Abstract
Neuropathic pain is caused by a lesion or disease affecting the somatosensory system and is difficult to manage, often proving refractory to existing treatments. In more than half of cases, it is localized and affects a specific, clearly circumscribed area of the body (localized neuropathic pain, or LNP). A recently developed screening tool enables patients with probable neuropathic pain/LNP to be identified quickly and easily. In view of the conflicting current treatment recommendations, an advisory board of pain specialists met in June 2015 to develop a complementary treatment guidance algorithm, for use in the primary care setting and by non-pain specialists. The starting point of the algorithm is a diagnosis of LNP and there was consensus that first-line treatment should be a topical analgesic agent, because the benefit/risk ratios are far better than for systemic agents. Topical application offers site-specific delivery, a lower total systemic dose and avoidance of first-pass metabolism, reducing the risk of adverse events and drug/drug interactions. The 5% lidocaine medicated plaster has most evidence supporting its use in LNP, producing effective analgesia and reducing the associated area of allodynia, but other topical agents include capsaicin, clonidine and botulinum toxin type A. Treatment should be commenced with the topical agent of choice, and the patient re-assessed after an appropriate period. Where the response is good the topical agent is continued, with a re-evaluation after 3–6 months. A systemic agent (e.g. gabapentin, pregabalin, duloxetine, venlafaxine) is added if there is only a partial response, or substituted if there is no response, and the patient re-assessed after a month. If there is poor or no response to the systemic agent the patient should be switched to an alternative one and, if this also proves ineffective, referred to a pain specialist.
Transparency
Declaration of funding
This study was funded by Grunenthal GmbH, Aachen, Germany.
Declaration of financial/other relationships
M.A. has disclosed that he has received grants from Grunenthal, MSD, and Mundipharma. R.B. has disclosed that he has received grants from Pfizer, Genzyme, Grunenthal, Mundipharma, and as a member of the European Innovative Medicines Initiative, the German Federal Ministry of Education and Research, the German research network on neuropathic pain, the NoPain system biology and the German Research Foundation. He is also a consultant to Pfizer, Genzyme, Grunenthal, Mundipharma, Allergan, Sanofi Pasteur, Medtronic, Eisai, Lilly, Boehringer Ingleheim, Astellas, Novartis, Bristol Myers Squibb, Biogen Idec, AstraZeneca, Merck, AbbVie, Daiichi Sankyo and Glenmark Pharmaceuticals. He is also on the speakers’ bureau of Pfizer, Genzyme, Grunenthal, Mundipharma, Sanofi Pasteur, Medtronic, Eisai, Lilly, Boehringer Ingleheim, Astellas, Desitin, Teva, Bayer-Schering, and MSD. G.H. and G.M. have disclosed that they have no significant relationships with or financial interests in any commercial companies related to this study or article. G.C.-I. has disclosed that he is a consultant to Grunenthal. M.S. has disclosed that he is a consultant to Grunenthal and is on the speakers’ bureau of Grunenthal and Astellas.
CMRO peer reviewers on this manuscript have received an honorarium from CMRO for their review work, but have no relevant financial or other relationships to disclose.
Acknowledgement
The authors thank Derrick Garwood Ltd, Cambridge, UK, for editorial support, which was sponsored by Grünenthal GmbH, Aachen, Germany.