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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
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.
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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.

Last updated on: January 10, 2012