The clinical signs, clinicopathologic test results, portal pressure, and gross appearance of the liver of dogs with idiopathic noncirrhotic portal hypertension may be identical to those of dogs with cirrhosis; therefore liver biopsy is crucial. Because the prognosis for idiopathic noncirrhotic portal hypertension is generally favorable, owners of affected dogs should be discouraged from choosing euthanasia.

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Vagus nerve stimulation (VNS) is an effective adjunctive treatment for intractable epilepsy. However, the optimal range of device duty-cycles [on/(on + off times)] is poorly understood. The authors performed a multicenter, randomized trial of three unique modes of VNS, which varied primarily by duty-cycle. The results indicate that the three duty-cycles were equally effective. The data support the use of standard duty-cycles as initial therapy.

We describe 8 young dogs with congenital dilatation of the intra- and extrahepatic bile ducts and diffuse cystic kidney disease, compatible with Caroli's disease in humans. The dogs were referred between 1980 and 2000 because of chronic disease at an age of 6 months to 3 years. These dogs included 3 Collies, 2 Frisian Stabyhouns, 2 Jack Russell Terriers, and 1 mixed-breed dog. The most common signs were vomiting (6/6), polyuria and polydipsia (4/6), and anorexia (4/6). Ascites was a common finding (4/6). Clinicopathologic abnormalities were available for 6 dogs. All had increased plasma alkaline phosphatase activity and fasting bile acids: increased alanine aminotransferase activity and urea and creatinine concentrations were present in 50% of dogs. Ultrasound examination of the liver showed severely dilated bile ducts without evidence of obstruction, and calcification in all cases but 1. Postmortem examination revealed severe dilatation of the larger intra- and extrahepatic bile ducts. The common bile duct and gall bladder were normal, and the bile system was patent. The ducts contained a clear viscid fluid often with calcified material. Microscopically, marked portal fibrosis was present, often with abnormally structured dilated bile ducts lined with columnar or cuboid epithelium and regularly small calcifications. The lesion was complicated by ascending cholangitis in 1 dog. The kidneys showed marked cortical and medullary fibrosis with a diffuse radial cystic pattern; only slight renal fibrosis was found in the oldest dog. Seven dogs were euthanized without treatment; the oldest dog was alive and well 5 months after diagnosis and was maintained on a protein-restricted diet.

In this retrospective study, we describe 14 cats diagnosed with hepatic abscesses. The objective of the study was to report the clinical signs, physical examination findings, clinicopathologic findings, and outcomes in affected cats. These findings were then compared with those previously reported in dogs and humans. Clinical signs were vague and included anorexia, lethargy, and weight loss. Only 23% of cats had fever, whereas 31% were hypothermic. Increases in serum activities of alanine aminotransferase and alkaline phosphatase were found in 45 and 18%, respectively, of the 11 cats that had laboratory work performed. Abdominal ultrasound examinations were performed in 7 cats, and abnormalities were found in 71% of them. Four cats had solitary abscesses, all of which were located in the right liver lobes. The other 10 cats had multifocal small abscesses or microabscesses, and all of these cats had clinical signs suggestive of sepsis. Cytologic evaluation of samples obtained by abdominocentesis indicated septic inflammation in 67% of cats in which peritoneal fluid was analyzed. Hepatic abscess cultures yielded polymicrobial growth in 66% of the cats: Escherichia coli was the most commonly cultured organism. Overall mortality rate was 79%. All survivors underwent exploratory laparotomy for partial hepatectomy to resect the abscess followed by medical management. Hepatic abscesses should be considered in cats with signs consistent with sepsis. More routine use of ultrasonography may aid in earlier diagnosis of hepatic abscesses, potentially improving prognosis and outcome.

The problem o€ recurrent seizures is a common and challenging one in veterinary medical practice. The pathophysiology and pharmacologic suppression of focal seizure activity have been studied extensively in basic research settings, yet little is known of the genesis, modulation, and termination of generalized seizures, the most common form of seizures noted to occur in companion animals. Knowledge concerning the pharmacokinetic fate of anticonvulsant drugs currently used in veterinary medicine is adequate, though prospective clinical studies of the efficacy of these drugs in the treatment of various types of seizures are lacking. This study will review the available literature regarding the pharmacology, use, and side effects of anticonvulsant drugs currently available for control of recurrent seizures in companion animals. Alternative anticonvulsant drugs will also be described. (Journal of Veterinary Internal Medicine 1990; 4:26-39) Pathophysiology of Seizure Generation SEIZURES are the clinical manifestation of rapid, excessive electrical discharge of neurons in the brain. Seizures may be classified by site of origin as primary (idiopathic, genetic) or secondary (acquired, symptomatic). The term epilepsy refers to recurrent seizures of intracranial origin. How seizure activity is expressed clinically, whether as localized or geneFalized motor or nonmotor (psychic, autonomic) activity, may determine the group of anticonvulsant drugs that would be appropriate for therapy, especially in human patients.In the normal resting state, the electrical difference across neuronal cell membranes is maintained by an active sodium-potassium pump, the net effect of which results in a resting membrane potential ( R M P ) of -70mV.' Transmission of changes in the RMP along axons ultimately causes release of a neurotransmitter with either excitatory or inhibitory effects on a network of postsynaptic neurons that includes adjacent and distant cells. A collateral feedback system allows each neuron to also influence its own excitability. Excitability is mediated by energy-dependent influx of sodium into

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