Feline Epilepsy: An update

ΔΕΝ ΔΙΑΤΙΘΕΤΑΙ ΠΕΡΙΛΗΨΗEpileptic seizures are the most common neurological disorder in the clinical setting. Their etiology is multifactorial and is mainly divided into structural, reactive and idiopathic epilepsy. Structural epilepsy can be caused by vascular events, inflammatory conditions (encephalitis), traumatic injuries, neoplasia, congenital and inherited (degenerative) disorders. Reactive epilepsy is caused by exposure in toxins or metabolic derangements. Although idiopathic epilepsy was thought to be rare in cats, it is now established as a common cause. Epileptic seizures in cats appear with various clinical presentations including generalized, focal with or without secondary generalization epileptic seizures. Diagnostic investigation is crucial in order to establish final diagnosis and to determine the therapeutic plan. Diagnostics include physical and neurological examination with detailed history (drug or toxin exposure), routine hematology (CBC, biochemistry, urinalysis), specific laboratory tests if concurrent or metabolic disease are suspected, advanced diagnostic imaging (CT/MRI) whether intracranial disease is suspected and cerebrospinal fluid (CSF) analysis. Most commonly used antiepileptic drugs (AED) in cats are phenobarbital and levetiracetam. Bromide is contraindicated in cats due to severe respiratory disease caused as an adverse life-threatening reaction. Diazepam is an emergency AED used to eliminate cluster seizures or status epilepticus but it should be avoided as a long-term medication because it has been associated with fatal hepatotoxicity. Gabapentin in another potential antiepileptic drug however its longterm efficacy has to be evaluated. Prognosis depends on the underlying etiology and treatment response. In most cats quality of life is improved and (>50% reduction of epileptic seizures) regardless of etiology. The complete remission of epileptic seizures in cats is rare and most cats should be maintained on anti-epileptic therapy

Relation of clinical signs to pathological changes in 19 cases of canine distemper encephalomyelitis

In an attempt to associate the clinical neurological syndromes with the neuropathological features of canine distemper (CD), 19 spontaneous cases with neurological involvement were examined, before and after euthanasia. Seventeen dogs were less than one year of age and all except two (89.4%) were unvaccinated against CD. Various extrancural signs associated with CD encephalomyelitis (CDE) were seen in 15 dogs. Generalized or localized myoclonus was the most common sign observed (13/19). Seventeen or the dogs presented with signs suggestive of one neuroanatomical location of lesions. Of these animals, seven had signs of cerebral, two of cerebellar, four of cervical, one of cervicothoracic, two of thoracolumbar and two of lumbosacral syndrome. The diagnosis of CD was confirmed immunohistochemically (detection of CD viral antigen), serologically (neutralizing serum antibody titre greater than or equal to16) and histopathologicaliy (CDV inclusion bodies, type of central nervous system lesions). An association of the neuroanatomical lesion location and the histopathological findings was noted in 14 out of 17 dogs (82.3%). Myoclonus could be attributed in lower motor neuron damage in eight out of 13 dogs (61.5%). (C) 2002 Harcourt Publishers Ltd