Chronic pain: How to approach these 3 common conditions

The diagnostic criteria for fibromyalgia were modified in 2011 to remove the tender point examination and to add in somatic symptoms.⁶ These criteria can be useful in the clinical setting in identifying not only fibromyalgia itself but also the degree of “fibromyalgianess” a patient has, which is an indicator of how large a role the centralization process plays in the maintenance of chronic pain.^23,24

Treatment: Multimodal and patient empowering. Evidence-based treatment options for fibromyalgia, as well as other conditions for which there is a high degree of centralized pain, can be found in TABLE 2.^25-36 Multimodal treatment, with an emphasis on patient knowledge and empowerment, is generally thought to be the most beneficial.^25,37 Treatment should almost always include CBT and exercise/activity therapies,^26,29 which have high degrees of efficacy with few adverse effects.

In terms of medication, centrally-acting agents (tricyclic antidepressants, serotonin norepinephrine reuptake inhibitors [SNRIs], and alpha 2 delta ligands) are the most effective. There is little to no data showing benefit from anti-inflammatories or opioids in the setting of fibromyalgia. There is some data to suggest that combination therapy, for example with an SNRI (milnacipran) and an alpha 2 delta ligand (pregabalin), may provide more benefit than treating with pregabalin alone.³⁸

Identify any factors that might be contributing to your patient's pain, such as co-occurring affect disorders, a history of trauma, poor sleep, or tobacco use.Complementary and alternative therapies (eg, yoga, chiropractic care, acupuncture, massage) are being studied more, and while evidence is only preliminary in terms of efficacy, there is increasing emphasis being placed on the need for patients with chronic pain to shift their treatment expectations to greater acceptance of pain and the need for ongoing self-care.²⁸ (For more advice on managing fibromyalgia, see the related videos at http://bit.ly/2lPEt0f and http://bit.ly/2lmjEcn.)

Osteoarthritis: An example of peripheral nociceptive pain

OA is a condition long thought to be characterized by damage to the cartilage and bone; however, as with many other pain diagnoses, there is frequently little correlation between damage seen on radiographs and the amount of pain that patients experience.

One study analyzed data on almost 7000 patients from the National Health and Nutrition Examination Survey (NHANES I) and found that between 30% and 50% of OA patients with moderate to severe radiographic changes were asymptomatic, and 10% of those with moderate to severe pain had normal radiographs or only mild changes.³⁹ Research is showing that many factors may contribute to this discrepancy, including the typical “wear and tear” of the disease, subacute levels of inflammation that can lead to peripheral sensitization,⁴⁰ and, in some patients, a centralized pain component. The patients with more centralized pain often have pain that is disproportionate to radiographic evidence, as well as more somatic symptoms such as fatigue, sleep disturbance, and memory issues.⁴¹

Treatment should be multimodal and include interventions targeted at halting the progression of damage as well as palliation of pain. All treatment plans for OA should also include exercise, weight reduction, and self-management, in addition to pharmacologic interventions, to reduce both the micro-inflammation and the centralized pain component (when present). Intra-articular injections of various types have been studied with some having more efficacy in pain reduction and functional improvement than others.^42-45 See TABLE 3^42-61 for a summary of evidence-based treatment options.

Low back pain—a mixed pain state

Low back pain (LBP) has been recognized as a mixed pain state for quite some time. While some patients may experience purely nociceptive and/or neuropathic pain, most cases are nonspecific with patients experiencing varying degrees of nociceptive (myofascial low back pain), neuropathic (lumbar radiculopathy), and central sensitization pain.^62,63 Evidence for centralized pain is demonstrated in studies showing hyperalgesia,⁶⁴ augmented central pain processing,⁶⁵ involvement of the emotional brain,⁶⁶ and delayed recovery influenced by poor coping strategies.⁶⁷

When developing a treatment plan for a patient with chronic low back pain, remember that the pain derives from a complex combination of pathophysiologic contributors. Identifying where a patient lies on the pain centralization spectrum can help you tailor treatment.

In one study of 548 patients presenting to a tertiary pain clinic with primary spine pain diagnoses, 42% met diagnostic criteria for fibromyalgia.⁶⁸ Compared to criteria-negative patients, these patients tended to be younger, unemployed, and receiving compensation; they had greater pain intensity, pain interference, and used stronger words to describe their neuropathic pain; they also had higher levels of depression/anxiety and a lower level of physical function.

Because low back pain is a condition with high prevalence and associated disability, many clinical boards have created guidelines for management. These guidelines tend to vary in the strength of evidence used, and the extent to which they are followed in clinical practice remains largely unknown. Recommendations frequently discourage the use of ultrasound/electrotherapy, but many encourage short-term use of medications (see “How effective are opioids for chronic low back pain?” J Fam Pract. 2015;64:584-584), supervised exercise therapy, CBT, and multidisciplinary treatment.