• Remigiusz Lecybyl, Juan Acosta, Joydeep Ghoshdastidar, Kinga Stringfellow, and Magdi Hanna.
• King's College London, Pain Clinical Research Hub, Denmark Hill Campus, London, UK.
• Bmc Neurol. 2010 Jan 1; 10: 5.

BackgroundSurrogate pain models have been extensively tested in Normal Human Volunteers (NHV). There are few studies that examined pain models in chronic pain patients. Patients are likely to have altered pain mechanisms. It is of interest to test patient pain responses to selective pain stimuli under controlled laboratory conditions.MethodsThe Institutional Ethic Committee approved the study. 16 patients with chronic neuropathic radiculopathy and 16 healthy volunteers were enrolled to the study after obtaining informed consent. During electrical stimulation (150 minutes for volunteers and 75 minutes for patients) the following parameters were measured every 10 minutes: Ongoing pain: Visual Analogue Scale (VAS) and Numeric Rate Scale (NRS)Allodynia (soft foam brush)Hyperalgesia (von Frey monofilament 20 g)Flare. For each endpoint, the area under the curve (AUC) was estimated from the start of stimulation to the end of stimulation by the trapezoidal rule. The individual AUC values for both periods were plotted to show the inter- and intra-subject variability. For each endpoint a mixed effect model was fitted with random effect subject and fixed effect visit. The estimate of intra-subject variance and the mean value were then used to estimate the sample size of a crossover study required to have a probability of 0.80 to detect a 25% change in the mean value. Analysis was done using GenStat 8th edition.ResultsEach endpoint achieved very good reproducibility for patients and NHV. Comparison between groups revealed trends towards: Faster habituation to painful stimuli in patients. Bigger areas of hyperalgesia in patients. Similar area of allodynia and flare (no statistical significance)ConclusionThe differences demonstrated between patients and NHVs suggest that the electrical stimulation device used here may stimulate pathways that are affected in the pathological state.

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