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9 Articles in Volume 10, Issue #3
Body Perception Disturbance (BPD) in CRPS
Diagnostic and Therapeutic Issues of Neuropathic Pain
Realizing the “Promise” of Pain Management and Palliative Care
Emergency Protocols for the Spinal Injectionist
Therapeutic Laser in the Management of Arthritis
Post-operative Inguinodynia from Hernia Surgery
Refractory Chronic Migraine
Taking Advantage of the Peripheral Opioid Receptor
Traumatic Brain Injury (TBI) Pain Phenomena

Diagnostic and Therapeutic Issues of Neuropathic Pain

The use of laboratory studies and imaging studies in the diagnosis of neuropathic pain present clinical challenges and, although medications remain the mainstay of therapy, it is frequently necessary to try multiple different medications and modalities for adequate treatment.

There are two types of pain: nociceptive and neuropathic. The former is of a mechanical nature and relates to nerve pain through direct nerve irritation, such as an arthritic joint. The latter implies a specific injury or insult to nerves causing pain and discomfort. Based on my clinical observations in treating patients with neuropathic pain for almost 20 years, it is my belief that neuropathic pain and, in particular, radicular pain has been under-diagnosed and under-treated for a variety of reasons. Partly it’s our reliance on electrodiagnostic testing in making the diagnosis of radicular pain and the difficulty in obtaining an accurate history from the patient, and an absence of other diagnostic testing to make this diagnosis. Also, health care professionals often overlook the neuropathic component of pain and focus on other causes of chronic pain. Further, the difficulty in the treatment of neuropathic pain presents a clinical challenge.

Neuropathic pain includes, but is not limited to diabetic neuropathy, all peripheral neuropathies, radiculopathy, complex regional pain syndrome, sympathetically mediated pain, fibromyalgia, and interstitial cystitis. A variety of medical conditions that cause peripheral neuropathy include inherited diseases, alcoholism, nutritional vitamin deficiencies, cancers, autoimmune reactions, medications, kidney and thyroid disease and infections such as Lyme disease, shingles or AIDS. Peripheral neuropathy of idiopathic etiology, diabetic peripheral neuropathy, radiculopathy and mono-neuropathies make up the majority of all the causes of neuropathic pain.

Diagnostic Issues

Although the diagnosis of a specific type of neuropathic pain can be complicated, distinguishing between neuropathic pain and nociceptive pain is not as complicated. It is important to distinguish pain patterns in making the diagnosis of neuropathic pain. Practitioners should evaluate the patients as to whether the pain involves an extremity and, if so, is it radiating from the spine or is it a separate pain of a joint or a separate part of the extremity.

Pain location is important and the patient needs to elaborate specifically where the pain occurs. It is helpful to use a pain diagram to show where their pain is located. The practitioner should then go over the diagram with the patient and complete an examination and have the patient show them physically on their body where the pain occurs. If the pain involves an extremity, is it sock-like pain or is it linear in fashion? Are there neurological changes on examination and does the patient have other neurological symptoms or complaints such as numb-ness or tingling?

For the purpose of this article, I examined 30 patients in my clinic with chronic back pain and confirmed compressive pathology in patients who also had extremity pain. Of those 30 patients, only two were able to adequately describe a radicular symptomatology that could be considered as anatomically accurate. Less than half the patients had EMG studies and, of those, about two thirds were reported as negative. In our practice, we have found that the treatment of radicular pain has frequently been denied specifically based on these two issues: that there is a lack of a clear dermatomal pain pattern, and that there is a normal EMG report.

A review of the literature seems to indicate that there is some information which substantiates these concerns. A study from the Journal of Neurology indicated, “The subsequent clinical course of patients examined in an EMG laboratory has not been adequately studied.”1 The purpose of this study, in addition to their observations of EMG results, was to review the existing literature and determine the treatment outcomes of patients based on those EMG findings. What they found in this retrospective review of patients was that those patients who had had a pathological EMG had significantly better clinical outcomes in the three year post period than those patients who did not. This indicates that practitioners were treating patients for neuropathy based on the EMG results and denying treatment on those patients who did not have positive results.1

A separate study, completed in 2002, attempted to determine specific protocols for the use of EMG. It recognized deficiencies in the diagnosis. The studies stated specifically, “The assessment of the spontaneous activity in extremity muscles alone minimizes the influence of error-causing factors on the EMG result. Nevertheless, lack of assessment of motor units potentials makes electromyographic investigation of chronic radiculopathy impossible. “Sensitivity and specificity of the method have to be determined before the clinical use of the assessment of motor unit potential, MUP, and chronic radiculopathy, especially in patients with motor weakness. This indicates shortcomings in needle EMG in diagnostic radiculopathy.”2

Further difficulties with paraspinal EMG and lumbar radiculopathies were outlined in a 2000 article regarding the use of a 0–4+ scoring scale in determining paraspinal muscle involvement in radiculopathies. They found deficiencies in the scoring system when the electromyographer suspected that the patient had radiculopathy. It was a more common use of equivocal paraspinal scoring and underscores the inconsistencies and subjectivities that may occur regarding EMG diagnosis.3 This seems to indicate that electrodiagnostic studies are not extremely accurate in some neuropathic pain and there seems to be inconsistencies regarding its use in determining the diagnosis of radicular pain. Since practitioners have frequently treated radiculopathy based on EMG findings and have neglected to treat as aggressively those patients who did not have positive EMG findings, I believe additional studies need to be done to clarify these issues.

Clinical Diagnosis of Neuropathic Pain

The diagnosis of neuropathic pain is also based on clinical examination and clinical history as well as laboratory studies and imaging studies. As far as examination and diagnosis of neuropathic pain, observations in our clinic have revealed that very few patients adequately describe what would be considered an anatomical dermatomal pain pattern for radicular pain. This was emphasized during my informal evaluation of a group of patients in our clinic. The difficulties patients have in describing neuropathic pain occur for a variety of reasons and was highlighted in a 2005 article: “Sensory examination could be challenging and confusing because responses are indirect and represent a patient’s interpretation of the test and questions. It is obviously easier to determine in patients if there is a stocking glove-type dermatomal or radiating type pattern, but as far as following a dermatomal pattern this difficulty remains.”4

The use of provocative tests is another clinical diagnostic tool. There are three provocative tests that are commonly used for the diagnosis of radicular type pain. The first is Spurling’s test which is a neural compressive maneuver. Also, there is the Valsalva maneuver and straight leg raising maneuver. A 2007 study, Comprehensive Review of Provocative Testing in Diagnostic Radiculopathy, showed that “Common methodological flaws included lack of an optimal reference standard, disease progression bias, spectrum bias and review bias.” A portion of the conclusion of this study stated, “The lack of evidence precludes any firm conclusions regarding their diagnostic value, especially in primary care. More highly qualified studies are necessary in order to resolve this issue.”5

The clinical diagnosis of chronic regional pain syndrome is different than some of the other neuropathic pains. There are no good diagnostic studies to rule in CRPS and it remains a clinical diagnosis of exclusion. The three-phase bone scan has been touted in some studies as a diagnostic tool for CRPS, but it is clinically obvious that this test is not accurate. While late stage CRPS with bone density changes can be diagnosed using the three-phase bone scan, it is otherwise of minimal value.

On clinical examination, hypesthesia and subtle temperature changes as well as skin coloration and swelling are the hallmark findings clinically for CRPS. Even though CRPS is a condition that 10 to 15 years ago doctors were battling with insurers and other healthcare administrators as being a bogus diagnosis, there are still some that refer to the old RSD criteria in denying treatment of CRPS. With the overwhelming clinical evidence of CRPS, I believe that these opinions are improper and indicate a lack of understanding of this condition.

Laboratory Studies

In general, laboratory testing in radicular pain is not helpful. However, lab testing is essential in peripheral neuropathy. The laboratory tests for peripheral neuropathy can be very extensive and expensive. There have been many articles dedicated solely to the diagnosis of peripheral neuropathy and we recommend this condition be evaluated by someone who has significant clinical experience in diagnosing and treating this condition. Careful examination and history can rule out many of the other etiologies of peripheral neuropathy.

Laboratories studies recommended for fibromyalgia should be limited and should generally include an ESR, CBC, chem profile and TSH. An ANA and RA Titer should not be completed unless clinically indicated.

Imaging Studies

Imaging studies do have value in diagnosing radiculopathy since they can identify a compressive lesion or neuro compromise. In peripheral neuropathy, however, there is limited value in imaging studies. Imaging studies are also of limited value in peripheral entrapment and mononeuropathies.

Radicular pain, in the absence of any imaging study showing neurocompressive pathology is frequently untreated. It is currently a clinical understanding that degenerative disc disease, spondylosis, ligamentous structures, spondylolisthesis and other conditions can cause neuro compromise and radicular pain without showing specific neurocompressive changes on imaging studies. Radicular pain can be present with a normal MRI due to undetected disc pathology, such as tears and also musculoligamentous structures that can cause compression. This can create a diagnostic and treatment dilemma in radiculopathy.

As stated previously, a three-phase bone scan is not helpful in RSD, but a bone scan can be indicated in certain cases of RSD, particularly when infection needs to be ruled out.

There have been reported cases of the use of ultrasound for detecting para-spinal tumors as the cause of an otherwise undiagnosed lumbar radiculopathy. A very careful history and, in the absence of other findings, a high level of suspicion of radiculopathy may justify this type of imaging. In general, ultrasound would not be used routinely as a diagnostic test for either radicular pain or neuropathic pain.

Treatment

Medications. The treatment of all neuropathic pain is similar. Medications are the mainstay of the treatment of neuropathic pain. The medications for treatment of neuropathic pain include alpha adrenergic agents (e.g., tizanidine and clonidine); anti-convulsants (e.g., gabapentin, pregabalin, topiramate and lamictal); and selective norepinephrine reuptake in-hibitors (e.g., venlafaxine, duloxetine, tricyclic antidepressants, amitriptyline, desipramine, and nortriptyline). The listed drugs are only a sample of medications used and there are others that are frequently used.

In our community, we have had difficulty with insurers denying the use of many of the medications that are non-generic. It is our custom to try non-generic medications first, but if ineffective or contraindicated, we will frequently try to use some of the newer drugs that do not have a generic equivalent. These limitations have led to non-treatment of some of our patients for neuropathic pain when generic medications have not been proven helpful or are contraindicated and they cannot afford the cost of the non-generic medication.

Neurostimulation. Neurostimulation is a very effective means in treating both radicular and neuropathic pain. One of the limitations of neurostimulation is that, frequently, patients with post-laminectomy syndromes will have back and leg pain. The neurostimulation works better on extremity pain. Percutaneous stimulation of the low back is an emerging use of percutaneous neurostimulation and can treat back pain separately from leg pain.

In our clinic we have had substantial success treating lower buttocks and leg pain and, in some cases, even back pain using neurostimulation. Peripheral neur-opathy and RSD have responded very well to neurostimulation. Mononeuritis conditions, including ulnar neuritis and inguinal neuritis, have shown promising results from peripheral neurostimulation.

“Medications are the mainstay of the treatment of neuropathic pain. The medications for treatment of neuropathic pain include alpha adrenergic agents...anti-convulsants...and selective norepinephrine reuptake inhibitors...”

Topicals. Topical agents are used quite a bit for neuropathic pain. Lidoderm© patches have proven to be effective, but we have experienced limitations from insurers because the original FDA approval was for postherpetic neuralgia. A 2000 journal assessment of Lidoderm patches found that they can be effective for chronic neuropathic pain conditions other than postherpetic neuralgia. The patch uses Lidocaine to provide a sodium channel block and effectively reducing peripheral nociceptive sensitization and ultimately central nervous hyperexcitability. It does this without absorbtion of large amounts of lidocaine and is one of the strong points in the use the Lidoderm patch.6 Large dose capsaicin may also be effective. A 1998 study showed that, “Intermittent application of large dose topical capsaicin may provide significant pain relief, decreased chronic analgesic dependency and decreased aggregate health care expenditures.”7

There are pharmacists who compound drugs for the use of neuropathic pain. We are fortunate to have such a pharmacy in our area. We do, however, have difficulty getting them reimbursed through insurance. There are a variety of different compounding options. In our clinic, we use a local pharmacy that utilizes a transdermal cream that has reported penetrating superiority over creams. We use a combination of a 60-gram tube with 6% ketamine, which is an NMDA receptor antagonist, combined with 5% gaba-pentin which is a glutamate antagonist that blocks pain transmission. We often add the local anesthetic agent lidocaine in a 5% concentration.

We do variations on this with slightly higher doses of ketamine and, in some cases, the addition of ketoprofen. We have found that patients who are able to afford, or have insurance coverage for, these compounded products do quite well with them.

TENS Units

Transcutaneous neurostimulators, or TENS units, can provide some nerve blockage using electrical stimulation on the more peripheral level. It also potentially increases blood flow and reduces spasm. It reduces the triad of chronic pain, pain spasm, pain and swelling cycle by providing a temporary electrical nerve block and improving circulation. It tends to have its maximum effect when being worn, but the slowing of the pain triad may reduce overall patient pain. We find that our patients who try TENS units use them, on average, at least once a day. It is therefore a reasonable and effective tool in the treatment of neuropathic pain.

Surgery

Surgery is indicated in neural compressive disorders. I have not experienced any cases where surgery has been an emergency situation. There have been urgent cases where patients have developed a cauda equine-type syndrome. Patients who are experiencing loss of motor function or a persistent sensory deficit should be evaluated for surgical intervention. It should be explained that if there is an associated lesion that is not treated, some of these conditions could become permanent.

Opiates

The use of opiates for most neuropathic pain is considered acceptable, however there have been reported hyperalgesia syndromes when used for fibromyalgia.8 Though I am very cautious in using opiates, I have a few patients with fibromyalgia who require opiates and they have done well.

Methadone has a weak NMDA antagonist effect which is felt to help with neuropathic pain. Many practitioners, including this author, believe that methadone is more effective in the treatment of neuropathic pain than some of the other opiates.9

Practitioners need to be more selective about who they recommend for methadone use. There have been some reports of increased risk of respiratory depression and respiratory arrests in the use of methadone and benzodiazepines. If you elect to use methadone, you should do so with extreme caution and only if you have significant experience with this medication.10

Summary

The diagnosis of neuropathic pain can be difficult and the patient history is often inaccurate in describing anatomical pain patterns. We must be intuitive and aggressive in diagnosing and treating neuropathic and radicular pain. Diagnostic testing has its limitations, particularly in radicular pain. We need to have a clear understanding of the limitations of electrodiagnostics and patient history in describing a clear anatomical pain pattern. There are challenges in the treatment of neuropathic pain and no clear or easy answers. Though medications remain the mainstay, their efficacy is limited and it is frequently necessary to try multiple different medications and modalities in order to adequately treat neuropathic pain.

Last updated on: January 28, 2012
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