Chairman and Gerald J. Friedman Chair
in Pain Medicine and Palliative Care
Department of Pain Medicine and Palliative Care
Beth Israel Medical Center
New York, N.Y.
Chief Medical Officer
MJHS Hospice and Palliative Care
Professor of Neurology and Anesthesiology
Albert Einstein College of Medicine
Dr. Russell Portenoy is chairman of the Department of Pain Medicine and Palliative Care and the Gerald J. Friedman Chair in Pain Medicine and Palliative Care at Beth Israel Medical Center, New York. He is the Chief Medical Officer of MJHS Hospice and Palliative Care and Professor of Neurology and Anesthesiology at the Albert Einstein College of Medicine.
Dr. Portenoy is past-president of the American Academy of Hospice and Palliative Medicine and past-president of the American Pain Society. He previously chaired the American Board of Hospice and Palliative Medicine and served on the Council of the International Association for the Study of Pain. He is a recipient of the Lifetime Achievement Award and the National Leadership Award of the American Academy of Hospice and Palliative Medicine, has received both the Wilbert Fordyce Award for Lifetime Excellence in Clinical Investigation and the Distinguished Service Award from the American Pain Society, and was given the Founder’s Award by the American Academy of Pain Medicine. Dr. Portenoy has been Editor in Chief of the Journal of Pain and Symptom Management for more than two decades, co-edits the Oxford Textbook of Palliative Medicine, and is editor for the palliative care section of The Oncologist. He has written, co-authored, or edited 21 books and more than 525 papers and book chapters on topics in pain and symptom management, opioid pharmacotherapy, and palliative care.
Neuropathic pain may be defined as a pain causally related to neurological injury. In a more sophisticated way, it also may be viewed as a construct, a clinical inference that the symptoms, signs and pathological findings associated with a pain complaint are related to mechanisms generated by nervous system injury that have the capability of sustaining the pain in the absence of ongoing activation of nociceptive neurons. Basic research has revealed a very large number of potential mechanisms for pain after nerve injury, including processes that lead to dysfunction in transduction of peripheral events into electrical signals and processes that lead to dysfunction of transmission or modulation in the peripheral nervous system, the central nervous system, or both. This dysfunction, which may involve neurons and glia, and more specifically relate to a large number of neuroanatomic and neurochemical changes, can lead to excessive or sustain signaling of central neurons. Both the site of aberrant ‘generators’ and the specific mechanisms driving them are never clear in the clinical setting, but the inference that the pain is neuropathic suggests important considerations in assessment or treatment. To label a pain neuropathic, a clinician must appreciate the variation in phenomenology that may be encountered in the clinical setting. Often, the presentation is not clearcut and the best clinical stance is that the pain has a ‘probable’ neuropathic component. This conclusion provides a rationale for different therapeutic strategies. Pharmacologically, opioids have efficacy in neuropathic pain and are first-line for moderate to severe pain, but numerous other drugs and drug classes provide great opportunities to help patients whose pain is relatively poorly responsive to an opioid. First-line drugs comprise the glucocorticoids, the gabapentinoids and the analgesic antidepressants. Other classes include a variety of anti-epileptics, alpha-2 adrenergic agonists, NMDA receptor antagonists, GABA agonists, cannabinoids, sodium channel blockers, and various topical agents. Non-pharmacological strategies include varied types of neural blockade, including sympathetic nerve blocks and peripheral nerve blocks; neurostimulation approaches; and neuraxial analgesia.