Neuropathic Pain: Navigating the Challenges of an Elusive Disease

The wide range of etiologies underlying neuropathic pain render this modality a particularly challenging condition to manage. In addition, most available treatment options have limited efficacy. As the population ages, and as both the incidence of diabetes and the survival rates after chemotherapy treatment increase, the number of patients with neuropathic pain is expected to rise, according to a recent Nature Reviews article.¹

“Pain is complex, and even if you identify a medication that has an effect on a specific aspect of the pain pathway, the ascending or descending pathway, it is an extremely complex condition,” said Vernon Williams, MD, a neurologist and director of the Kerlan-Jobe Center for Sports Neurology and Pain Medicine at Kerlan-Jobe Orthopaedic Clinic in Los Angeles, California, in an interview with Clinical Pain Advisor.

“It is not just sensory; there’s an emotional and cultural aspect,” he explained. This is true for nociceptive pain as well, he said, but it is particularly true for neuropathic pain because it tends to cause much worse quality of life than nociceptive pain does, and it is an unfamiliar kind of pain that people can have difficulty understanding.

Preventing Neuropathic Pain

The challenge of treating neuropathic pain makes prevention a particularly high priority. Genetic etiologies cannot be prevented; however, preventing shingles, which often causes postherpetic neuralgia, with herpes zoster vaccination is critical to the prevention of neuropathic pain.

In addition, providers can work with patients to manage conditions or treatments known to increase the risk for neuropathic pain, such as diabetes, chemotherapy, and perioperative interventions, to reduce the likelihood of postsurgical pain.

Screening and Diagnosing Neuropathic Pain

In cases in which prevention fails or is not an option, 3 diagnostic classifications exist for neuropathic pain: possible, probable, and definite.² A “possible” diagnosis applies when the patient’s history suggests a neurological lesion or disease or an account of one’s pain consistent with biological plausibility, but such categorization requires further testing. A “probable” diagnosis, determined on the basis of clinical examination of sensory signs with bedside and/or quantitative sensory testing, indicates a need to start treatment. Only those patients who have undergone an objective diagnostic test (eg, skin biopsy, neurophysiological assessment) that indicates either a lesion or dysfunction of the somatosensory nervous system would receive a “definite” diagnosis.

Validated screening tools for neuropathic pain, which can suggest a probable diagnosis requiring treatment initiative, include the following: Leeds Assessment of Neuropathic Symptoms and Signs, Douleur Neuropathique 4 questions, Neuropathic Pain Questionnaire, painDETECT, ID Pain, and Neuropathic Pain Symptom Inventory. Each of these tools relies on varying requirements in assessing specific symptoms or descriptors of pain, clinical exam items, affect or location of pain, provoking factors of pain, and/or temporal aspects.

“From a practical standpoint, the things most commonly done have to do with the patient history and physical examination,” Dr Williams said. “If the character and distribution of the pain by patient history is consistent with neuropathic pain, that is often sufficient.” Pain descriptions that include burning, electric, or radiating pain are common, as are presence of allodynia  or hyperpathia. Bedside assessment of sensory symptoms might involve observing the response to pressure, vibration, pinpricks, cold, heat, or light touch (to assess allodynia).

Several objective tests for nerve damage are of varying utility:

• Quantitative sensory tests, using standardized mechanical and thermal stimuli, provide reliable information about loss and gain of function of different afferent nerve fibers classes and can be useful in identifying different phenotypes.³
• Laser-evoked potentials most reliably assess integrity of Aδ and C fibers, whereas  nerve conduction studies, trigeminal reflexes, or somatosensory-evoked potentials assess Aβ function.⁴
• Skin biopsy is highly sensitive for identifying small-fiber neuropathies, but evidence linking neuropathic pain to skin biopsy findings is limited.⁵
• Corneal confocal microscopy is noninvasive, but costly, and not widely available; in addition, evidence linking neuropathic pain with corneal abnormalities is scarce, and nonneuropathic eye conditions may affect the results.⁶

This article originally appeared on Clinical Pain Advisor