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The Paclitaxel Acute Pain Syndrome: Sensitization of Nociceptors as the Putative Mechanism

Loprinzi, Charles L. MD*; Maddocks-Christianson, Kami MD; Wolf, Sherry L. RN, MS*; Rao, Ravi D. MBBS*; Dyck, P James B. MD; Mantyh, Patrick PhD§; Dyck, Peter J. MD

doi: 10.1097/PPO.0b013e31815a999b
Original Article

Purpose: Paclitaxel therapy often result in a unique subacute pain syndrome, commonly termed “myalgia” or “arthralgia.” The pathophysiology of this syndrome is unknown and has not been demonstrated to be associated with any structural alteration of muscles or joints. We hypothesized that this syndrome was caused by a neuropathic nerve injury from paclitaxel. Herein, we characterize the clinical characteristics of this syndrome using detailed patient interviews and consider the putative mechanism(s) for these symptoms.

Methods: Oncology patients who were treated with paclitaxel and developed a subacute pain syndrome were questioned using a detailed structured interview. Data were tabulated descriptively.

Results: Eighteen patients were interviewed. The symptoms (ie, pain) typically began 1–2 days after the infusion and lasted for a median of 4–5 days. Pain was most commonly located in the back, hips, shoulders, thighs, legs, and feet, with the most common descriptors used being “aching” or “deep pain.” Commonly used adjectives to describe the pain were radiating, shooting, aching, stabbing, and pulsating. Some patients described increased pain with weight bearing, walking, or tactile contact. When asked directly whether the pains appeared to be specifically localized to either joints or muscles, 15 of 18 patients denied localization.

Discussion: Based on the nature and temporal occurrence of the paclitaxel acute pain syndrome symptoms, we infer that the paclitaxel acute pain syndrome occurs as a result of sensitization of nociceptors, their fibers, or the spinothalamic system. This proposed neurologic etiology of this pain may also explain the subsequent development in some patients of a symmetric length-dependent sensorimotor polyneuropathy. The mechanism of this syndrome needs further study.

From the *Division of Medical Oncology, †Department of Internal Medicine, and ‡Peripheral Neuropathy Research Laboratory, Mayo Clinic College of Medicine, Rochester, MN; and §Neurosystems Center and Departments of Preventive Sciences, Psychiatry, Neuroscience, and Cancer Center, University of Minnesota and VA Medical Center, Minneapolis, MN.

Reprints: Charles L. Loprinzi, MD, Mayo Clinic College of Medicine, Division of Medical Oncology, 200 First Street SW, Rochester, MN. E-mail:

© 2007 Lippincott Williams & Wilkins, Inc.