For example, in a patient with rheumatoid arthritis (RA), peripheral nociceptive input (in the form of inflammation) is likely the initial mechanism at work, but as time goes on, central processing becomes more involved. The patient may then begin to experience pain that is disproportional to what is generally expected with RA and may develop other somatic symptoms. The diagnosis then becomes pain primarily related to RA with central sensitization, and both need to be addressed in a treatment plan. In rheumatic conditions, comorbid fibromyalgia (indicative of central sensitization) is thought to occur in 15% to 30% of patients.5
FPs can utilize the underlying mechanisms to cut across diagnostic labels and tailor treatments to those that are most likely to be effective. For a patient with more prominent peripheral involvement, a procedural intervention such as injections or surgery alone may suffice, whereas a broader approach including psychotherapy, medications, exercise, and other lifestyle interventions may be necessary for a patient with pain caused predominantly by central sensitization.
Addressing both peripheral and central components is essential. One prospective, observational cohort study of more than 600 patients scheduled for unilateral total knee or total hip arthroplasty found that those patients with a higher degree of centralization of pain (as measured by widespread pain index and modified fibromyalgia screening scales6) were less likely to report improvement in the affected body part and in overall body pain following the surgery.7
There is a high degree of overlap among many of the chronic pain syndromes (fibromyalgia, irritable bowel syndrome, interstitial cystitis, chronic headaches) that have been found to have a central sensitization component.8 Providers of primary care are aptly positioned to recognize central sensitization as the underlying pathology and target treatment effectively.
Tailor the treatment plan to the underlying mechanisms of pain
As with any chronic condition, a thorough work-up (complete with history, physical exam, and diagnostic testing, as appropriate) is indicated. In the setting of chronic pain, it’s important to identify both the primary mechanism, as well as secondary factors that may be contributing to the patient’s pain, before developing your treatment plan. These secondary factors may include co-occurring affect disorders,9 a history of trauma,10 poor sleep,11 and tobacco use,12 among others. A history of trauma, for example, co-exists with many pain syndromes. For these patients, central sensitization is responsible for much of their pain. As a result, traditional cognitive behavioral therapy (CBT) may not be the best option because of its focus on accepting pain as a chronic diagnosis; more trauma-focused treatments such as those dealing in emotional awareness and understanding of the central nervous system’s role in chronic pain need to be considered.13
3 common conditions. Below we present evidence-based treatment approaches for 3 conditions that are typically associated with each of the major mechanisms of chronic pain generation: fibromyalgia (a central sensitization cause), OA (a peripheral nociceptive cause), and low back pain (a mixed pain state).
Fibromyalgia: A case of central sensitization
Fibromyalgia is a hallmark diagnosis for those patients in whom central sensitization is the dominant cause of pain. These patients usually present with widespread, diffuse pain, as well as somatic symptoms such as fatigue, memory difficulties, and poor sleep quality.8 When explaining the pain mechanism (ie, central sensitization) to patients, it may be useful to use the analogy of a volume control dial that is stuck in the “high” position and can’t be turned down.
Genes, the environment, and neurotransmitters play a role.The origin of the pain amplification process is believed to be multifactorial.
Genetic factors are thought to contribute to a predisposition for amplification. To date, 5 sets of genes have been implicated in increased sensitivity to pain leading to increased risk of the development of chronic pain during a patient’s lifetime.14-19
Environmental factors (eg, early life trauma, physical trauma especially to the trunk, certain infections such as Lyme disease and Epstein-Barr virus, and emotional stress) may trigger or exacerbate symptoms.8 Of note: Only about 5% to 10% of people who experience these triggers actually develop a chronic pain state, while the rest regain their baseline health.4 This raises the question of whether there is a point during an acute pain episode in which one can intervene and prevent the acute pain from becoming chronic in those at higher risk.4
Imbalances of neurotransmitters (high glutamate;20 low norepinephrine, serotonin,21 and gamma-aminobutyric acid [GABA]22) play a role in central amplification. These substances not only affect sensory transmission, but also control levels of alertness, sleep, mood, and memory.
