Epileptic 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.

The purpose of the current review is to summarize data regarding hereditary myelopathies in dogs. Canine degenerative myelopathy (DM) is a progressive disease prevalent in senior (≥8 years old), large breed-dogs, predominating in German shepherd dog. Neurolocalization indicates a thoracolumbar, upper motor neuron, lesion; it can progress to the thoracic limbs and later to lower motor neurons of all limbs resembling human amyotrophic lateral sclerosis (ALS). Tentative diagnosis is based on ruling out other progressive myelopathies. Clinical similarities between ALS and DM made superoxide dismutase 1 gene (SOD1) a viable candidate gene as an etiopathogenic factor. Α E40K missense mutation of the SOD1 has been linked to DM. A genetic test for DM exists, which will aid breeding programs to eliminate the disease. Exercise and physiotherapy are important to slow the progression of DM. Long-term prognosis is poor as dogs become non-ambulatory within 4-6 months from the time of diagnosis. Dystrophic myelopathies include Afgan hound myelopathy/hereditary necrotizing myelopathy in Kooikerhondje dogs, leukoencephalomyelopathy and neuroaxonal dystrophy in Rottweilers and spongiform leukoencephalomyelopathy. A similar myelopathy is Jack Russell and Fox terrier hereditary ataxia. Their etiology is suspected to be hereditary and they appear at a young age. They are diagnosed solely postmortem with histopathological examination. There is no etiologic treatment and the prognosis is poor except for Rottweiler neuroaxonal dystrophy and Jack Russel ataxia due to the extremely slow progression of symptoms. Syringomyelia is characterized by the formation of fluid filled cavities within the spinal cord and outside the central canal that may communicate with the central canal and it is caused mainly due to Chari-like malformation (CLM). The most important clinical sign is neuropathic pain and is localized in the cervical region of the spinal cord. Progression of the disease varies, there are severe disabilities due to pain or it can be an incidental finding. CT and MRI are the preferable ways to detect the lesions. For CLM, therapy includes surgical and medical management. Drugs can be divided into analgesics (non-steroidal anti-inflammatory, gabapentin, pregabalin, tramadol), drugs reducing cerebrospinal fluid (CSF) production (omeprazole, acetazolamide, furosemide) and corticosteroids. Medical therapy diminishes the severity of clinical signs but never succeeds full resolution.