Abstract
Canine neuropathic pain (NeuP) has been poorly investigated. This study aimed to evaluate the pain burden, sensory profile and inflammatory cytokines in dogs with naturally-occurring NeuP. Twenty-nine client-owned dogs with NeuP were included in a prospective, partially masked, randomized crossover clinical trial, and treated with gabapentin/placebo/gabapentin-meloxicam or gabapentin-meloxicam/placebo/gabapentin (each treatment block of 7 days; total 21 days). Pain scores, mechanical (MNT) and electrical (ENT) nociceptive thresholds and descending noxious inhibitory controls (DNIC) were assessed at baseline, days 7, 14, and 21. DNIC was evaluated using ΔMNT (after-before conditioning stimulus). Positive or negative ΔMNT corresponded to inhibitory or facilitatory pain profiles, respectively. Pain scores were recorded using the Client Specific Outcome Measures (CSOM), Canine Brief Pain Inventory (CBPI), and short-form Glasgow Composite Measure Pain Scale (CMPS-SF). Data from baseline were compared to those of sixteen healthy controls. ΔMNT, but not MNT and ENT, was significantly larger in controls (2.3 ± 0.9 N) than in NeuP (-0.2 ± 0.7 N). The percentage of dogs with facilitatory sensory profile was similar at baseline and after placebo (61.5-63%), and between controls and after gabapentin (33.3-34.6%). The CBPI scores were significantly different between gabapentin (CBPI pain and CBPI overall impression) and/or gabapentin-meloxicam (CBPI pain and interference) when compared with baseline, but not placebo. The CBPI scores were not significantly different between placebo and baseline. The concentration of cytokines was not different between groups or treatments. Dogs with NeuP have deficient inhibitory pain mechanisms. Pain burden was reduced after gabapentin and/or gabapentin-meloxicam when compared with baseline using CBPI and CMPS-SF scores. However, these scores were not superior than placebo, nor placebo was superior to baseline evaluations. A caregiver placebo effect may have biased the results.
Highlights
Neuropathic pain (NeuP) is caused by a lesion or disease of the somatosensory system [1]
Its diagnosis relies on sensory examination of nerve fibers involved in nociception/proprioception for both loss and gain of function via quantitative sensory testing (QST) [2]
Dogs with NeuP were older than controls (P = .021) but there was no difference for body weight (P = .36)
Summary
Neuropathic pain (NeuP) is caused by a lesion or disease of the somatosensory system [1]. QST is a psychophysical method that evaluates the somatosensory function from receptor to cortex using calibrated innocuous or noxious stimuli It offers useful insight into the underlying pain mechanisms and the characterization of painful conditions [3]. Changes in QST before and after the application of a conditioning stimulus provide useful information about the diffuse noxious inhibitory control (DNIC) as a representation of central descending modulatory pain mechanisms. The latter could predict people’s response to drugs acting on central pain modulation [6]. It has been proposed that inflammatory cytokines play a role in the development and maintenance of NeuP and could be an avenue for future therapeutic options [7]
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