The scientific approach to pain management demands a step-wise approach, which utilizes lower risk interventions first. In many cases, these lower-risk interventions are helpful for relieving chronic pain. For example, a recent review found that exercise and behavioral therapy were effective at decreasing pain and increasing functioning among patients with chronic pain (Hassett 2011). Other nonpharmacologic interventions that may be useful for chronic pain include meditation, biofeedback, acupuncture, electrical stimulation, and surgery (NIH MedlinePlus 2012). However, in those cases that do not respond to initial pain management treatment options with lower risk interventions, patients with chronic pain may have no other choice but to initiate pharmacologic therapy.
Pharmacologic therapy is one of the most popular treatment options for managing chronic pain. While initial treatment recommendations will vary based upon diagnosis (e.g., nociceptive vs. neuropathic), the most commonly used agents include (Bajwa 2012):
- Non-opioid analgesics (acetaminophen and/or NSAIDs)
- Antidepressants (tricyclics and serotonin-norepinephrine reuptake inhibitors [SNRIs])
- Antiepileptic drugs (gabapentin, pregabalin, and other anticonvulsants)
- Muscle relaxants
- Topical analgesic agents
Despite the wide variety of pharmacologic therapies available for patients with chronic pain, a recent report published by an international panel of experts has pointed out that current conventional treatment schemes are lacking in efficacy and often impose unacceptable side effects (Coluzzi 2011). For example, opioids are the most commonly prescribed class of medication in the United States for short-term relief of chronic pain, and yet, their efficacy and negative side effect profile have many experts questioning their use in this way; especially since the increase in opioid availability has been accompanied by an epidemic of opioid abuse and overdose (Von Korff 2011; Friedrich 2012). In addition to the potential for dependence, patients beginning opioid therapy should also be aware of other common side effects, which include (Friedrich 2012):
- Excessive sleepiness
- Itchiness (i.e., pruritus)
- Respiratory depression
According to the World Health Organization’s (WHO) "analgesic ladder", opioids are not recommended for chronic pain unless the pain can be described as moderate to severe, and/or has not responded to previous (non-opioid) treatment approaches. Consensus xxpert guidelines only recommend opioid therapy for managing chronic (non-cancer) pain once all other reasonable lower risk and lower cost pain management interventions have failed (WHO 1990; Chou 2009).
In an effort to reduce the risk of serious adverse outcomes associated with narcotic pain relievers, Congress has recently mandated that the FDA create the Risk Evaluation and Mitigation Strategies (REMS), which requires drug companies to develop special educational programs for physicians and for patients who are prescribed these potentially dangerous medications (Okie 2010). While opioid therapy can be used for chronic (non-cancer) pain in a safe way, it must be initiated properly, and only in select patient populations (i.e., physicians should carefully screen for mental disorders and history of substance abuse) (Edlund 2007; Chou 2009).
Centrally-acting Drugs for Pain Relief
Chronic activation of peripheral pain sensors (nociceptors), such as occurs in osteoarthritis, for example, can alter central neural pain processing over time. The ongoing nature of chronic pain, and the adaptive nature of the central nervous system both contribute to biochemical alterations that increase pain sensitivity and cause the brain to become accustomed to processing pain. This phenomenon is known as central sensitization.
When the central nervous system has become "sensitized" to pain, painful sensations can be augmented because they are no longer only a nociceptive response, but are now being reinforced by mechanisms within the brain and spinal cord (Mease 2011).
Thus, chronic pain has a peripheral and a central element.
Evidence shows that patients with osteoarthritis of the knee are more sensitive to pain at other sites on their body than are healthy controls (Bradley 2004). This is because the brains of people afflicted with chronic pain have adapted to processing pain and have become hyper-responsive to painful stimuli.
The central element of chronic pain does not respond to traditional therapies such as anti-inflammatory drugs because they cannot modulate the transmission of pain within the sensitized central nervous system. Therefore, drugs such as antidepressants and antiepileptics can complement traditional anti-inflammatory drugs by modulating central biochemistry.
In the case of antidepressant drugs, it appears that the mechanism by which they provide pain relief is somewhat independent from their mood-altering affects (McCleane 2008), while antiepileptics alter pain signaling by modulating calcium signaling in the brain, which is also a mechanism by which they control seizures (Mease 2011).
For many people with chronic pain, centrally acting drugs are effective adjuvants to traditional pain therapies. Moreover, because central processing is a critical element of neuropathic pain, centrally-acting drugs are a mainstay of treatment in this setting (Yalcin 2009).