Dogs with epilepsy are among the commonest neurological patients in veterinary practice and therefore have historically attracted much attention with regard to definitions, clinical approach and management. A number of classification proposals for canine epilepsy have been published during the years reflecting always in parts the current proposals coming from the human epilepsy organisation the International League Against Epilepsy (ILAE). It has however not been possible to gain agreed consensus, “a common language”, for the classification and terminology used between veterinary and human neurologists and neuroscientists, practitioners, neuropharmacologists and neuropathologists. This has led to an unfortunate situation where different veterinary publications and textbook chapters on epilepsy merely reflect individual author preferences with respect to terminology, which can be confusing to the readers and influence the definition and diagnosis of epilepsy in first line practice and research studies.In this document the International Veterinary Epilepsy Task Force (IVETF) discusses current understanding of canine epilepsy and presents our 2015 proposal for terminology and classification of epilepsy and epileptic seizures. We propose a classification system which reflects new thoughts from the human ILAE but also roots in former well accepted terminology. We think that this classification system can be used by all stakeholders.

This article outlines the consensus proposal on diagnosis of epilepsy in dogs by the International Veterinary Epilepsy Task Force. The aim of this consensus proposal is to improve consistency in the diagnosis of epilepsy in the clinical and research settings. The diagnostic approach to the patient presenting with a history of suspected epileptic seizures incorporates two fundamental steps: to establish if the events the animal is demonstrating truly represent epileptic seizures and if so, to identify their underlying cause. Differentiation of epileptic seizures from other non-epileptic episodic paroxysmal events can be challenging. Criteria that can be used to make this differentiation are presented in detail and discussed. Criteria for the diagnosis of idiopathic epilepsy (IE) are described in a three-tier system. Tier I confidence level for the diagnosis of IE is based on a history of two or more unprovoked epileptic seizures occurring at least 24 h apart, age at epileptic seizure onset of between six months and six years, unremarkable inter-ictal physical and neurological examination, and no significant abnormalities on minimum data base blood tests and urinalysis. Tier II confidence level for the diagnosis of IE is based on the factors listed in tier I and unremarkable fasting and post-prandial bile acids, magnetic resonance imaging (MRI) of the brain (based on an epilepsy-specific brain MRI protocol) and cerebrospinal fluid (CSF) analysis. Tier III confidence level for the diagnosis of IE is based on the factors listed in tier I and II and identification of electroencephalographic abnormalities characteristic for seizure disorders. The authors recommend performing MRI of the brain and routine CSF analysis, after exclusion of reactive seizures, in dogs with age at epileptic seizure onset <6 months or >6 years, inter-ictal neurological abnormalities consistent with intracranial neurolocalisation, status epilepticus or cluster seizure at epileptic seizure onset, or a previous presumptive diagnosis of IE and drug-resistance with a single antiepileptic drug titrated to the highest tolerable dose.This consensus article represents the basis for a more standardised diagnostic approach to the seizure patient. These recommendations will evolve over time with advances in neuroimaging, electroencephalography, and molecular genetics of canine epilepsy.Electronic supplementary materialThe online version of this article (doi:10.1186/s12917-015-0462-1) contains supplementary material, which is available to authorized users.

In Europe, the number of antiepileptic drugs (AEDs) licensed for dogs has grown considerably over the last years. Nevertheless, the same questions remain, which include, 1) when to start treatment, 2) which drug is best used initially, 3) which adjunctive AED can be advised if treatment with the initial drug is unsatisfactory, and 4) when treatment changes should be considered. In this consensus proposal, an overview is given on the aim of AED treatment, when to start long-term treatment in canine epilepsy and which veterinary AEDs are currently in use for dogs. The consensus proposal for drug treatment protocols, 1) is based on current published evidence-based literature, 2) considers the current legal framework of the cascade regulation for the prescription of veterinary drugs in Europe, and 3) reflects the authors’ experience. With this paper it is aimed to provide a consensus for the management of canine idiopathic epilepsy. Furthermore, for the management of structural epilepsy AEDs are inevitable in addition to treating the underlying cause, if possible.

The medical records of 220 dogs with inflammatory/infectious diseases of the central nervous system (CNS) were retrospectively examined. The aims of the study were to determine if clinical and clinicopathologic data (not including biopsy or necropsy examination) could distinguish inflammatory CNS diseases from diseases of other types, and to search for criteria allowing differentiation of specific inflammatory diseases. The signalment, historical findings, extraneural and neurological signs, and the lesion site contributed marginally to a specific diagnosis. Multifocal signs were only noticed in one third of the dogs with inflamrnatory/infectious diseases. Particular neurological abnormalities were more frequent in certain diseases than in others (eg, myoclonus was frequent in dogs with distemnflammatory and infectious diseases of the central ner-I vous system (CNS) are an important group of disorders in all animal species. They usually cause severe neurological impairment, often resulting in the death of the animal and/ or massive economic losses. In addition, several of these diseases are zoonoses.Over distinguishing the cause of meningoencephalomyelitides remains a diagnostic and therapeutic challenge for the clinician.Review articles on meningoencephalomyelitis in dogs have compiled and summarized the available clinical information on this subject.8" ' Surprisingly, very few attempts2' have been made to evaluate how well inflammatory lesions of the CNS can be differentiated from each other on the basis of clinical and clinicopathologic data.In the present study, the medical records of 220 dogs with inflammatory/infectious diseases of the CNS were evaluated retrospectively. The aims of this study were to determine if inflammatory/infectious lesions can be distinguished as a group from other lesions and to search for criteria that would be helpful for recognizing specific inflammatory diseases.

Steroid responsive meningitis‐arteriitis (SRMA) is an immunemediated disorder commonly recognised in dogs in small animal practice. Two different forms of SRMA may occur. The typical, acute form of SRMA is characterised by cervical rigidity, pain, pyrexia and a polymorphonuclear pleocytosis of the cerebrospinal fluid (CSF). In a less common, chronic form of SRMA, additional neurological deficits consistent with a spinal cord or a multi‐focal neurological disorder may be present, often accompanied by a mononuclear CSF pleocytosis. The prognosis for young dogs in the acute stage of SRMA is relatively good with early and aggressive anti‐inflammatory or immunosuppressive therapy. In more protracted, relapsing cases of SRMA the prognosis is guarded, and therapy requires more aggressive, long term immunosuppression. The complete etiopathogenesis of SRMA is unknown; however, an aberrant immune response directed against the central nervous system (CNS) is most likely. Neutrophilic pleocytosis in SRMA seems to be facilitated by chemotactic factors in the CSF and upregulation of integrins and metalloproteinases that disrupt the blood brain barrier. Upregulation of IgA, induced by a Th2 immune response, also plays a central role in the pathogenesis of SRMA.