Analgesic medications are commonly used for low back pain (LBP). Evidence on the efficacy of pharmacologic therapy for LBP comes from clinical trials that have many limitations, including short-term studies and selective trial populations. Evidence currently supports the use of short-term pharmacologic treatment for LBP. However, the safety and efficacy of long-term pharmacologic therapy for LBP is uncertain and therefore best used with caution, monitoring, and as one component of a comprehensive paincare approach emphasizing rehabilitation.
Low back pain (LBP) is a highly prevalent health problem. Most adults experience LBP, pain in the lumbar region with or without leg pain (sciatica), at some time in their lives. Classification of LBP is generally based on duration of pain (acute or chronic) and location of pain (nonspecific or secondary). LBP is defined as acute when it lasts less than 1 month, subacute when it lasts 1 to 3 months, and chronic when it lasts longer than 3 months. About 90% of patients presenting to primary care with LBP have nonspecific LBP, which is LBP that cannot be attributed to a specific cause, such as infection, tumor, or fracture. Up to 90% of patients with acute nonspecific LBP have improvement of symptoms within 3 months; however, recurrence rates are high, and a number of patients may develop some degree of chronic LBP. This article addresses the pharmacologic treatment of nonspecific LBP and not the treatment of secondary LBP. This article also discusses the most commonly prescribed oral medications for LBP but not the less commonly prescribed pharmacologic treatments, such as transdermal and intrathecal therapy.
The evidence on pharmacologic treatment of LBP comes from clinical trials that have multiple limitations, including short-term trials only, selected trial populations that may not reflect clinical practices, trials using single treatments, and trials measuring pain reduction without evidence of improved functioning. Also, acute LBP is frequently self-limiting, and thus, nearly any treatment administered in the acute phase may seem to be effective. The most commonly prescribed oral medications for LBP include acetaminophen and nonsteroidal anti-inflammatory drugs (NSAIDs), muscle relaxants, antidepressants, antiepileptics, and opioids. Current evidence shows that these medications all have equal efficacy in reducing pain, provide only partial pain reduction at best, and are each associated with different adverse side effects. Evidence supports the efficacy of short-term analgesic therapy for LBP; however, the safety and efficacy of long-term analgesic therapy is not clear. Therefore, current evidence-based guidelines recommend limiting the duration of use for most medications in the treatment of LBP.
Pharmacologic treatment of LBP
Acetaminophen and NSAIDS
Because studies show all analgesics to have equal efficacy in pain reduction, it is recommended that the agents with least risk of harm be used first. Therefore, acetaminophen or NSAIDs are recommended as first-line agents for LBP. A systematic review found no clear difference between acetaminophen and NSAIDs for pain relief in patients with LBP. Acetaminophen, unlike NSAIDs, is not known to be associated with myocardial infarction or gastrointestinal bleeding and may be preferable for patients at risk of these conditions. All NSAIDs appear to be equivalent in efficacy for acute LBP, so the choice of agent may be based on patient preference and cost.
Recommendation
Evidence supports a short course of acetaminophen or NSAIDs for acute or chronic LBP. Long-term use should be avoided.
Muscle Relaxants
Muscle relaxants are divided into 2 categories:
- 1.
Antispastic agents, baclofen, tizanidine, dantrolene, and diazepam, are not recommended for nonspecific LBP. These agents are indicated for spasticity related to central nervous system injury, such as multiple sclerosis.
- 2.
Antispasmodic agents, cyclobenzaprine, methocarbamol, metaxalone, and carisoprodol, may be used short-term (2 weeks) for acute LBP. Long-term use is not recommended.
Evidence from clinical trials regarding muscle relaxants is limited because of short-term trials, poor methodological design, and small numbers of patients. There is no clear evidence that one muscle relaxant is superior to another, so the choice of agent should be based on risk of side-effects, drug interactions, and cost. Adverse effects, particularly dizziness and drowsiness, are consistently reported with all muscle relaxants. Cyclobenzaprine (Flexeril) has been the most heavily studied muscle relaxant with proven short-term effectiveness. Cyclobenzaprine 5 mg is as effective as 10 mg, with fewer adverse effects. The sedative properties of cyclobenzaprine may benefit patients with sleep disturbance. Methocarbamol (Robaxin) is less sedating but has also been less studied. Metaxalone (Skelaxin) has not been studied since the 1970s. One fair-quality study showed no difference between metaxalone and placebo. Carisoprodol (Soma) is metabolized to meprobamate (sedative controlled substance) with addiction potential. Benzodiazepines also have addiction potential and are not recommended for the treatment of muscle spasm. The only trial evaluating a benzodiazepine available in the United States found no difference between diazepam and placebo for muscle spasm.
Recommendation
Evidence supports a short course (2 weeks) of antispasmodic agents, such as cyclobenzaprine or methocarbamol, for acute LBP. Long-term use is not recommended. All muscle relaxants should be used with caution in older patients. Carisoprodol and diazepam should not be used for LBP, because of their addiction potential and lack of efficacy over other muscle relaxants.
Antidepressants
Tricyclic medications (amitriptyline, nortriptyline, desipramine) have been shown in randomized trials to provide a small pain reduction in patients with chronic LBP without clinical depression. These trials did not show functional improvements and side effects occurred in more than 20% of patients. The analgesic effect from tricyclics is believed to be because of inhibition of norepinephrine reuptake rather than serotoninergic activity. Selective serotonin-reuptake inhibitors (SSRIs) have not been shown to be more effective than placebo in patients with chronic LBP. Antidepressants with serotonin-norepinephrine reuptake inhibitor (SNRI) effects, such as bupropion (Wellbutrin), venlafaxine (Effexor), and duloxetine (Cymbalta), have been shown to provide analgesia for certain conditions; however, there are few studies on their use for LBP.
Recommendation
Evidence supports the use of tricyclic medications for chronic low LBP in patients who have not responded to first-line agents. These medications should be started at a low dosage; for example, amitriptyline 10 to 25 mg at bedtime, increased by 10 to 25 mg per week, up to 75 to 150 mg at bedtime or as tolerated. Limited evidence exists on the efficacy of SNRIs for LBP. Evidence does not support the use of SSRIs for LBP.
Depression is common in patients with LBP; as many as 50% of individuals with chronic LBP may have comorbid depression. Clinicians need to address and treat depression appropriately. Studies have shown that treating pain and depression together results in better outcomes than treating either one alone. The patient should be informed of the impact that pain can have on mood and vice versa, and thus, the importance of treating both together. This holds true for other comorbid mental health disorders, such as posttraumatic stress disorder and anxiety.
Antiepileptic Medications
The efficacy of antiepileptic medications for subacute or chronic LBP is based on a few small studies. The precise mechanism of their analgesic effect remains unclear. These agents are thought to limit neuronal excitation, and their sites of action include receptors and sodium and calcium ion channels. Gabapentin (Neurontin) for chronic sciatic pain was evaluated in 2 small short-term trials. There was some evidence of effect for gabapentin titrated to 3600 mg/d; however, the trial lacked a double-blind design. Adverse events reported with gabapentin include drowsiness, loss of energy, and dizziness. Gabapentin for spinal stenosis was evaluated in one small trial. The addition of gabapentin titrated to 2400 mg/d to a regimen of supervised exercise therapy, lumbar supports, and NSAIDs in patients with spinal stenosis and neurogenic claudication resulted in some pain improvement.
Recommendation
Gabapentin may be tried for chronic LBP in selected patients (eg, those with spinal stenosis and neurogenic claudication or evidence of nerve root pain) who have not responded to first-line agents. Starting at a low dosage, it should be increased as tolerated; for example, 100 to 300 mg at bedtime, increased by 100 mg every 3 days, up to 1800 to 3600 mg/d taken in divided doses 3 times daily. Other antiepileptic drugs, such as carbamazepine (Tegretol), pregabalin (Lyrica), and lamotrigine (Lamictal), are not recommended for LBP given the limited evidence.
Opioids
Two systematic reviews and meta-analyses of opioid use for chronic LBP identified few high quality or long-term trials. There are no published trials on the safety and efficacy of long-term opioid therapy for LBP. One systematic review of opioid use for LBP showed a lack of evidence of long-term therapy because the trials were short-term with mean study duration of 8 weeks only. In addition, this review showed that substance use disorders were common in patients taking opioids for chronic LBP. One meta-analysis found that opioid medications compared with placebo or nonopioid analgesics did not significantly reduce pain in patients with chronic LBP. Tramadol, an SNRI combined with a weak opioid, has been shown to be minimally more effective than placebo for improving pain and function. Clinical trials on opioid therapy for chronic LBP often do not show functional improvement and rarely quantify the risk of adverse events, such as abuse or addiction. A recent study observed an increased risk of opioid overdoses in patients receiving higher prescribed doses of opioids for pain. This study showed more overdoses among patients diagnosed as suffering from depression or substance abuse or concurrently receiving benzodiazepines. Patients with mental and substance use disorders are at higher risk for developing opioid misuse and yet some studies have found that opioid prescribing is more strongly associated with the presence of mental and substance use disorders than with pain severity or clinical findings.
In the 1980s, opioids were largely limited to cancer and acute pain. In 1986, Dr Russell Portenoy, a cancer pain expert, published a review of 38 patients on chronic opioids and concluded that chronic opioid therapy can be safe for patients with noncancer pain. During the 1990s, Portenoy and others encouraged the use of opioids for chronic pain, equating effective pain treatment with opioid therapy and using the terms undertreatment, pseudoaddiction, and “opiophobia.” Clinicians were informed that opioid therapy had no ceiling and that it was appropriate to escalate “to effect,” regardless of the amounts prescribed. In 1995 Purdue Pharma introduced OxyContin, claiming it had low abuse potential. In the last decade opioid prescribing for chronic pain has increased dramatically and during this time there has been a dramatic rise in opioid-related abuse, overdoses, and deaths. A public outcry in 2001 over OxyContin-related deaths, lead to investigations and in 2007 top executives of Purdue Pharma pleaded guilty to claiming OxyContin had low abuse potential when they had no evidence to support this. Portenoy has admitted to misgivings about how he and others used the research.
Opioids are now the most commonly prescribed medication in the United States, there has been no evidence that opioids for LBP improve functional disability or self-assessed health status, and prescription opioid-related abuse, overdoses, and deaths have become a public health crisis.
Recommendation
Evidence supports the use of short-term opioid therapy for severe acute LBP. There are no quality studies looking at the safety and efficacy of long-term opioid therapy for LBP. Therefore, long-term opioid therapy must be used with caution and close oversight and to help rehabilitation toward clear and established treatment goals. The use of an opioid treatment agreement informing the patient of safe and appropriate use of opioid therapy can be helpful. Routine urine drug testing is recommended for safety reasons. Regular reassessment is recommended to monitor treatment adherence and progress toward treatment goals. Continuing opioid therapy needs to be contingent on active treatment participation and clear improvements in function and quality of life. Opioid therapy needs to be discontinued when there is evidence of treatment failure or repeated unsafe behavior, such as active substance use disorder.
When opioids are taken on a daily basis for pain, it is recommended that they be taken on a time-contingent rather than pain-contingent or as-needed basis and that long-acting opioids be used to provide more sustained analgesia. Daily use of short-acting opioids or “breakthrough” dosing of opioids is generally not recommended for chronic pain, because of the short duration of benefit and the development of roller-coaster serum levels. Recent evidence shows that larger prescribed opioid doses for chronic pain can result in a greater risk of overdosing on opioids, and therefore, prescribing within a low to moderate daily dosage range may be important. Recently published guidelines on the use of opioid therapy for chronic pain suggest limiting daily opioid doses to a maximum of 120 mg to 180 mg of morphine or its equivalent and to refer patients for additional help before escalating opioid doses further.
Related posts:
Functional Anatomy and Pathophysiology of Axial Low Back Pain: Disc, Posterior Elements, Sacroiliac Joint, and Associated Pain Generators
Myofascial Low Back Pain: A Review
Imaging the Back Pain Patient
Epidural Steroid Injections for Low Back Pain
Sacroiliac Joint and Lumbar Zygapophysial Joint Corticosteroid Injections
The Use of Spinal Cord Stimulation and Intrathecal Drug Delivery in the Treatment of Low Back-Related Pain
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