Medical Rehabilitation

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CHAPTER 81 Medical Rehabilitation

Howard Liss, Donald Liss, Steven Helper

INTRODUCTION

This chapter will provide the reader with a strategy for treating radicular pain and radiculopathy caused by lumbar disc herniations, stenosis, synovial cysts, and spondylolisthesis. These strategies rely on identifying the cause of nerve root irritation and tailoring the treatment algorithms based on the specific causes. The methods are based on the evidence-based literature and our groups’ collective experience. Because there is little or no evidence that commonly used treatments for radicular pain are either effective or not effective, our approach emphasizes the history and physical examination rather than imaging and electrodiagnostic studies. We will argue that the ultimate patient outcome is best predicted by the clinical presentation and early response to treatment.

The main reason why we base our prescription on the history and presentation is because the history and presentation are the best indicators of what prescription will work.

The art of treating a patient with lumbar radiculopathy involves considering many factors before deciding on or changing a course of action (Table 81.1).

Table 81.1 Medical treatment of lumbar radiculopathy – overview

image

Blanket statements such as, ‘A patient should have physical therapy for 6 weeks before considering imaging,’ fail to take into account many and varied factors. For example, the patient’s medical conditions, emotional state, magnitude of pain, and personal and/or social situation must be considered before treatment recommendations are made. Ideally, the risks and benefits of any considered treatment, including the absence of any treatment, should be carefully explained so that the patient can contribute as much as possible to the decision as to how to proceed.

In the ideal world, as long as we can measure an ongoing positive response to treatment which is better than the expected natural course of the condition, continued treatment is appropriate. On the other hand, if the rate of recovery is not acceptable to the patient, or if there is no measurable response to treatment, then other treatment options should be explored. Unfortunately, this ideal is seldom achieved because third-party payers often put limits on continued therapy and may not authorize changes in therapy or further diagnostic tests

By far the most common cause of lumbar radicular pain is a paramedian herniated nucleus pulposus (HNP) and the treatment for this specific cause will be described in detail. How treatment differs when caused by a lateral or foraminal HNP, sequestered HNP, lumbar stenosis, synovial cysts, and spondylolisthesis will be described in each specific case.

THE MANAGEMENT OF LUMBAR RADICULOPATHY SECONDARY TO A PARAMEDIAN HERNIATED NUCLEUS PULPOSUS

Natural history

A paramedian herniated disc presents with a characteristic history and physical examination. Imaging studies and electrodiagnostic testing will help confirm the diagnosis and help rule out other etiologies of pain or neurological deficits.

Most patients with a paramedian HNP report a history that includes both low back and lower extremity pain. The pain is often worse in the morning, is usually aggravated by sitting more than standing or walking, or upon arising after a sustained period of sitting. Valsalva maneuvers, such as coughing, sneezing, or straining, may also aggravate the patient’s symptoms.

The physical examination usually reveals positive straight leg raising. When a positive crossed straight leg raising sign is present, there is a very high correlation with an extruded HNP, although the location is not necessarily paramedian.

In a review article, Benoist reported that approximately 60% of patients with a symptomatic herniated disc will report a marked decrease in back and leg pain during the first 2 months, while 20–30% will still complain of back and/or leg pain at 1 year.1

Most studies indicate that most patients with a paramedian HNP can be satisfactorily treated with conservative measures.2–6

Komori et al. report: ‘Several well-designed studies of patients with HNP have revealed the satisfactory results of conservative treatment, although some authors have reported that about 20% of all patients had to be treated surgically during follow-up because of prolonged or aggravated leg pain.’7

Saal and Saal performed a retrospective cohort study on the success of nonoperative treatment of herniated lumbar discs with radicular pain and radiculopathy without associated spinal stenosis. All patients had a chief complaint of leg pain, positive straight leg raising of less than 60 degrees, herniated discs on computed tomography (CT) scan, and a positive electromyogram (EMG). The average follow-up time was 31.1 months. The patients underwent aggressive physical rehabilitation, including back school and stabilization training. Ninety percent reported a good or excellent outcome, and 92% returned to work after an average sick leave of 15.2 weeks.3–5,8

The patient’s history and examination not only are critical in making a diagnosis, but also allow us to forecast the likelihood of a patient’s responding to therapy alone as opposed to requiring epidural steroid injections or surgery.

Early indications for surgery

Although only 0.0004% of patients have a cauda equina syndrome, symptomatic compression of the cauda equina must be ruled out before proceeding with conservative care. Cauda equina compression usually presents with urinary retention. In addition, patients will infrequently have bowel incontinence, and may note sexual dysfunction. There is often diminished perineal sensation, bilateral lower extremity complaints, and absent bilateral Achilles reflexes. When any of these symptoms are present, magnetic resonance imaging (MRI) must be immediately performed, and if significant compression is shown patients must undergo immediate surgical decompression.

Other patients who are usually candidates for prompt surgical decompression are those who have progressive neurological deficits despite conservative care. There are, however, two situations where surgery is probably not the next step.

If patients have multiple medical comorbidities or advanced age that make the risk–benefit ratio of surgical intervention questionable, one may treat the neurological deficit with an orthotic device to support weakness and ambulation aids rather than performing surgery.

In the early stages after the onset of radicular pain, patients may present with severe pain, positive mechanical signs, and mild or no neurological deficits. These patients may demonstrate worsening of neurological deficits within the next 3–7 days but a lessening of radicular pain and improving mechanical signs. In this case, the patients probably had significant compression of the nerve root causing evolving neurological deficits. Unless the deficit is profound, these patients usually will improve neurologically as well and will not require surgery.

Since no literature is available to predict outcomes in patients with radicular pain and radiculopathy, it is very difficult to advise them with confidence. Nonetheless, our anecdotal experience treating many patients with radicular pain and radiculopathy who refuse surgical intervention has shown that the vast majority of these patients will reach full or nearly full neurological resolution.

Review of the surgical literature reveals an interesting paradox. The results from surgical studies suggest that patients who do require surgery face a greater likelihood of successful outcome if they are operated on relatively soon after the onset of radicular pain. One study reported a worse overall prognosis for patients whose surgery takes place 12 months or more after the initial onset of radicular symptoms.9 Only with a clear understanding of both the natural history and effective conservative interventions for paramedian disc herniations can informed decisions be made regarding surgical consultation.

There are several studies that help predict which patients will respond best to nonoperative care. Patients who present with negative crossed straight leg raising, and the ability to extend the lumbar spine without associated radicular pain, usually respond well to conservative management.10 Patients with normal or very mild neurological deficits also have a better chance of responding to nonoperative care. We also feel that outcome is better when the onset of discogenic radicular symptoms was acute rather than insidious.

There are numerous reports of significant shrinkage, or even disappearance, of extruded herniations that usually occurs over a 3–6-month period.1,11–14 Subligamentous disc herniations, however, are often more stubborn and resolve more slowly than extruded herniations.

Treatment goals

The primary goal of conservative treatment of lumbar radiculopathy is to accelerate the recovery process and educate patients on methods to help prevent or reduce the intensity of future occurrences. We discuss their chances of recovery with conservative care as opposed to requiring spinal injections or surgery. They should be carefully informed as to their chances of recovery from each course of treatment, and should understand the risk of complications and any other negative aspects associated with each approach, including time of recovery.

Conservative treatment seeks to help improve nerve root inflammation, reduce the further expansion of the outer anulus or extrusion of material into the epidural space, and to help the patient compensate for reduced mobility and reduced neurological function.

Functional deficits

Patients occasionally present with significant neurological deficits that may be concerning or disabling. Many of these patients may not require surgery, but until adequate neurological recovery occurs they will need assistance in compensating for these deficits and minimizing the risk of falls. Patients with motor deficits may require lower extremity support.

Patients with S1 deficits have poor push-off and a rocker-bottom shoe can improve the cosmesis of the gait, and a flexible posterior leaf orthosis may help compensate for a patient’s lack of push-off.

Patients with L5 deficits may have significant dorsiflexion weakness and may benefit from wearing boots that fit firmly above the ankle. They may also benefit from ankle–foot orthoses such as a lightweight, flexible posterior leaf orthosis. If there is substantial mediolateral weakness of the ankle, more rigidity must be incorporated into the orthosis. Often overlooked, patients with L5 radiculopathies infrequently have significant weakness of hip abduction with a Trendelenburg gait abnormality and may require the use of a cane on the contralateral side in addition to specific strengthening exercises.

Patients with significant quadriceps weakness from upper lumbar deficits are at risk of falling, particularly when they step off curbs, go down stairs, or walk downhill. These patients should be instructed in compensatory mechanisms that minimize the risk of the knee buckling. On occasion, a knee extension orthosis is advisable.

Patients with significant sensory deficits face the risk of ankle sprains and may benefit from mediolateral ankle support.

Patients with disc disease should also be selectively counseled regarding various assistive devices, such as reachers, as well as on reorganizing and relocating their personal items in order to make the activities of daily living easier while also reducing the strain on their lumbar discs.

Activity modification

Activity modification is one of the least studied areas of treatment, but a particularly important component of our practice.

In a review of ten trials of bed rest and eight trials of advice to stay active, Waddell et al. reported consistent findings showing that bed rest is not an effective treatment for acute low back pain, and in fact may delay recovery.15 Although these patients were not carefully separated into those with axial back pain as opposed to those with radicular pain, the authors concluded that patients should be advised to remain active.

In a trial comparing 2 days of bed rest with 7 days of bed rest for patients with mechanical low back pain without neurological deficits, Deyo et al. reached a similar conclusion: the group with the shorter period of bed rest missed fewer days of work.16 No other difference was noted between the two groups in terms of their functional, physiological, or perceived outcomes.

In fact, there is no evidence that bed rest hastens recovery or improves outcome in patients with radicular pain and radiculopathy. On the contrary, numerous studies demonstrate the deterioration of many physiological systems as a result of bed rest. Abnormalities that develop include, but are not limited to, decreased cardiac output, atelectasis, orthostatic hypotension, decreased aerobic capacity, diffuse muscular atrophy, constipation, renal lithiasis, osteopenia, and depression.

On the other hand, Wiesel et al. conducted a study on military recruits with nonradiating back pain and found that those who were on brief periods of bed rest had a faster return to full duty than those who remained ambulatory.17

Despite numerous studies indicating that continued activity is preferable to bed rest, many patients have too much pain to get out of bed and will require a short period of bed rest until the severe pain lessens. Pain can often be reduced by the following: lying supine with hips and knees both in significant flexion, supported by pillows underneath the calves; lying on either side in a fetal position with the pillow between the knees; and short periods of lying prone with a pillow under the mid-abdomen. In addition, patients are advised to use firmer mattresses, with a soft, thin surface layer.18

Patients with radiculopathy caused by paramedian herniated discs should keep sitting to an absolute minimum. To encourage them to limit time spent sitting, we instruct patients to imagine a nail coming out of their buttock, and to envision it being driven in further if they sit. We also advise them to limit their commute to work and, if possible, being driven in a reclined position as opposed to driving themselves. If they must drive, patients are instructed to tilt up the front of the seat and recline the back, with the use of a lumbar support.

Walking, on the other hand, places fairly minimal pressure on the discs and is well tolerated by the vast majority of patients with paramedian disc herniations. Patients should also be cautioned to keep bending, twisting, and lifting to a minimum.

Clinical use of medications

There is no evidence that any oral medication will change the course of lumbar radiculopathy due to a herniated disc. On the other hand, medication can help control symptoms. Patients are, however, warned to avoid activities that they know would be painful or inadvisable when not taking their medications because such activity could ultimately exacerbate rather than alleviate their symptoms (Table 81.2).

Table 81.2 Medications for lumbar radiculopathy – summary

Non-narcotic analgesics NSAIDs Anticonvulsants
Analgesic effect only Analgesic effect primarily For pain with neuropathic quality, ???, burning
Acetaminophen – max 4 g per day Disease altering for: synovial cyst, Facet syndrome Most common: gabapentin, titrate up to 1800 mg per day for most, max. 3600 mg per day
Tamadol – max 100 g every 6 h Selective COX-2 inhibitors, meloxicam
Caution: interaction with serotonergic drugs Salsalate – ↓GI toxicity, normal bleeding time Caution: somnolence, dizziness, nausea
Caution: fluid retention, GI toxicity – add PPI, misoprostol, ↑ bleeding time, ↑ vascular events
Narcotic analgesics Oral corticosteroids Antidepressants
Analgesic effect only Theoretically decrease root inflammation For pain with neuropathic quality
Short acting Not proven to alter course Tricyclics – most common is amitriptyline, variable sedation, variable anticholinergic
Long acting – for hours, for chronic pain Caution: AVN, multiple side effects
Caution: sedation – add provigil, constipation – add laxatives, nausea, pruritus, addictive potential   SSRIs – not well studied
Effexor, Paxil, duloxetine – theoretical benefit of increasing both central serotonin and neuroepinephrine
Muscle relaxants Anti-TNF Topical agents
Variably sedating Experimental For pain with neuropathic quality
Role when diffuse muscular tenderness Anti-inflammatory – disease modifying Lidocaine patch, capsaicin
Some with anticholinergic effect
Some with addictive potential

Nonnarcotic analgesics

Acetaminophen, in doses of 500–1000 mg every 4–6 hours, up to a maximum of 4000 mg per day provides mild but relatively safe analgesia. Side effects are rare and there is no gastrointestinal toxicity and no sedation. There is no impact on bleeding time and organ toxicity is rare if the dosage is limited to less than 4000 mg per day.

Tramadol (Ultram) is a weak opioid agonist with analgesic properties equal to acetaminophen/codeine combination preparations that is well tolerated by most, including the elderly. Tramadol is often prescribed as 50 mg to a maximum of 100 mg every 6 hours. It is also available in a combination tablet, which includes 37.5 mg of tramadol and 325 mg of acetaminophen (Ultracet). Tramadol has the advantage of causing less sleepiness and constipation than narcotics, with a similar analgesic benefit to mild narcotics. Uncommon side effects include sleepiness, dizziness, and nausea. Tramadol may decrease the seizure threshold in patients with epilepsy.19

Practitioners must be cautious when treating concomitantly with tramadol and other drugs that increase serotonin activity, such as monoamine oxidase inhibitors (MAOIs), tricyclic antidepressants, Paxil, and Effexor. Patients taking significant doses of Ultram in combination with these medications can develop a ‘serotonin syndrome,’ which includes various autonomic, neuromotor, and cognitive–behavioral symptoms. Symptoms may include diaphoresis, hyperthermia, nausea, diarrhea, shivering, hyperreflexia, myoclonus, muscular rigidity, tremor, and ataxia. There have been reports of agitation, mania, hallucinations, and even seizures and death.

Narcotic analgesics

Narcotics are a mainstay in the treatment of severe pain and when used appropriately in patients without a prior history of addiction present a low risk of addiction. Side effects include somnolence, nausea, pruritus, and constipation. Constipation is of particular concern in patients with disc herniation, since straining not only causes pain, but could also cause worsening of symptoms. Time-released preparations of oxycodone, morphine, or fentanyl should be considered for those patients who are unable to sleep due to severe pain.

Nonsteroidal antiinflammatory drugs

No studies show that nonsteroidal antiinflammatory drugs (NSAIDs) improve either the objective signs or the long-term outcome in patients with lumbar radiculopathy. There is, however, some evidence that NSAIDs are effective for short-term symptomatic relief in patients with acute low back pain, but no specific type appears to be more effective than the others.20

There is evidence that antiinflammatories can reduce inflammatory mediators in animal studies.21 A comparison of indomethacin with placebo did not demonstrate a difference in objective neurological signs or subjective reports of pain relief.22 One study revealed a symptomatic improvement with meloxicam in acute sciatica when compared with placebo and diclofenac in a double-blinded trial.23

Neverthless, NSAIDs are frequently used to treat patients with lumbar radiculopathy. Although the course of the condition is not changed, there is probably a role for these drugs in many patients. At the time that this book was going to press, rofecoxib (Vioxx) and valdecoxib (Bextra) had been withdrawn from the market, and other selective COX-2 inhibitors, such as celecoxib (Celebrex), were under investigation in the wake of studies indicating an increased risk of adverse cardiovascular events.

NSAIDs have several advantages when used for pain relief in lumbar radiculopathy, including lack of sedation and the ability to reduce the demand for narcotics. Side effects include gastrointestinal (GI) toxicity and some alteration in bleeding time. Under investigation are NSAIDs that do not appreciably increase bleeding time, including meloxicam (Mobic) and salsalate (Disalcid). However, the prolonged use of all NSAIDs and, in particular the COX-2 inhibitors, may increase the risk of heart attacks and stroke.

The first concern about the cardiovascular safety of rofecoxib emerged with the VIGOR study, reported in 2000. It involved a fivefold increase in myocardial infarction and a twofold increase in stroke, or cardiovascular death among 8076 rheumatoid arthritis patients treated for a median of 9 months with rofecoxib compared with naproxen.24–27 Further questions about the cardiovascular safety of rofecoxib were raised in 2001 by an overview of the clinical trial data.28 These data prompted the FDA to initiate a label change in 2002, highlighting the potential cardiovascular risks of rofecoxib. Despite more recent observational studies also suggesting an increased early (within the first 30 days of treatment) and late (beyond 30 days) risk of acute myocardial infarction or sudden cardiac death with rofecoxib,29,30 conclusive evidence of increased cardiovascular risk from adequately powered randomized trials was lacking.31

The decision by Merck to withdraw rofecoxib worldwide was prompted by an unexpected source. APPROVe (Adenomatous Polyp Prevention On Vioxx) was a multicenter, placebo-controlled trial of 2600 patients designed to examine the effects of treatment with rofecoxib on the recurrence of neoplastic polyps of the large bowel in patients with a history of colorectal adenoma.27 An interim analysis of this trial demonstrated an almost twofold increase in cardiovascular events in patients treated with rofecoxib (25 mg daily) compared with placebo. When these data are extrapolated to the Australian population, the increased risk of 16 events per 1000 patients treated for up to 3 years equates to a potential excess of several thousand cardiovascular events caused by rofecoxib. This may represent an underestimate of the number of events caused by rofecoxib, because patients with inflammatory arthritis are likely to be at higher baseline risk of cardiovascular events than the ‘low-risk’ population included in APPROVe.27

Selection of a particular NSAID type is primarily based upon pharmacokinetics. Prior tolerance of a drug and a low incidence of GI toxicity, as well as minor effects on bleeding time, are all significant factors to consider in choosing the appropriate NSAID. Proton pump inhibitors and misoprostol (Cytotec) are well tolerated and can significantly reduce the incidence of gastrointestinal bleeding and other gastrointestinal side effects. NSAID types that must only be taken once or twice daily are better tolerated than a three-times-a-day schedule.

Muscle relaxants

Some studies support a weak benefit of muscle relaxants over placebo for the treatment of axial back and neck pain,32–35 but we are not aware of any trials on the use of muscle relaxants for lumbar radiculopathy.

Muscle relaxants do affect the musculature, as well as the central nervous system. All relaxants are sedating and therefore are useful when sedation is desired. Muscle relaxant drugs can cause addiction and some are associated with a withdrawal syndrome. Serious toxicity is rare if one keeps within the prescribed dosage range.

Lioresal (baclofen) facilitates gamma-aminobutyric acid (GABA) transmission, and has been demonstrated to be effective in trigeminal neuralgia and may reduce neuropathic pain.

Tizanedine (Zanaflex) is a centrally acting alpha2-adrenergic agonist and effects an inhibition of spinal reflexes. Zanaflex may be useful in patients with diffuse muscular tenderness.

Cyclobenzaprine (Flexeril) is chemically similar to amitriptyline (Elavil) and, because of the anticholinergic effects, may not be suitable for patients with close-angle glaucoma or benign prostatic hypertrophy.

Antidepressants

Tricyclic antidepressants are known to reduce neuropathic pain, but no known studies are specific to lumbar radiculopathy. Although amitriptyline is the best-studied and most accepted drug for the treatment of neuropathic pain, it is also the most sedating of the tricyclic antidepressant medication. All tricyclic drugs have anticholinergic side effects.

The use of selective serotonin reuptake inhibitors (SSRIs) in the treatment of radicular pain is largely unsupported. In studies comparing tricyclic antidepressants with SSRIs for chronic pain syndromes, tricyclics were found to be more effective in every case.36

On the other hand, venlafaxine (Effexor) shares similarities with the tricyclic antidepressants but lacks their most troublesome side effects. In addition, venlafaxine has a similar structure to tramadol. There are case reports, open trials, and preclinical work that support the efficacy of venlafaxine for both nociceptive and neurogenic pain. In addition, paroxetine (Paxil) has been found to inhibit the reuptake of both norepinephrine and serotonin. Therefore, theoretically, it should be a more effective analgesic than the other SSRIs.

Duloxetine (Cymbalta), a selective serotonin and norepinephrine reuptake inhibitor (SSNRI), is available in doses of between 20 mg and 120 mg per day, administered either once or twice daily. Efficacy has been demonstrated in diabetic peripheral neuropathy in two randomized, double-blind, 12-week, placebo-controlled studies in which patients were followed for at least 6 months.37,38 Improvements were seen as early as 1 week after initiating the drug. Doses above 60 mg per day did not offer greater improvement. The drug is contraindicated in patients with narrow-angle glaucoma, as well as in patients with end-stage renal disease or hepatic insufficiency. Most commonly observed adverse effects include nausea, dry mouth, constipation, fatigue, decreased appetite, somnolence, and increased sweating. The overall discontinuation rate due to adverse events was 14%, compared with 7% for placebo.

Anticonvulsants

Most anticonvulsant agents have shown effectiveness in the reduction of neuropathic pain, and may be useful in reducing pain caused by lumbar radiculopathy. Three relatively newer antiepileptic agents – gabapentin (Neurontin), lamotrigine (Lamictal), and topiramate (Topamax) – have become drugs of choice for neuropathic pain syndromes.

Gabapentin is the most often prescribed medication for the symptomatic control of neuropathic radicular pain both because it has the most favorable side effect profile and, due to its low incidence of organ toxicity, because blood levels are not required‥ To help avoid side effects, treatment is usually started at 100–200 mg b.i.d. and 200–300 mg h.s. and slowly titrated upward, by 100 mg per dose. Side effects can include sedation, dizziness, ataxia, and gastrointestinal distress. Maximum daily dosage is 3600 mg per day. Gabapentin is usually tolerated in dosages up to 1800 mg per day, and is generally taken three times per day. The drug can also be used only at bedtime to reduce nocturnal pain.

The antiepileptic drug lamotrigine (Lamictal) has recently been studied in the management of intractable sciatica.39 The study demonstrated improvements in lumbar range of motion, straight leg raising, and a short form of the McGill pain questionnaire.

Newer promising anticonvulsant drugs include tiagabine (Gabitril), oxcarbazepine (Trileptal), zonisamide (Zonegran), felbamate (Felbatol), and levetiracetam (Keppra).

Oral corticosteroids

Although short courses of corticosteroids are often prescribed for radicular pain, there are no double-blind, placebo-controlled trials supporting or not supporting the use of corticosteroids for the treatment of radicular pain caused by a herniated disc or spinal stenosis.40 Because of the risk of avascular necrosis of joints with the intake of 60 mg doses of dexamethasone,41 we only occasionally treat radicular pain with oral corticosteroids.

Antitumor necrosis factor medications

Several recent studies show that tumor necrosis factor TNF-α may be a significant pain mediator in radicular pain.42,43 According to Murata et al.,43 TNF-α is produced and released from chondrocyte-like cells of the nucleus pulposus and acts to reduce nerve conduction velocity, induce intraneural edema and intravascular coagulation, reduce blood flow, and cause myelin splitting. Murata treated rats with intraperitoneal infliximab (Remicade), a selective inhibitor of TNF-α and showed that injected rats produced a significant reduction in histologic changes in the dorsal root ganglion.

Korhonen et al. demonstrated the beneficial effect of a single infusion of infliximab, 3 mg per kg, for herniation-induced sciatica.44 Eight of the 10 patients treated with infliximab remained pain-free 1 year after injection, and no ill effects were reported in any of the 10 patients. Six of the 10 had achieved pain-free status at 2 weeks, seven at 4 weeks, and nine at 3 months. All had severe sciatic pain below the knee, positive straight leg raising at less than or equal to 60 degrees, and a disc herniation concordant with symptoms on MRI. By comparison, only 43% of the 62 control patients, who also had disc herniation-induced sciatica, were pain free at 12 months.

Topical agents

Lidocaine 5% patch reduces pain associated with postherpetic neuralgia without toxicity. The only side effect is an occasional local rash. Lidoderm patches have been tried in various conditions associated with neuropathic pain. Although the drug’s insert instructs that the use should be an on-and-off 12-hour schedule, there does not appear to be any physiological risk to 24-hour use of the patch. There are, however, no studies demonstrating efficacy in lumbar radiculopathy.45

Topical capsaicin (Zostrix), applied three times a day, has been shown to reduce neuropathic pain in concentrations of both 0.025% and 0.075%. Effectiveness is generally unappreciated for at least 2 weeks, and some patients have significant discomfort due to an initial local burning sensation. There is no evidence that this agent is effective in lumbar radiculopathy. Considering the long onset of action and questionable efficacy, we rarely use capsaicin in patients with acute lumbar radiculopathy.

Physical therapy

It is critical for the treating physician and therapist to work closely together and agree on the details of ongoing treatment. The most important role of the physical therapist is to educate patients in proper body mechanics, as well as to guide them through centralization exercises.

Several physical therapy modalities can benefit patients with lumbar radiculopathy. Some patients may respond to lumbar traction and some may benefit from soft tissue modalities. Transcutaneous electrical nerve stimulation (TENS) has an occasional role as an analgesic modality. Selected patients may respond to spinal and neural mobilization techniques. Stabilization and core strengthening exercises are theoretically beneficial, particularly in the prevention of future discogenic episodes. Thermotherapy, electrotherapy, and cryotherapy can temporary relieve pain and are often combined with stretching techniques to reduce soft tissue pain.

Superficial cold (cryotherapy)

Application of cold packs placed in wet towels or ice massage can afford temporary analgesia.46 Cold causes vasoconstriction of superficial vessels, indirectly resulting in vasodilatation of deeper vessels. Contraindications to cryotherapy include cold hypersensitivity and urticaria, Raynaud’s phenomenon, cryoglobulinemia, and paroxysmal cold hemoglobinuria. In addition, cryotherapy should not be applied to areas of skin anesthesia or decreased circulation. Vapo-coolant spray and stretching (spray and stretch) can also be used for the management of myofascial pain. This is often used in combination with trigger point injections as described by Travell and Simons.47

Heat (thermotherapy)

Heat can be used as a temporary analgesic,48 and can be administered by hydrocollator packs, heating pads, hydrotherapy, or thin wraps that can be placed on the skin for a prolonged application. In fact, heat wraps have been demonstrated to be more effective than ibuprofen and acetaminophen for acute low back pain,49 and are helpful for relieving overnight pain.50 Diathermy and ultrasound are usually ineffective in reducing radicular pain.

Heat should not be used in patients with inadequate or altered sensation of pain, and should not be applied to regions of acute trauma, anesthetic skin, or compromised circulation.

Electrotherapy

Various forms of electrical stimulation, such as high-voltage pulsed galvanic stimulation or interferential electric stimulation, can be applied in the office setting, either in isolation or in conjunction with heat or cold. These modalities seem to contribute to relaxation and temporary analgesia, perhaps through decreasing spasm. Electrical stimulation should not be applied to patients with cardiac pacemakers or defibrillators, or to anesthetic areas or incompletely healed wounds.51

TENS uses a small pulse generator clipped to the skin connected to one to four variously placed transcutaneous electrodes. The pulse frequency, amplitude, and wave form are adjusted to achieve maximal effect. TENS can provide analgesia,52

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