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6 Articles in Volume 1, Issue #3
Breaking Down the Barriers of Pain: Part 3
CES: A Practical Protocol for theTreatment of Pain
HeadacheRelief
New Directions
Pharmaceutical Therapies
The Neural Plasticity Model of Fibromyalgia Theory, Assessment, and Treatment: Part 1

Breaking Down the Barriers of Pain: Part 3

Part three of this series discusses clinical presentation, exam, and treatment options for a variety of conditions.

Nerve Compression, Nerve Root

Clinical presentation: The presenting symptom of disc herniation with root compression is a radicular, dermatomal pattern of pain and paresthesias (numbness and tingling). The onset is typically associated with a specific event such as lifting a heavy object or sudden bending or twisting.

Exam: Classically the exam should show root specific changes in at least sensation, if not strength and reflexes, but once again this is the exception not the rule. Most patients with MRI documented root compression have no strength or reflex changes.

Tests: In contrast to AHCPR guidelines, any patient with a radicular pattern of pain should have an MRI within six weeks of onset, especially if the symptoms are progressing, even in the absence of examination findings. An EMG-NCV is rarely helpful.

Treatment: It is likely the MRI will be abnormal since 70 percent of the healthy adult population has bulges or herniations without root compression. If the MRI shows no root compression then either the patient has a residual radiculopathy and the source of compression or damage is no longer present, or the pain is not radicular. For instance, muscle pain associated with piriformis or thoracic outlet syndromes can be confused with radiculopathy.

If the patient has a radicular pattern of pain and/or paresthesia that has persisted for more than six weeks, an MRI should be performed to identify nerve or root compression. This is true even in the absence of “objective findings” such as weakness, reflex asymmetry, or sensory loss. If the MRI shows disc herniation with nerve root compression, consistent with the dermatome of pain, the goal is to allow enough time for the swelling to reduce and take the pressure off the nerve, but not to wait so long that the nerve root becomes permanently damaged by the on-going root compression. The patient should be seen every two to three weeks. If the pain and paresthesias are improving, one waits; if worsening or unchanged, then decompression should proceed. There is no evidence nor compelling logic that physical therapy can decompress MRI-proven disc herniation with root compression.

Nerve Compression, Peripheral Nerve

Clinical presentation: True carpal tunnel syndrome (CTS) is the prototypical nerve compression syndrome and is widely over-diagnosed. Most patients with this diagnosis actually have either epicondylitis or repetitive (muscle) strain. In true CTS the pain and paresthesias should be in the median nerve distribution, i.e., the palmar surface of the thumb, index, middle, and half the fourth finger.

Exam: Exam is typically normal, although in severe cases, thenar atrophy and sensory loss can be found. A positive Tinel's is helpful in confirming the diagnosis.

Tests: An EMG-NCV should be performed. It can confirm the diagnosis and document the severity of nerve compression. However, it can also be normal in mild cases.

Treatment: It is important to distinguish true CTS from the more common muscular and tendon conditions such as epicondylitis and repetitive strain. Typically, nerve compression is due to inflammation and edema in surrounding tendons and ligaments, caused by over-activity. Thus the best treatment is to instruct the patient to avoid that activity or eliminate it completely until the pain subsides, then gradually re-introduce the activity as tolerated. The patient will often resist this recommendation because he or she believes “there is no choice” but to continue that activity, because it is their job or hobby, etc. In addition, patients may have been told that surgery is an option, and might want to go for the “quick fix.” Patients should understand that even if surgery is performed, it may aggravate the condition and that avoiding the aggravating activity will still be necessary post-operatively. The patient can also be provided with a splint, but with the instruction that the splint does not prevent movement and functions. It should be used more as a reminder to avoid the aggravating activity. The proper splint to prescribe is a “neutral position wrist support.”

Nerve Damage, Peripheral Nerve

Clinical presentation: The prototypical painful peripheral neuropathy is diabetic polyneuropathy. Typically, burning pain begins in the soles of the feet and gradually progresses over months and years.

Exam: On examination, there is a loss of ankle reflexes and a “stocking” pattern of loss of light touch and pinprick. Vibration sense is also typically diminished.

A neuroma is another type of peripheral nerve damage, caused by trauma, typically to the bottom of the foot. The damaged nerve forms a tangle of nerve endings that grow into a mass that can range in size from a millimeter to a centimeter. The neuroma is sensitive to pressure, resulting in a localized, sharp, often shock-like pain at the site of the neuroma and distal to it. It is much more localized than a muscle trigger point, which is not typically found in the small muscles of the feet. If large enough, the neuroma can be palpated manually. Diagnosis is made by tapping or firmly palpating over the neuroma and eliciting the painful shock sensation.

A neuroma is distinguished from a ganglion, which is a thickening of the tendon sheath. The pain of a ganglion is experienced as a “catching” sensation when the tendon slides through its sheath. It is typically not painful to light tapping and the pain is reproduced by tendon movement. This is not the case with a neuroma.

Typically, nerve compression is due to inflammation and edema in surrounding tendons and ligaments, caused by over-activity.

Treatment: A key component of treatment is to help the patient understand that nerve damage, whether from diabetes or the residua of decompression surgery, cannot be “cured.” If this is not made clear to the patient then he or she may believe that additional surgery might cure it or by going to another doctor he or she may provide another solution.

The mainstay of treatment is anti-convulsants or anti-depressants. Clinically the anti-convulsant gabapentin (Neurontin) is most effective, but again, not curative. It may take several weeks to be effective and the dose may need to be raised several times in increments. A minimal trial of gabapentin or any other medication is four to six weeks.

If gabapentin is not helpful in reducing pain, then others that are worth trying are amitriptyline (Elavil) and carbamezepine (Tegretol). It is important to start with very low doses. In the case of amitriptyline, even 10 mg hs can cause unacceptable sedation, especially in the morning. The patient must be warned about this side effect and encouraged to take even less for a few days to get past the sedating effect. If Tegretol is used, blood counts must be checked every few months.

SSRI anti-depressants, such as Prozac, are not effective for nerve pain, although effective in treating depression that can accompany chronic pain.

Nerve Damage, Root

Clinical presentation: The most common cause of root damage is prolonged root compression from a disc protrusion or damage during decompression surgery. The symptoms and signs are identical to root compression, a dermatomal pattern of pain and paresthesia.

Exam: Examination is often normal, although with an S1 radiculopathy there may be a reduced ankle reflex on that side.

Tests: Because root damage cannot be distinguished from root compression clinically, an MRI should be obtained to distinguish the two. If surgery has been done in the past, the MRI may show scar tissue around and intermingled in the root. Scar tissue cannot be decompressed from the root and therefore is another form of residual root damage.

Treatment: It is reasonable to attempt a series of three epidural steroid injections in the hope of reducing whatever edema or inflammation is present. Unfortunately these blocks typically give only temporary relief.

Residual radiculopathy is the only indication for a dorsal column stimulator. This device essentially provides a “masking” sensory afferent at the dorsal root ganglion, in an attempt to compete with the nociceptive afferent. Before a permanent device is implanted, the localization and stimulus intensity should be tested for pain relief with a temporary probe insertion. The method carries the risk of further root damage and infection, and unfortunately loses its effectiveness over time (typically less than a year).

The most reliable treatment for residual radiculopathy is the same medications that are used for peripheral neuropathy.

As always, a key component of treatment is education. The patient with residual radiculopathy after decompression surgery will have the same symptoms as before surgery and will probably conclude that the surgery was not successful. He or she may feel that additional surgery must be necessary. If the physician managing the pain condition does not explain this clearly, the patient will search for a surgeon willing to perform more surgery, often a fusion, in the mistaken belief that spinal instability is causing pain. However, the pain arises from the residual radiculopathy that cannot be improved by a fusion.

Joint/Tendon Conditions

Clinical presentation: Joint and tendon conditions are covered together because they present similarly and are treated similarly. These conditions generally involve some degree of inflammation of the synovia, tendon insertions, or ligament attachments. These structures are either injured traumatically or over time from repetitive awkward motions without the opportunity to heal.

Exam: Examination shows local tenderness over the joint.

Treatment: The key to successful treatment of joint and tendon disorders is for the patient to avoid the activity that causes pain, and then gradually re-introduce that activity as tolerated. If a patient will do this, they will recover, although it can take several months. The difficulty is that patients either won't or can't take that advice and expect that injections or surgery will be a quick fix. Injections can provide temporary relief, sometimes lasting a few weeks, but are not a substitute for avoiding the aggravating activity. Also, it can only be used a few times or the steroid will result in atrophy of the tissue. Surgery to repair a tear must also be weighed against the recovery period that will still require avoidance of the aggravating activity.

The most common joint/tendon conditions are discussed individually.

Epicondylitis

Clinical presentation: Pain is experienced at the elbow, radiating into the forearm, especially during strenuous or repetitive flexion and extension of the forearm.

Exam: There is exquisite tenderness just distal to the elbow at the origin of the wrist extensor muscles.

Treatment: Epicondylitis is typically accompanied by muscular involvement that must be treated as described in the muscle injury section described previously. The patient must be instructed to avoid the aggravating activities for a period of time that can extend unfortunately to several months.

A proper forearm cuff can be very helpful and often provides immediate relief. The patient should use it whenever engaged in aggravating activities, but he or she must be reminded that the cuff is not an alternative to avoiding those activities. In addition, the patient should take frequent breaks from forearm activities to stretch the affected muscle tendons.

Local injection of a steroid will reduce the inflammation, but will recur if the patient continues to pursue the aggravating activities. Repeat injections will lead to tissue atrophy and thus should be limited to no more than three to four injections over a four to six month period. The steroid, such as 0.5cc of Celestone, is infiltrated into the tissues around the tendon insertion but not into the tendon directly. The injection should not contain a local anesthetic because this gives patients the false impression that they can return to normal activities because they are pain-free while the anesthetic lasts.

DeQuervain's Tendonitis

Clinical presentation: Pain is experienced at the wrist, just proximal to the radial surface of the thumb (“the snuff box”), especially during strenuous or repetitive flexion and extension of the wrist and thumb.

Exam: There is exquisite tenderness in the “anatomical snuff box” where the thumb extensor inserts on the thumb.

Treatment: The same principles apply here, as with epicondylitis, only a different splint is needed. A Universal Thumb Splint is most effective.

Shoulder Impingement Syndromes

Clinical presentation: Pain is localized to the shoulder and precipitated and aggravated by strenuous or repetitive use of the arm.

Exam: Passive range of motion reproduces the pain.

Treatment: The best treatment is having the patient do Codman Pendulum Exercises. These exercises allow movement of the glenohumeral joint, stretch the joint capsule without impinging the supraspinatus tendon, avoid active abduction, and minimize the scapula elevation or “shrugging” that occurs while standing or sitting, all without contracting the shoulder girdle musculature. This is accomplished as follows:

Have the patient lean forward from the waist with knees slightly bent. Rest the patient's head upon the unaffected (non-painful) arm on a firm object such as a counter or high stool. Allow the affected (painful) arm to dangle freely. Permit the arm to move forward, backward, and in a circular motion clockwise and counter clockwise. If necessary, add a small amount of weight to the dangling arm. Diligent adherence to regular practice of these exercises, plus avoiding the aggravating activities, will result in resolution but will take several months.

Vertebral Facet Arthropathy

Clinical presentation: Pain is localized to a small area just lateral to the spinous process and is typically not severe, often described with words such as “it feels stuck.” When present in the cervical vertebra, the patient experiences a localized stiffness that is relieved by “popping the neck.” Facet pain is mild. If the pain is severe it is likely that the pain is arising in the muscles around the spine rather than the vertebral facet joint.

Exam: Exam is usually normal, although there may be localized tenderness to deep palpation just lateral to the spinous process. The pain can be reproduced, and relieved, by a spinal adjustment maneuver.

Tests: Plain X-rays will typically show degenerative spine changes but are not diagnostic.

Treatment: This is the bread and butter, and virtually the sole province, of chiropractic and osteopathic manipulation. A single treatment should resolve the pain and “stuckness.” The condition is likely to recur but should not require follow-up adjustments more than once or twice a year.

Osteoarthritis of the Spine

Clinical presentation: Osteoarthritis of the spine is essentially normal wear and tear associated with aging. It is usually painless in the spine with the rare exception of a bony spur becoming so large that it causes root compression, in which case there will be radicular pain.

Tests: Plain X-rays will show degenerative changes, primarily bony thickening. These changes do not correlate with presence of or severity of pain.

Treatment: No treatment is indicated for this condition. While it may seem reasonable to prescribe NSAIDs, these medications are not without side effects. NSAIDs give patients the misperception that back pain is caused by inflammation of the spine, when it is much more likely that the pain arises from the paraspinal musculature.

Migraine

Clinical presentation: Migraine is not a synonym for “severe headache.” The key to the diagnosis of migraine is the time course. Migraine is an episodic disorder. Typically migraine attacks occur after 30 minutes and last from an hour to several days. The pain can be severe or mild, and those suffering from mild migraines typically don't seek medical care. In less than 25 percent of cases, the pain may be preceded by neurological symptoms, the aura. The most well known auras are visual obscurations including scintillating scotomas, wavy lines, and visual field cuts. Typically the attack is accompanied by nausea, which can be as mild as a hardly noticed lack of appetite or overt vomiting. The pain is unilateral in only about 30 percent of cases. If the attacks are frequent, more than a few a month, it is common for the patient to have muscular pain between the attacks, so called Mixed Migraine. Many patients who have been diagnosed with migraine have muscular headaches that are readily distinguishable because the pain of muscular headaches is daily and fluctuating, not episodic.

Exam/Tests: Examination is normal; there are no diagnostic tests for migraine.

Treatment: The mainstay of migraine treatment is proper use of triptans such as Imitrex. It is not necessary to take triptans at migraine attack onset, but the dose has to be adequate to stop the migraine. The subcutaneous form is still the best, but not covered by some insurance plans. The sublingual forms are no more effective than the higher oral doses.

Triptans are short acting, and so patients often report that the triptan “didn't work” when in fact it worked well, but the migraine returned a few hours later. The solution to this problem is a “follow-on” strategy. After the initial migraine-stopping triptan dose, several doses of caffeine or a lower dose triptan can be spread out over the window of risk, typically 24 to 72 hours. The easiest way to use caffeine is Excedrin, which contains 65 mg. No-Doz contains 100 mg of caffeine.

Preventative medications are unfortunately often not very effective. The most effective remains propranolol, with nadolol a close second. Amitriptyline is sometimes effective. Calcium channel blockers are rarely effective – the only one to be tested in FDA trials, Procardia, failed. Anti-convulsants such as valproate (Depakote) are also rarely effective. Each should be given a trial of at least four to six weeks.

The outstanding feature of RSD is that the patient's distress and disability is dramatically out of proportion to the objective findings.

Eliminating triggers is central to migraine management. Triggers occur minutes to several hours prior to the onset of an attack. The easiest-to-recognize triggers are food triggers such as monosodium glutamate or red wine. The most difficult to recognize are interpersonal triggers, and there are several reasons for this. Migraine patients tend to be reluctant to admit a “stress” component to their migraine attacks. Interpersonal triggers tend to be delayed, typically several hours from the triggering event to the onset of migraine. The interpersonal triggers are not necessarily “bad” in the typical social sense. For example, it is common to have a migraine attack on the first day of a vacation, presumably after the time-urgency of preparing for the trip. The best method of helping migraine patients recognize their triggers is thermal biofeedback. A temperature probe is taped to one of the fingers and registers subtle changes in blood flow to the periphery, including presumably the meninges. Normal temperature is approximately 92 degrees. Migraine sufferers will often show temperatures below 80 degrees. Using thermal biofeedback, a migraine sufferer can learn to recognize the sensation in the body when the temperature is dropping. The most typical sensation is a racy, queasy sensation in the belly, just below the sternum presumably related to gastric ischemia. Recognizing this sensation when it starts and becomes more intense is the best way to recognize one's migraine triggers. If this sensation is ignored and allowed to progress, a migraine attack is likely to occur within a few hours. When patients learn to attend to these warning signs, they can take actions to eliminate or reduce it.

Repetitive Stress Disorder (RSD)

Clinical presentation: The hallmark of RSD is allodynia — light touch is perceived as painful — of the distal extremity, most commonly the hand. The allodynia involves the whole hand or foot, is not limited to the finger tips as is Renaud's, nor does it follow a nerve distribution and so is readily distinguishable from median neuropathy. The outstanding feature of RSD is that the patient's distress and disability is dramatically out of proportion to the objective findings. For example, the typical RSD patient is totally disabled, even when the symptoms are limited to one hand.

Exam: To make a definitive diagnosis of RSD there must be objective findings of disturbed blood flow to the extremity. This is typically manifested as a coldness or clamminess of the skin of the hand, but can progress to frank edema, skin and nail texture changes, and eventually atrophy and contractures of the wrist and finger joints. Nevertheless, in the absence of at least a skin temperature or color change as minimal objective findings, a diagnosis of RSD cannot be made even with the complaint of severe distal light touch sensitivity. A bone scan adds nothing to findings present on clinical examination. The condition typically follows trauma to the extremity, often minor trauma, even as minor as a paper cut. The most common trauma is surgery, especially carpal tunnel releases.

Pathogenesis: Pathogenesis is unknown. There is no evidence of any specific lesion in the peripheral or central nervous system, including the autonomic system, although the disturbed peripheral blood flow is presumably sympathetically mediated. A useful explanation to patients is as follows: “It's as if the brain thinks that you are bleeding in the area of injury and is trying to stop the bleeding by constricting the blood flow to the area. The pain is not unlike the pain you would experience making snowballs in freezing weather without gloves. The trick is to get your brain to realize that you are not bleeding and that this emergency reflex is no longer needed.”

Treatment: Since the condition is hypothesized to be sympathetically mediated, there has been some experimentation with adrenergic blockers such as phentolamine and phenoxybenzamine. The half-life of phentolamine is 40 minutes so this may be used to determine if it is in fact sympathetically mediated but not a viable treatment. Phenoxybenzamine is a non-competitive blocker and therefore has a rationale as a treatment. However, it is currently available only as an oral tablet and is limited by the systemic cardiovascular side effects. There is research interest in an intravenous form of phenoxybenzamine, but this also has systemic limitations. Local anesthetics also have short half-lives, up to a few hours, and thus are also of questionable value. It is common practice to perform a series of three or four sympathetic blocks in the hope of “breaking the cycle” but if this is not successful, the blocks should be discontinued because they foster co-dependence and are a further source of trauma that often aggravates the condition.

Practically speaking, the first task in taking over pain management of a patient with RSD is to wean them from dependence on the blocks. Patients generally realize the relief is only temporary but are happy to have even temporary relief and develop co-dependent relationships with their anesthesiologist. Thus, weaning the blocks constitutes a real challenge, as the blocks should not be discontinued abruptly. Instead, the pain-managing physician should negotiate with the patient a gradual increase in the interval between blocks, typically adding one or two days to the interval each time a block is done. This will not be successful if the anesthesiologist decides to perform additional “ad lib” blocks when the patient demands it.

The next challenge is getting the patient to begin moving the extremity. Some patients with RSD will not even look at their involved extremity and many will not use it for any tasks. Patients are traditionally referred to occupational therapists specializing in hand therapy. The problem here is that these therapists are trained primarily to treat hand-injury patients that require strengthening of atrophied muscles and adapting functional activities. This is not effective for RSD patients. RSD patients are, in essence, afraid of their affected hand (or foot).

The best way to overcome the RSD patient's fear of using the affected extremity is put the patient in charge of a very gradual escalation in activity. The best place to begin is having patients placing their hand (or foot) in lukewarm water that they adjust themselves. This can be a surprisingly prolonged exercise and may require several therapy sessions over several weeks. Patients must adjust the temperature on their own, using pitchers of cold and warm water to add to the bath until they find a temperature they can tolerate. This will typically be below 92 degrees, but each patient is different. Once they can accomplish this task easily, comfortably, and without anxiety, the next step is to move the extremity in the bath and to experiment with lower and higher temperatures, again in a very gradual manner. The next stage is to begin similar movements outside the bath. The next stage is to begin brief functional uses of the hand such as writing or holding light objects. Obviously, for this program to be successful, utilize a therapist who understands this process and is able and willing to depart from traditional hand therapy treatment precepts.

At the same time this process is undertaken, a counseling program must also begin. There are three necessary components to this counseling. The first is education about the condition. RSD patients typically have distorted images of what RSD is. The very name is confusing and frightening. It is helpful to use the “brain-thinks-you're bleeding” analogy. Often, in addition to the RSD, there is an issue of nerve involvement. For example, many cases of RSD follow carpal tunnel surgery. So, the issue of residual damage to the median nerve remains. If the patient has had carpal tunnel surgery it is best to assume there is some nerve damage, even if clinical exam and NCV are negative. The second component revolves around disability. Many of these patients are on workers' compensation. These patients tend to be on disability out of proportion to their injury. More specifically, most are on total disability despite the fact that their condition is limited to one extremity. Eventually these patients need to begin to think about getting on with their lives despite the residual pain and dysfunction. Finally, there are always other pre-existing or concurrent psychology issues with RSD patients. Most typically there are serious financial or family issues that fuel a chronic state of anxiety, which at the very least can be expected to aggravate whatever sympathetically-mediated pro-cess is on going. Typically a psychologist performs this counseling. As with the occupational therapist, it is necessary to find the right psychologist who understands this condition and does not fall into a mere commiseration role.

These patients are typically drug dependent as well. Nevertheless, RSD is the exception to the rule in that it is more effective to maintain or even increase the amount of narcotics during the treatment process, and then deal with the drug dependence as the condition stabilizes.

Last updated on: January 10, 2012
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