Comparison of gabapentin versus topiramate on clinically affected dogs with Chiari-like malformation and syringomyelia.

To date there is no evidence-based data for efficacious treatment of neuropathic pain in dogs with Chiari-like malformation (CM) and syringomyelia (SM). The objective of this prospective cross-over study was to compare the effect of gabapentin versus topiramate, as an add-on treatment to carprofen, on quality of life (QoL) of dogs experiencing signs of neuropathic pain due to CM/SM. A visual analogue scale (VAS) was used to assess the QoL: (1) on day 0; (2) after 1 week of carprofen only; (3) after 2 weeks on carprofen and gabapentin; and (4) after 2 weeks on carprofen and topiramate. No significant difference was observed between VAS after gabapentin or topiramate (P=0.91). However, an improvement in QoL was observed when gabapentin was compared with baseline (P=0.009), but not for topiramate. In conclusion, the addition of gabapentin was more effective in improving QoL than carprofen alone, but the study failed to identify that gabapentin was more efficacious than topiramate. Perhaps the more favourable side effect profile of the former makes it more suitable for the treatment of neuropathic pain associated with CM/SM but further placebo-controlled trials are required to assess the efficacy of these drugs.

Migraine-like episodic pain behavior in a dog: can dogs suffer from migraines?

Migraines and other primary headache disorders commonly affect people. There is evidence to suggest that migraines can occur in dogs. In this review, we present a dog with paroxysmal episodes that have a striking resemblance to human migraine, and we give an overview of migraine in people. The current classification, clinical signs, and diagnosis in people are discussed, as well as the anatomy of head pain, pathophysiology, pharmacology, and treatment options.

Long-term outcome of Cavalier King Charles spaniel dogs with clinical signs associated with Chiari-like malformation and syringomyelia.

The disease complex Chiari-like malformation (CM) and syringomyelia (SM) has been associated with the development of neuropathic pain (NeP), and commonly affects Cavalier King Charles spaniels (CKCS). This prospective cohort study followed 48 CKCSs with CM and/or SM and clinical signs suggestive of NeP for a period of 39 (±14.3) months from diagnosis. At the end of the study, 36 dogs were still alive; five dogs died of an unrelated or unknown cause, and seven were euthanased due to severe clinical signs suggestive of NeP. During the follow-up period, the clinical signs of scratching, facial rubbing behaviour, vocalisation and exercise ability were evaluated. Nine out of 48 dogs stopped scratching (P<0.001), but there was no statistically significant change in the number of dogs exhibiting exercise intolerance, vocalisation or facial rubbing behaviour. The overall severity of clinical signs based on a visual analogue scale (VAS) (0 mm: no clinical signs 100 mm: severe clinical signs) increased (from median 75 mm (interquartile ranges (IQR) 68-84) to 84 mm (IQR 71.5-91), P<0.001). A quarter of the dogs were static or improved. In general, the majority of the owners felt that the quality of life of their dogs was acceptable. Medical treatments received were gabapentin or pregabalin and/or intermittently, carprofen. The owner's perception of their animal's progress, and progress based on VAS, had strong positive correlation (Spearman's rank correlation (s(r)) 0.74, P<0.001). Overall, this study suggests that clinical signs suggestive of NeP progress in three-quarters of CKCSs with CM and/or SM.

Neuromyotonia in a dachshund with clinical and electrophysiological signs of spinocerebellar ataxia.

A 10-month-old dachshund was presented with a recent history of episodic muscle rippling and generalised stiffness. An uncoordinated gait was present since eight weeks of age. On presentation the dog showed cerebellar-like ataxia and poor menace responses. Myokymic contractions were visible in the appendicular and truncal muscles and neuromyotonic discharges were detected by electromyography. Central components of the brain auditory evoked potentials were absent and the onset latencies of the tibial sensory-evoked potentials recorded at the lumbar intervertebral level were delayed. Response to slow-release phenytoin was temporary. The clinical picture together with the electrophysiological findings in this dachshund are identical to the findings in Jack Russell terriers with hereditary ataxia and neuromyotonia. This is the first description of neuromyotonia associated with clinical and electrophysiological signs of spinocerebellar ataxia in a breed other than the Jack Russell terrier. This case also strengthens the theory that spinocerebellar ataxia and neuromyotonia are related. An ion channel dysfunction is presumed to link both disorders.