A 4-year-old, male Bernese mountain dog was evaluated for a 1-year history of right hemiparesis. Computed tomography revealed a large hypoattenuating mass severely deforming the C5 vertebral arch, invading the C6 spinal canal, and causing spinal cord compression. The signal characteristics of magnetic resonance imaging indicated a lesion composed of adipose tissue. The mass was removed via right hemilaminectomy, and histopathological examination confirmed it was an infiltrative lipoma. The compressive lesion remained unresolved, so the dog underwent a second operation, after which he regained some ambulatory function. Although postoperative adjunctive radiation therapy was performed, the dog died 201 days after the first operation.

Enhanced responses of the chorda tympani nerve to sugars in the ventromedial hypothalamic obese rat. J Neurophysiol 90: 128 -133, 2003. First published March 12, 2003 10.1152/jn.01170.2002. Sweet taste sensitivity in obese rats with lesions of the ventromedial hypothalamus (VMH) was studied by examining chorda tympani nerve responses to various taste stimuli including sugars. In the early progressive phase of obesity (2 wk after creating VMH lesions), there was no significant difference in the nerve responses to any taste stimulus between sham-operated and VMH-lesioned rats. In contrast, in the late phase of obesity (15-18 wk after VMH lesions), the magnitude of responses to sugars (except for fructose) was prominently greater than that in age-matched controls. High-fat diet-induced obese rats and streptozotocin-diabetic rats also showed greater chorda tympani nerve responses to sugars as was observed in VMH-lesioned obese rats, indicating that VMH lesions might not be specifically related to the enhanced gustatory neural responses to sugars. Although it has been demonstrated that the enhanced responses of the chorda tympani nerve to sugars in genetically diabetic db/db mice is largely attributable to the lack of the direct suppressive effect of leptin on the taste receptor cells, plasma leptin levels were not correlated with the changes in chorda tympani responsiveness to sugars in these models of obesity and diabetes. Accordingly, our results suggest that some chronic factors, including high blood glucose, inefficiency of insulin action, or leptin resistance may be related to the enhancement of chorda tympani nerve responses to sugars. I N T R O D U C T I O NDestruction of the ventromedial area of hypothalamus (VMH) results in a chronic and persistent elevation of food intake, a hyperphagia that may exceed two to three times normal intake (Corbit and Stellar 1964;Graff and Stellar 1962;Weingarten 1982). A striking characteristic of VMH lesioned rats is their hyperreactivity to the stimulus properties of foods (Corbit and Stellar 1964; Graff and Stelilar 1962;Weingarten 1982). When given a relatively palatable diet including standard laboratory chow, they eat far more than normal animals. In contrast, if the palatability of the standard diet is reduced by the addition of quinine-HCl (QHCl), the hyperphagic animals reduce their food intake markedly, while normal animals maintain a relatively constant food intake. These feeding characteristics have been represented as "finickiness."Although alteration in taste sensitivity and preference in VMH-lesioned rats have been well documented at the behavioral level, possible changes in peripheral taste nerve responsiveness accounting for the behavioral alterations are not known. In genetically diabetic db/db mice, it has been demonstrated that responses of the chorda tympani (CT) nerve to sugars are greater than those of lean control mice (Ninomiya et al. 1995). Recently, Kawai et al. (2000) showed that leptin directly suppresses the sensitivities of taste receptor cells ...

A 4-year-old male Toy Poodle was presented with a history of status epilepticus. On presentation, neurological examination revealed a delay in postural reactions in the right pelvic limb. Magnetic resonance imaging showed a fluid-containing cystic lesion that compressed the mesencephalon, hippocampus, and amygdala. The cyst was surgically removed via left rostrotentorial craniotomy. The final diagnosis was an intracranial ectopic choroid plexus cyst. The patient has remained free of seizures for 18 months after surgery. This is the first case report of an intracranial ectopic choroid plexus cyst that was surgically removed in a dog.

A 4-month-old cat with epileptic seizures and nasal discharge was presented, and diagnosed with intranasal meningoencephalocele based on the clinical symptoms and findings of CT and MRI. As liquorrhea was suspected, the meningoencephalocele was surgically excised and the postoperative course was favorable. For cribriform plate reconstruction, the autologous tunica vaginalis was used. Rhinorrhea of the cerebrospinal fluid and seizures disappeared after surgery. On CT and MRI at 7 months after surgery, septum formation between the cranial and nasal cavities was confirmed. Currently, no seizures have occurred even though no oral antiepileptic agent was administered. There are few reports of surgical treatment for meningoencephalitis, and there are no reports of reconstruction of the cribriform plate using tunica vaginalis, so we reported the details.

A fatal case of malignant atrophic papulosis (Degos disease) with optic nerve and spinal cord involvement is described. Magnetic resonance imaging (MRI) of the optic nerve showed abnormal signal enhancement on fat suppressed T1 weighted images after intravenous meglumine gadopentetate infusion. On T2 weighted sagittal images, a sawtooth pattern was observed over seven vertebral segments of the spinal cord. On necropsy, a severe loss of myelinated nerve fibres in the left optic nerve was seen, with thrombotic obstruction of the central retinal artery. Spongy degeneration was observed in all levels of the spinal cord, with patchy and motheaten patterns caused by thromboses and endothelial proliferation in subarachnoid vessels. Findings on MRI were consistent with findings on pathological examination.