Chronic Pain
Maunak Rana
Scott W. Jellish
The International Association for the Study of Pain defines chronic pain as pain that is present for 3 months beyond the inciting event. Persistent pain is a serious health problem because it dramatically impacts the economic, physical, and bio-psychosocial well-being of society. This chapter presents an overview of the classification and treatment of chronic pain states.
I. TYPES OF CHRONIC PAIN
The sensation of pain can be broadly classified into “neuropathic, musculoskeletal, and psychological.”
A. Neuropathic pain
is described as “electric, burning, or shock-like.” Sources of neuropathic pain can be metabolic, nutritional, infectious, genetic, autoimmune, and vasculitic in nature. These problems can lead to muscle cramps, numbness, and weakness of an affected extremity, causing mononeuropathy or polyneuropathy.
B. Musculoskeletal pain
is described as “aching” (superficial or deep). Discomfort is associated with muscle spasms and a decreased range of motion. If persistent, pain may lead to disuse atrophy and contractures. Causes include myofascial pain, fibromyalgia, posttraumatic/iatrogenic, myopathy, metabolic bone/muscle disease, and/or intervertebral disc disease.
C. Psychological pain
may present as any of the above. Patients may also describe difficulty sleeping, diminished physical, mental, and social functions. Treatment involves addressing the problem with the patient and acknowledging that depression and anxiety may be part of chronic pain, which requires treatment. Primary psychological derangement or a secondary underlying cause of chronic pain may be the problem.
II. MANAGEMENT OF CHRONIC PAIN
Treatment for chronic pain may involve pharmacologic therapy, interventional options, and biofeedback.
A. Medications.
1. Nonsteroidal anti-inflammatory drugs (NSAIDs).
These agents lead to analgesia via central and peripheral mechanisms. They function through the inhibition of the arachidonic acid cascade, which leads to decreased production of prostaglandins. Patients may have varying responses to different agents in this class. These agents can be classified based on their action against cyclooxygenase I/II activity (COX). COX I/II nonselective agents include ibuprofen, naproxen, and piroxicam. Celecoxib is currently the only COX II selective agent available in the United States. parecoxib, an intravenous COX II selective agent, is not currently available in the United States. Common side effects of NSAIDs include renal dysfunction, gastrointestinal (GI) bleeding, and ulcer formation. The antiplatelet effects are not seen with celecoxib and other COX II selective agents.
2. Opioids.
These drugs are either naturally occurring alkaloids or are synthetically produced. They function, to varying degrees, at opioid receptors in the CNS and periphery. These agents are classified based on chemical structure. Opium plant derivatives (phenanthrenes) include morphine and codeine. Agents that are synthetically derived from the phenanthrenes (semi-synthetic) are hydrocodone, oxymorphone, and oxycodone. Synthetic agents not derived from the phenanthrenes include the aniliodopiperidines, fentanyl
(transdermal, buccal, and sublingual), sufentanil, and remifentanil. The phenylpiperidines are meperidine and tramadol; phenylpropylamines include propoxyphene, methadone, and loperamide. Pentazocine is a benzomorphane, oripavine (buprenorphine), and morphinan drugs include butorphanol and nalbuphine. Buprenorphine is an opioid receptor agonist/antagonist that has also been used in pain management (Table 50.1).
(transdermal, buccal, and sublingual), sufentanil, and remifentanil. The phenylpiperidines are meperidine and tramadol; phenylpropylamines include propoxyphene, methadone, and loperamide. Pentazocine is a benzomorphane, oripavine (buprenorphine), and morphinan drugs include butorphanol and nalbuphine. Buprenorphine is an opioid receptor agonist/antagonist that has also been used in pain management (Table 50.1).
Clinicians should utilize preparations with the least abuse potential and side effects. Agents that contain an anti-inflammatory/acetaminophen, to decrease the dose of opioid required for analgesia, should be considered first-line drugs. Common side effects of opioids include respiratory depression, sedation, cognitive impairment, liver dysfunction, and testosterone deficiency in men both with long-term use. Tolerance, addiction potential, and withdrawal from sudden cessation are also common.
3. Antidepressants.
Antidepressants are also utilized in chronic pain management. These agents act via mechanisms that include a direct antidepressant effect, a decrease in synaptic transmission, and the enhancement of the action of endogenous opioids (Table 50.2). They are classified based on their mechanism of action. Tricyclic antidepressants include amitriptyline and nortriptyline. Common side effects of these agents include dry mouth, sedation, sexual dysfunction, hyponatremia, and the risk of withdrawal if discontinued. Selective serotonin reuptake inhibitors (SSRI) are another class of antidepressant and include fluoxetine and duloxitene. Duloxetine is a dopamine, serotonin, and norepinephrine reuptake inhibitor. This drug is used for diabetic neuropathy and is contraindicated in patients with concomitant monoamine oxidase inhibitor therapy, hypersensitivity, and narrow angle glaucoma. Common side effects of SSRI agents include dry mouth, constipation, orthostatic hypotension, weight gain, dizziness, unmasking of mania in bipolar patients, and risk of seizures in patients receiving tramadol. Other agents in this class include buproprion, trazadone, and venlafaxine. Clinicians should be aware that lower doses of antidepressants are usually used for analgesia.
4. Anticonvulsants.
Anticonvulsants are also used in the treatment of chronic painful conditions. Many agents in this category have a common historical use for the prevention and suppression of seizure disorders. These drugs act via different mechanisms including increasing inhibitory neurotransmitters, decreasing excitatory transmitters, and blocking ion channels. These agents are most effective for neuropathic pain, although medications of the other classes may be utilized (Table 50.2).
Phenytoin is used to treat diabetic neuropathy. Treatment is initiated at 300 mg per day, with increased dosage as needed. Side effects include gingival hyperplasia, hirsutism, acne, and coarsening of features. This agent activates the P-450 enzyme system in the liver, resulting in a decreased efficacy of mexiletine, haloperidol, and carbamazepine. Co-administration with antidepressants may lead to increased blood levels of phenytoin.
Carbamazepine is used for trigeminal neuralgia (tic douloureux), post-stroke pain, post-herpetic neuralgia, and diabetic neuropathy. The drug is believed to act via central and peripheral mechanisms, selectively targeting actively firing C and A delta fibers. Treatment is started at 100 mg twice a day and titrated to effect. The typical dose range is 300 to 1,000 mg per day in divided doses. Side effects include gait alterations, hyponatremia, leukopenia, aplastic anemia, and agranulocytosis. As a result of these potential hematologic alterations, blood tests are recommended every 2 to 4 months. Oxcarbazepine is an analogue of carbamazepine less likely to cause CNS/blood alterations. Side effects include hyponatremia (sodium of <125 mmol per L), sedation, and dizziness.
Lamotrigine prevents the release of glutamate in addition to blocking active sodium channels. This agent is used for cold-induced discomfort, trigeminal neuralgia, diabetic, and HIV neuropathy. The starting dose is 20 to 50 mg at bedtime, slowly increased to 300 to 500 mg per day in twice daily divided doses (over 2 weeks). A rash, the most common side effect, is commonly seen in pediatric patients, patients receiving valproic acid, and in patients receiving rapid titration of lamictal. The rash may also lead to Stevens-Johnson syndrome. Clinicians should note a decreased efficacy of lamotrigine with concomitant administration of carbamazepine and phenytoin.
Topiramate acts at both sodium and calcium channels, enhancing the action of gamma-aminobutyric acid (GABA), and inhibiting AMPA receptors. The agent is used in diabetic neuropathy, post-herpetic and intercostal neuralgia, and complex regional pain syndrome (CRPS) (see Chapter 51). Dosing is begun at 50 mg at bedtime, increasing to 200 mg twice daily. Side effects include sedation, development of kidney stones, and ocular granuloma due to the inhibition of carbonic anhydrase.
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