YHua, WQ and XC analysed the data and drafted the manuscript CL,

YHua, WQ and XC analysed the data and drafted the manuscript. CL, DZ and JH collected the data. YW, YHu and DX revised the manuscript. YHu and DX participated in administrative and technical support. Funding: This research received no specific grant from any funding agency in the public, commercial or not-for-profit sectors. Competing interests: None. Patient consent: http://www.selleckchem.com/products/CP-690550.html Obtained. Ethics approval: Health Authority Research Ethics Board of the First People’s Hospital of Shunde, Foshan, People’s Republic of China. Provenance and peer review: Not commissioned; externally peer reviewed. Data sharing statement: No additional data are available.
Postherpetic neuralgia (PHN) is

a syndrome characterised by pain persisting for more than

3 months following the resolution of herpes zoster.1–4 In addition, the clinical manifestations include allodynia, dysaesthesia and pruritus along the distribution of the involved dermatome. The incidence of PHN is 4/1000 per year, which further increases to 12/1000 among people aged over 80 years.5 The relevant risk factors for PHN include old age, female gender, greater severity of acute pain, greater rash severity, degree of sensory impairment, psychological distress, a painful prodrome, diabetes mellitus, nutritional deficiencies and diminished cell-mediated immunity.6–10 However, the most relevant risk factor is old age.11 12 It is uncommon in people aged under 50 years, but approximately 83% of PHN occurs in those aged above 50 years. 13 Owing to the persisting or intermittent spontaneous pain, PHN has a serious impact on the patients’ daily activities (eg, dressing, bathing, sleep), quality of life, general health, psychological health (eg, depression and difficulty with concentration), and social and economic well-being.14 15 Though the pathophysiology of PHN is poorly understood, postmortem studies in patients with PHN have found demyelination and axonal loss in peripheral nerves and sensory roots.16 Since PHN frequently resolves spontaneously

over time and the evaluation is unclear regarding the efficacy of treatments,17 18 pain reduction may be incorrectly attributed to current treatments for PHN. There are conventional treatments for PHN, such as tricyclic antidepressants Cilengitide (TCAs), antiepileptics, opioids, tramadol, lidocaine and capsaicin, which are probably effective to relieve some of the pain for a period of time. However, approximately 50% of patients may still not obtain satisfactory analgesia despite treatments with these medications.4 Moreover, being the first-line treatment suggested worldwide for PHN, TCAs and antiepileptics (gabapentin and pregabalin) still bring a high incidence of adverse events, including sedation, xerostomia, confusion, dysrhythmia, weight gain, dizziness, somnolence, fatigue and ataxia.

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