@article{schwartz_munana_nettifee-osborne_2013, title={Assessment of the prevalence and clinical features of cryptogenic epilepsy in dogs: 45 cases (2003-2011)}, volume={242}, ISSN={["1943-569X"]}, url={http://www.scopus.com/inward/record.url?eid=2-s2.0-84873910001&partnerID=MN8TOARS}, DOI={10.2460/javma.242.5.651}, abstractNote={Abstract Objective—To determine the prevalence and clinical features of cryptogenic epilepsy among dogs. Design—Retrospective case series. Animals—214 client-owned dogs with onset of epileptic seizures at ≥ 7 years of age. Procedures—A diagnostic imaging database was searched for dogs with symptomatic or cryptogenic epilepsy. Signalment, seizure history, and diagnostic information were recorded. Information regarding seizure frequency, administration of antiepileptic drugs (AEDs), owners' perceptions regarding quality of life, survival times, and causes of death for dogs with cryptogenic epilepsy was obtained via questionnaire. Variables were compared among dogs grouped according to diagnosis and age. Results—45 (21%) dogs had a diagnosis of cryptogenic epilepsy, and 169 (79%) had symptomatic epilepsy. In dogs 7 to 9 years and ≥ 10 years of age at the time of seizure onset, 31 of 106 (29%) and 14 of 108 (13%), respectively, had a diagnosis of cryptogenic epilepsy. At last follow-up, most (40 [89%]) dogs with cryptogenic epilepsy were receiving ≥ 1 AED. Thirty-one of 37 (84%) dogs typically had ≤ 1 seizure/mo following hospital discharge. Death was confirmed in 20 (44%) dogs with cryptogenic epilepsy and was related to seizures or AEDs in 7 Median survival time from onset of seizures was 52 months for all dogs with cryptogenic epilepsy. Median quality-of-life score (scale, 1 [poor] to 10 [excellent]) indicated by 34 owners of dogs with cryptogenic epilepsy was 10 before diagnosis and initiation of AED treatment and 8 afterward. Conclusions and Clinical Relevance—Cryptogenic epilepsy was diagnosed in a substantial proportion of dogs with an onset of epileptic seizures at ≥ 7 years of age. Seizure control was considered acceptable in most dogs.}, number={5}, journal={JAVMA-JOURNAL OF THE AMERICAN VETERINARY MEDICAL ASSOCIATION}, author={Schwartz, Malte and Munana, Karen R. and Nettifee-Osborne, Julie}, year={2013}, month={Mar}, pages={651–657} } @article{schwartz_munana_nettifee-osborne_messenger_papich_2013, title={The pharmacokinetics of midazolam after intravenous, intramuscular, and rectal administration in healthy dogs}, volume={36}, ISSN={["0140-7783"]}, url={http://www.scopus.com/inward/record.url?eid=2-s2.0-84883647308&partnerID=MN8TOARS}, DOI={10.1111/jvp.12032}, abstractNote={Intravenous benzodiazepines are utilized as first‐line drugs to treat prolonged epileptic seizures in dogs and alternative routes of administration are required when venous access is limited. This study compared the pharmacokinetics of midazolam after intravenous (IV), intramuscular (IM), and rectal (PR) administration. Six healthy dogs were administered 0.2 mg/kg midazolam IV, IM, or PR in a randomized, 3‐way crossover design with a 3‐day washout between study periods. Blood samples were collected at baseline and at predetermined intervals until 480 min after administration. Plasma midazolam concentrations were measured by high‐pressure liquid chromatography with UV detection. Rectal administration resulted in erratic systemic availability with undetectable to low plasma concentrations. Arithmetic mean values ± SD for midazolam peak plasma concentrations were 0.86 ± 0.36 μg/mL (C0) and 0.20 ± 0.06 μg/mL (Cmax), following IV and IM administration, respectively. Time to peak concentration (Tmax) after IM administration was 7.8 ± 2.4 min with a bioavailability of 50 ± 16%. Findings suggest that IM midazolam might be useful in treating seizures in dogs when venous access is unavailable, but higher doses may be needed to account for intermediate bioavailability. Rectal administration is likely of limited efficacy for treating seizures in dogs.}, number={5}, journal={JOURNAL OF VETERINARY PHARMACOLOGY AND THERAPEUTICS}, author={Schwartz, M. and Munana, K. R. and Nettifee-Osborne, J. A. and Messenger, K. M. and Papich, M. G.}, year={2013}, month={Oct}, pages={471–477} } @article{schwartz_munana_olby_2011, title={Possible Drug-Induced Hepatopathy in a Dog Receiving Zonisamide Monotherapy for Treatment of Cryptogenic Epilepsy}, volume={73}, ISSN={["0916-7250"]}, url={http://www.scopus.com/inward/record.url?eid=2-s2.0-82955171529&partnerID=MN8TOARS}, DOI={10.1292/jvms.11-0164}, abstractNote={A 9-year old female spayed Rottweiler was diagnosed with cryptogenic epilepsy and started on zonisamide monotherapy (8.3 mg/kg, PO, q 12 hr). Three weeks after the 1st dose of zonisamide the dog presented for vomiting, inappetence and icterus. Serum biochemistry showed marked elevation of liver enzymes, consistent with hepatocellular damage and cholestasis. No underlying cause for liver disease was identified and a drug-induced hepatopathy was suspected. Zonisamide was discontinued and replaced by potassium bromide. Supportive therapy consisted of intravenous fluids, antiemetics, antibiotics and hepatoprotectants. The dog made a complete recovery and serial serum biochemical examinations showed complete normalisation of liver parameters 8 weeks after discontinuation of zonisamide. Based on a human Drug-induced Liver Injury Diagnostic Scale, the likelihood for zonisamide-induced hepatopathy was classified as "possible". Veterinary practitioners and owners should be educated about the potential for an idiosyncratic drug reaction to zonisamide. If signs of hepatotoxicity are recognised early and zonisamide is discontinued, complete recovery is possible.}, number={11}, journal={JOURNAL OF VETERINARY MEDICAL SCIENCE}, author={Schwartz, Malte and Munana, Karen R. and Olby, Natasha J.}, year={2011}, month={Nov}, pages={1505–1508} }