened and the medication previously prescribed (gabapentin 300 mg tid) is no longer working. She asks to try oxycodone.
CASE 2 › Matt P is a 59-year-old truck driver with severe hip osteoarthritis (OA). His orthopedist recommended against hip replacement at this time because of his young age and a heart condition that makes him high risk. His pain makes sitting for long periods very difficult. He presents to you for help because he is worried he will be unable to continue working.
CASE 3 › Keith B is a 56-year-old construction worker who has been suffering from bouts of back pain for many years. The pain has become more debilitating over time; currently, it is constant, and Mr. B can hardly make it through his work day. He has been getting hydrocodone/acetaminophen from urgent care centers and emergency rooms, but he isn’t sure it is helping and is coming to you to assume his pain management.
Chronic pain (defined as pain >3 months in duration), is a complex, heterogeneous condition affecting an estimated 116 million US adults.1 Much of the management of chronic pain occurs in primary care settings, placing family physicians (FPs) on the front lines of 2 epidemics: that of chronic pain itself and that of the abuse and misuse of opioid pain medications.
In an effort to improve communication about the risks and benefits of opioid therapy and the safety and effectiveness of pain treatments in general, many professional organizations, health care institutions, and recently the Centers for Disease Control and Prevention,2 have published guidelines on the use of opioids for non-malignant chronic pain. With these guidelines in mind—and in light of the latest evidence—we propose the paradigm that follows for the treatment of chronic pain. A critical aspect of this paradigm is determining the pathophysiology underlying a patient’s pain in order to develop a well-rounded, multimodal, evidence-based treatment plan. Detailed here is the application of this approach to the treatment of 3 common chronic pain diagnoses: fibromyalgia, osteoarthritis, and low back pain.
Look to the central and peripheral nervous system
Acute pain begins with activation of peripheral nociceptors at the site of injury. This causes depolarization up the spinal cord and through the brain stem to higher cortical centers where the pain is perceived and localized. Descending neural pathways transport both excitatory and inhibitory information from the brain to the periphery via the spinal cord, which either increases or decreases the perception of pain.3
When damage/injury doesn’t correlate with the perception of pain
Until recently, it was assumed that chronic pain worked much the same way as acute pain and was caused by ongoing nociceptive input in the periphery, but research has shown us that the central nervous system can play a large role in the modulation of nociception. This new understanding comes from the lack of evidence pointing to any pain state in which the degree of nociceptive input correlates with the degree of pain experienced.
With central sensitization, pain is often accompanied by other systemic symptoms such as fatigue—often in the setting of little to no actual stimulation of the peripheral nociceptors.For most patients with chronic pain, regardless of their diagnosis, there is some degree of alteration in the processing of nociceptive signals by the central nervous system contributing to the experience of pain.4 This alteration is thought to be the result of peripheral nociceptive signaling persisting past the point of tissue healing, leading to a hypersensitivity of nerve fibers; the fibers then continue to respond to low, or even absent, sensory stimuli.
Central sensitization is the term used when this hypersensitivity develops in the superficial, deep, and ventral cord nerves. When this happens, pain is often accompanied by other systemic symptoms such as fatigue and slowed cognitive processing, often in the setting of little to no actual stimulation of the peripheral nociceptors.3 (For more on this, see “A new paradigm for pain?” J Fam Pract. 2016;65:598-605 or go to http://www.mdedge.com/jfponline/article/111257/pain/new-paradigm-pain.)
TABLE 14 lists the possible mechanisms of pain, which can be broken down into 4 categories: peripheral nociceptive (inflammatory or mechanical), peripheral neuropathic (underlying damage to a peripheral nerve), central (referring to when the central nervous system is the primary entity involved in maintaining the pain), or any combination of the 3.
As pain becomes chronic, multiple mechanisms overlap
It is important to remember that for any single pain diagnosis, there is likely to be—at least initially—a principle underlying mechanism generating the pain. But as the pain becomes chronic, an overlap of multiple mechanisms develops, with central sensitization often playing a more dominant role than peripheral stimulation (regardless of the diagnosis).
