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Background: The tick-borne bacteria Borrelia burgdorferi sensu lato (sl) and Anaplasma phagocytophilum have been suspected to cause neurological signs in dogs. Diagnosis often has been made based on positive antibody titers in serum of dogs with neurological signs, but a high seroprevalence in dogs in at-risk populations makes diagnosis difficult., Objective: To determine if the neurological signs in dogs examined were caused by any of these bacteria., Animals: Fifty-four dogs presented to a board-certified neurologist., Methods: Prospective study. We divided dogs into 2 groups: those with inflammatory diseases of the central nervous system (CNS) and those with neurological signs from other diseases. Blood and cerebrospinal fluid (CSF) from all dogs were analyzed., Results: Dogs with inflammatory CNS diseases showed no serum antibodies against any of the agents. Among dogs with neurological signs from other diseases, 10.3% had serum antibodies for B. burgdorferi sl and 20.5% for A. phagocytophilum. All blood samples analyzed for bacterial deoxyribonucleic acid (DNA) and all CSF analyzed for antibodies and bacterial DNA for the 2 agents were negative., Conclusions and Clinical Importance: Based on this study, these bacteria are unlikely causes of neurologic disease in dogs and the presence of serum antibodies alone does not document or establish a definitive diagnosis of CNS disease caused by these organisms. Dogs that have neurologic disease and corresponding serum antibodies against these agents should have additional tests performed to assess for other potential etiologies of the signs.

A retrospective cohort study was carried out to evaluate whether seropositivity for the tick-transmitted bacterial species Borrelia burgdorferi sensu lato and/or Anaplasma phagocytophilum was associated with one or more specific categories of nervous system disorders in dogs. A total of 248 dogs with nervous system disorders were serotested for these agents and categorised into six main diagnostic categories: degenerative diseases of the spine, epilepsy, inflammatory diseases, neoplasia, peripheral neuropathies, and other diseases. Multivariable analysis using logistic regression was used to model whether a dog was diagnosed as being in any of these categories. The independent variables included were sex, age, year of serological testing, and whether the animal tested positive for B burgdorferi sensu lato and/or A phagocytophilum. In one model, a statistically significant association was found between a positive titre for A phagocytophilum and the risk of a dog developing neoplastic disease. Although statistically significant, it was concluded that the association was not of clinical relevance.

Injury to a sensory nerve often results in a clinically poor long term outcome, possibly as a result of the extensive loss of neurons within the dorsal root ganglia (DRG), which has been shown in several experimental studies. This loss is possibly caused by interruption of the sensory input and axonal transport in the damaged afferent nerve. To investigate the importance of sensory afferent input into a nerve a pulsed electric stimulation was applied on the proximal part of the superficial radial nerve after transsection and microsurgical repair. The purpose was to simulate nerve impulses and thereby mask the severity of the injury. To test this hypothesis a pilot study was undertaken in eight cats. The neuronal tracer showed that the median neuronal loss was 38% of the neurons of the dorsal root ganglia that received afferents from the nerve investigated, which corresponds to the figure in a previous study in which electric stimulation was not used. Artificial sensory stimulation during regeneration in a transsected and repaired peripheral nerve therefore does not seem to reduce neuronal loss.