Magnetic resonance imaging (MRI) examinations from 18 dogs with a histologically confirmed peripheral nerve sheath tumor (PNST) of the brachial plexus were assessed retrospectively. Almost half (8/18) had a diffuse thickening of the brachial plexus nerve(s), six of which extended into the vertebral canal. The other 10/18 dogs had a nodule or mass in the axilla (1.2-338 cm3). Seven of those 10 masses also had diffuse nerve sheath thickening, three of which extended into the vertebral canal. The majority of tumors were hyperintense to muscle on T2-weighted images and isointense on T1-weighted images. Eight of 18 PNSTs had only minimal to mild contrast enhancement and many (13/18) enhanced heterogeneously following gadolinium DTPA administration. Transverse plane images with a large enough field of view (FOV) to include both axillae and the vertebral canal were essential, allowing in-slice comparison to detect lesions by asymmetry of structures. Higher resolution, smaller FOV, multiplanar examination of the cervicothoracic spine was important for appreciating nerve root and foraminal involvement. Short tau inversion recovery, T2-weighted, pre and postcontrast T1-weighted pulse sequences were all useful. Contrast enhancement was critical to detecting subtle diffuse nerve sheath involvement or small isointense nodules, and for accurately identifying the full extent of disease. Some canine brachial plexus tumors can be challenging to detect, requiring a rigorous multiplanar multi-pulse sequence MRI examination.

Long-term administration of phenobarbital has been reported to cause hepatic injury in dogs. Phenobarbital induces hepatic enzymes, and it may be difficult to distinguish the effect of enzyme induction on serum liver enzyme activities from actual hepatic damage. The hepatotoxicity of phenobarbital and the impact of enzyme induction on serum liver enzyme activity were investigated prospectively in 12 normal dogs. Phenobarbital was administered for 29 weeks at 5 mg per kilogram of body weight (range, 4.8-6.6 mg/kg) PO q12h, resulting in therapeutic serum phenobarbital concentrations (20-40 microg/mL). Serum alkaline phosphatase (ALP), alanine transaminase (ALT), aspartate transaminase (AST), gamma-glutamyltransferase (GGT), fasted bile acids (fBA), total bilirubin, and albumin were determined before and during treatment. Lateral abdominal radiographs, abdominal ultrasounds, and histopathologic examinations of liver tissue obtained by ultrasound-guided biopsy were performed before and during treatment. Radiographs revealed a moderate increase in liver size in most dogs. Ultrasonographic examination revealed no change in liver echogenicity or architecture. No evidence of morphologic liver damage was observed histopathologically. ALP and ALT increased significantly (P < .05), GGT increased transiently, and albumin decreased transiently during the study. There were no significant changes in AST, bilirubin, and fBA. These results suggest that increases in serum ALP, ALT, and GGT may reflect enzyme induction rather than hepatic injury during phenobarbital treatment in dogs. Serum AST, fBA, and bilirubin, and ultrasonographic evaluation of the liver are not affected by the enzyme-inducing effect of phenobarbital and can therefore be helpful to assess liver disease in dogs treated with the drug.

Cervical intervertebral disk disease is commonly treated surgically by ventral decompression through a ventral slot. Nine dogs with documented vertebral subluxation following surgical creation of a ventral slot are reported. The location of the subluxation was at the fourth cervical (C4) to fifth cervical (C5) intervertebral space in two dogs, C5 to sixth cervical (C6) intervertebral space in four dogs, and C6 to seventh cervical (C7) intervertebral space in three dogs. The ventral slot width to vertebral body width ratio ranged from 0.39 to 0.80, with the ratio being 0.50 or greater in seven of eight cases evaluated radiographically. Surgical reduction and stabilization were performed in seven of nine dogs.

Phenobarbital can interfere with the thyroid axis in human beings and rats by accelerating hepatic thyroxine metabolism because of enzyme induction. In human beings, it also can interfere with the low-dose dexamethasone suppression test (LDDST) used to assess adrenal function by accelerating dexamethasone metabolism. This effect can cause a lack of suppression of pituitary ACTH and subsequent adrenal cortisol release after dexamethasone administration. The effects of phenobarbital on the thyroid axis, the adrenal axis, and adrenal function tests were prospectively investigated in 12 normal, adult dogs. Phenobarbital was administered at 5 mg per kilogram of body weight (range, 4.8-6.6 mg/kg) PO q12h for 29 weeks, resulting in therapeutic serum concentrations (20-40 g/mL). Serum total thyroxine (TT4), free thyroxine (FT4) by equilibrium dialysis, total triiodothyronine (TT3), thyrotropin (TSH), and cholesterol were determined before and during phenobarbital treatment. LDDST, ACTH stimulation tests, and ultrasonographic evaluation of the adrenal glands were performed before and during treatment. TT4 and FT4 decreased significantly (P Յ .05), TT3 had minimal fluctuation, TSH had only a delayed compensatory increase, and cholesterol increased during phenobarbital treatment. The delayed increase in TSH, despite persistent hypothyroxinemia, suggests that accelerated hepatic thyroxine elimination may not be the only effect of phenobarbital on the thyroid axis. There was no significant effect of phenobarbital on either of the adrenal function tests. With the methods employed, we did not find any effects of the drug on the hormonal equilibrium of the adrenal axis. Key words: Adrenal axis, Adrenal function tests, Phenobarbital, Thyroid axis. In rats and human beings, anticonvulsant drugs have considerable effects on the thyroid gland and thyroid hormone metabolism. Phenobarbital increases hepatic metabolism and biliary excretion of thyroxine by inducing hepatic enzymes, such as thyroxine-glucuronosyltransferase and cytochrome P450 enzymes. [1][2][3][4][5] In rats, a primary increase of hepatic thyroxine uptake stimulates hepatic deiodinative and excretory processes. Increased fecal and deiodinative clearance of thyroxine and triiodothyronine activates the thyroid axis, resulting in increased pituitary thyrotropin (TSH) secretion and subsequent establishment of a new steady state with normal thyroxine concentrations and somewhat increased TSH concentrations.2,4,6 Thyroid gland weight remains increased, indicating chronic stimulation. 2Several textbooks and review articles in the veterinary literature mention that phenobarbital decreases basal serum thyroxine concentrations in dogs.7-10 However, more recent data suggest that phenobarbital treatment at 30-45 mg q12h for 3 weeks has no significant effect on total thyroxine University, Baton Rouge, LA 70803; email: jtaboada@ mail.vetmed.lsu.edu. Submitted June 26, 1998; Revised March 12, 1999, and July 1, 1999; Accepted October 19, 1999 (TT4), free thyroxine (FT4), and TSH ...

An echogenic line in the outer zone of the renal medulla, paralleling the corticomedullary junction is described as the renal medullary rim sign. This renal ultrasonographic change is demonstrated in 4 dogs and 2 cats with a range of renal diseases. The renal medullary rim sign provides additional ultrasonographic criteria indicating primary renal disease in some patients. However the renal medullary rim sign may prove to be a poor correlate for prognosis across the range of differentials present in these clinical patients.

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This report compares results from imaging of transitional cell carcinoma of the urinary bladder in 15 dogs using intravenous urography, double‐contrast cystography, and ultrasonography. Intravenous urography demonstrated filling defects in the urinary bladder in 3 of the 5 cases examined with this modality. Double‐contrast cystography identified bladder masses in 8 of 10 animals. Ultrasonography was the only imaging modality which detected bladder masses in all patients.

Chronic hypertrophic pyloric gastropathy was diagnosed using ultrasound in six dogs that were presented for chronic vomiting. An evenly thick hypoechoic layer surrounding the pyloric lumen was visualized ultrasonographically in dogs with grades 1 or 2 chronic hypertrophic pyloric gastropathy. This was histologically found to correspond with a thickened muscular layer. Gastric wall thickness was greater than or equal to 9 mm in all six dogs. In dogs with grade 1 or 2 chronic hypertrophic pyloric gastropathy, the hypoechoic muscular layer was greater than or equal to 4 mm.