排序方式： 共有54条查询结果，搜索用时 46 毫秒
1.
M. Podell H.A. Volk M. Berendt W. Löscher K. Muñana E.E. Patterson S.R. Platt 《Journal of veterinary internal medicine / American College of Veterinary Internal Medicine》2016,30(2):477-490
This report represents a scientific and working clinical consensus statement on seizure management in dogs based on current literature and clinical expertise. The goal was to establish guidelines for a predetermined, concise, and logical sequential approach to chronic seizure management starting with seizure identification and diagnosis (not included in this report), reviewing decision‐making, treatment strategies, focusing on issues related to chronic antiepileptic drug treatment response and monitoring, and guidelines to enhance patient response and quality of life. Ultimately, we hope to provide a foundation for ongoing and future clinical epilepsy research in veterinary medicine. 相似文献
2.
3.
Fatzer R Gandini G Jaggy A Doherr M Vandevelde M 《Journal of veterinary internal medicine / American College of Veterinary Internal Medicine》2000,14(1):100-104
The clinical records of 38 cats (1985-1995) with a neuropathologically confirmed diagnosis of necrosis of the hippocampus and occasionally the lobus piriformis were evaluated retrospectively. There was no sex or breed predisposition. Most cats were between 1 and 6 years of age (mean age 35 months) and had either generalized or complex-partial seizures of acute onset and rapid progression. The seizures had a tendency to become recurrent and to present as clusters or even status epilepticus later in the course of the disease. Fourteen cats died spontaneously, and 24 were euthanized. Histopathologic examination revealed bilateral lesions restricted to the hippocampus and occasionally the lobus piriformis. The lesions seemed to reflect different stages of the disease and consisted of acute neuronal degeneration to complete malacia, affecting mainly the layer of the large pyramidal cells but sometimes also the neurons of the dentate gyrus and the piriform lobe. The clinical, neuropathologic, and epidemiologic findings suggest that the seizures in these cats were triggered by primary structural brain damage, perhaps resulting from excitotoxicity. The cause remains unknown, but epidemiologic analysis suggests an environmental factor, probably a toxin. 相似文献
4.
Thyroid function and serum hepatic enzyme activity in dogs after phenobarbital administration 总被引：2，自引：0，他引：2
Gieger TL Hosgood G Taboada J Wolfsheimer KJ Mueller PB 《Journal of veterinary internal medicine / American College of Veterinary Internal Medicine》2000,14(3):277-281
Phenobarbital is the drug of choice for control of canine epilepsy. Phenobarbital induces hepatic enzyme activity, can be hepatotoxic, and decreases serum thyroxine (T4) concentrations in some dogs. The duration of liver enzyme induction and T4 concentration decreases after discontinuation of phenobarbital is unknown. The purpose of this study was to characterize the changes in serum total T4 (TT4), free T4 (FT4), thyroid-stimulating hormone (TSH), cholesterol and albumin concentrations, and activities in serum of alanine aminotransferase (ALT), alkaline phosphatase (ALP), and gamma-glutamyl transferase (GGT) after discontinuation of long-term phenobarbital administration in normal dogs. Twelve normal dogs were administered phenobarbital at a dosage of approximately 4.4-6.6 mg/kg PO q12h for 27 weeks. Blood was collected for analysis before and after 27 weeks of phenobarbital administration and then weekly for 10 weeks after discontinuation of the drug. The dogs were clinically normal throughout the study period. Serum ALT and ALP activity and TSH and cholesterol concentrations were significantly higher than baseline at week 27. Serum T4 and FT4 were significantly lower. Serum albumin and GGT were not changed from baseline at week 27. Changes in estimate of thyroid function (TT4, FT4, TSH) persisted for 1-4 weeks after discontinuation of phenobarbital, whereas changes in hepatic enzyme activity (ALT, ALP) and cholesterol concentration resolved in 3-5 weeks. To avoid false positive results, it is recommended that thyroid testing be performed at least 4 weeks after discontinuation of phenobarbital administration. Elevated serum activity of hepatic enzymes 6-8 weeks after discontinuation of phenobarbital may indicate hepatic disease. 相似文献
5.
ZHAO Shuang KANG Yu-ming ZHANG Sheng-chang WANG Shu-qiu WANG Shao-qing MA Xiao-ru ZHANG Ting 《园艺学报》2007,23(6):1153-1156
AIM: To investigate the effect of Ganoderma lucidum spores powder on the expression of insulin-like growth factor-1 (IGF-1), nuclear factor-κB (NF-κB) and apoptosis of nerve cells in rats with epilepsy established by pentetrazole. METHODS: The sub-eclampsia dosage of pentetrazole (PTZ) was used to make epilepsy model. Ganoderma lucidum spores powder group was given from stomach. The enduring time and latent period were recorded. The immune reactivity of IGF-1, NF-κB/P65 and apoptosis of nerve cells were measured with immunohistochemical staining and TUNEL method. RESULTS: In high power sight (×400), there were much more apoptosis cells in hippocampus and brain cortex of model group (18.80±2.13, 16.87±2.00) than those in control group (0.97±0.52, 0.58±0.25). The expressions of IGF-1, NF-κB in model group were higher than those in control group. Compared with model group, the latent period of Ganoderma lucidum spores powder group at the 17th, 21th, 25th days were longer (P<0.05, P<0.05, P<0.01, respectively).There were less apoptosis cells in hippocampus and brain cortex of Ganoderma lucidum spores powder group (12.30±2.46, 10.48±1.33) than those in model group. The expression of NF-κB/P65 in Ganoderma lucidum spores powder group was lower than that in model group, but the immune reactivity of IGF-1 increased more distinctly in Ganoderma lucidum spores powder group than that in model group. CONCLUSION: IGF-1, NF-κB and apoptosis of nerve cells may have play a role in occurrence and development of PTZ-induced epilepsy. Ganoderma lucidum spores powder can suppress expression of NF-κB strongly, and facilitate the immune reactivity of IGF-1, which may be one of the mechanisms by which Ganoderma lucidum spores powder restrains the apoptosis of nerve cells caused by epilepsy to prevent the damages of nerve cells. 相似文献
6.
Behavioral Abnormalities in Lagotto Romagnolo Dogs with a History of Benign Familial Juvenile Epilepsy: A Long‐Term Follow‐Up Study 
下载免费PDF全文
下载免费PDF全文 T.S. Jokinen K. Tiira L. Metsähonkala E.H. Seppälä A. Hielm‐Björkman H. Lohi O. Laitinen‐Vapaavuori 《Journal of veterinary internal medicine / American College of Veterinary Internal Medicine》2015,29(4):1081-1087
Background
Lagotto Romagnolo (LR) dogs with benign juvenile epilepsy syndrome often experience spontaneous remission of seizures. The long‐term outcome in these dogs currently is unknown. In humans, behavioral and psychiatric comorbidities have been reported in pediatric and adult‐onset epilepsies.Hypothesis/Objectives
The objectives of this study were to investigate possible neurobehavioral comorbidities in LR with a history of benign familial juvenile epilepsy (BFJE) and to assess the occurrence of seizures after the remission of seizures in puppyhood.Animals
A total of 25 LR with a history of BFJE and 91 control dogs of the same breed.Methods
Owners of the LR dogs in the BFJE and control groups completed an online questionnaire about each dog''s activity, impulsivity, and inattention. Principal component analysis (PCA) served to extract behavioral factors from the data. We then compared the scores of these factors between the 2 groups in a retrospective case–control study. We also interviewed all dog owners in the BFJE group by telephone to inquire specifically about possible seizures or other neurological problems after remission of seizures as a puppy.Results
Lagotto Romagnolo dogs with BFJE showed significantly higher scores on the factors Inattention and Excitability/Impulsivity than did the control group (P = .003; P = .021, respectively). Only 1 of the 25 BFJE LR exhibited seizures after remission of epilepsy in puppyhood.Conclusions and Clinical Importance
Although the long‐term seizure outcome in BFJE LR seems to be good, the dogs exhibit behavioral abnormalities resembling attention deficit hyperactivity disorder (ADHD) in humans, thus suggesting neurobehavioral comorbidities with epilepsy. 相似文献7.
8.
AIM: To study the role of gap junction(GJ) in the pathogenesis of epilepsy. METHODS: The expression of connexin(Cx) 32 and Cx43 was evaluated in penlylenetetrazol(PTZ)-induced epilepsy rats at different time points with immunohistochemistry and real-time RT-PCR. The uncoupler of gap junction,carbenoxolone (CBX), and anti-epilepsy drug,carbamazepine (CBZ), were introduced to investigate the role of gap junction in epilepsy. RESULTS: The expression of Cx32 in the cortex and hippocampus of rats increased 2 h after PTZ administration, and was more obvious 8 h later, so was the expression of Cx43. CBX not only notably inhibited the expression of Cx32 and Cx43, but also suppressed the seizures. CBZ had no obvious effect on Cx32/43 expression. Real-time RT-PCR examination showed that the level of Cx32 mRNA went up rapidly 2 h after seizures, and began to decrease 10 h later. The level of Cx43 mRNA in PTZ group was higher than that in control group from 2 h to 5 h. CBX inhibited both the seizures and the increase in the mRNA expression of Cx32/43, while CBZ only suppressed the seizures and did not affect the expression of Cx32/43. CONCLUSION: GJ between neurons is reinforced after epileptic activities and takes part in the pathophysiological mechanism of synchronization and epilepsy. CBZ has no effect on the expression of Cx32 and Cx43, indicating that the anti-epileptic mechanism of CBZ is independent of GJ. 相似文献
9.
10.
Recent studies show that epileptic seizures result in mass free radical production and induce oxidative damage because of relative deficiency in anti-oxygen system. Mitochondrium is crucial to sustaining energy metabolism, regulating cell death, synthesising neurotransmitter and oxidating fatty acid. Mitochondrium is not only the place for free radical production, but also the target of oxidative damage. Mitochondrial oxidative stress and resultant dysfunction enhance epileptic susceptibility. Seizure-induced free radical can influence energy metabolism, destroy DNA construction and induce apoptosis in neurontoxic consequences in epilepsy. 相似文献