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Objective: To characterize lysosomal storage body accumulation in the retina and brain of Tibetan Terriers with ceroid-lipofuscinosis and determine whether the disease in these dogs is accompanied by impaired retinal function and retinal degeneration., Animals: Three 7- to 10-year-old Tibetan Terriers with ceroid-lipofuscinosis and 1 healthy 5-year-old Tibetan Terrier., Procedure: Owners completed a questionnaire to identify behavioral and physical signs indicative of ceroid-lipofuscinosis. Neurologic, behavioral, and ophthalmologic evaluations, including full-field electroretinograms, were performed on each dog. Fluorescence, light, and electron microscopy were performed on specimens of retina, cerebral cortex, and cerebellum of all dogs postmortem., Results: Behavioral assessments of the affected dogs revealed moderate visual impairment in low-light conditions but good vision in bright light. On funduscopic evaluation of these dogs, abnormalities detected ranged from none to signs of moderately advanced retinal degeneration. Compared with findings in the control dog, electroretinography revealed depressed rod cell function with some impairment of cone cell function in the affected dogs. Morphologically, disease-specific storage bodies were detected in retinal Müller cells and neurons, particularly in ganglion cells, and in cells of the cerebral cortex and cerebellum in affected dogs. Substantial photoreceptor cell loss and disruption of photoreceptor outer segment morphology appeared to develop late in the disease. IMPLICATIONS FOR HUMAN MEDICINE: The similarities between ceroid-lipofuscinosis in Tibetan Terriers and some forms of ceroid-lipofuscinosis in humans suggest that the canine disease may have a genetic and biochemical basis similar to that of one of the ceroid-lipofuscinosis disorders in humans.

Objective: To determine clinical characteristics and mode of inheritance of idiopathic epilepsy (IE) in English Springer Spaniels., Design: Original study., Animals: 45 dogs with IE and 74 siblings and their respective parents., Procedure: IE was diagnosed on the basis of age at the time of seizure onset and results of laboratory testing and neurologic examinations. Simple segregation analysis was performed with the Davie method., Results: Median age at the onset of seizures was 3 years; however, 9 (20%) dogs were between 5 and 6 years old at the time of the onset of seizures. Twenty-one dogs (47%) had generalized seizures, and 24 (53%) had focal onset seizures. Results of segregation analysis were consistent with partially penetrant autosomal recessive or polygenic inheritance. Simulated linkage indicated that there was a 58% chance of obtaining suggestive linkage with the available pedigrees., Conclusions and Clinical Relevance: Results of the present study suggest that in English Springer Spaniels, IE segregates in a manner that is consistent with partially penetrant autosomal recessive inheritance (ie, a single major locus with modifying genes) or polygenic inheritance. Given enough families with accurate phenotypic information and available DNA, it should be possible to use genetic linkage analysis to identify chromosomal segments containing the causative gene or genes.

Objective: To identify risk factors associated with dysautonomia in dogs., Design: Case-control study., Animals: 42 dogs with dysautonomia examined between October 1988 and January 2000 and 132 control dogs examined during the same period for an unrelated problem., Procedure: Information was gathered from medical records and surveys mailed to owners of case and control dogs., Results: 42 case and 132 control dogs were included; completed surveys were returned by owners of 30 case and 103 control dogs. Dogs with dysautonomia were significantly younger (median, 18 months) than control dogs (median, 60 months) and more likely to come from rural areas and to spend > or =50% of their time outdoors. Compared with rural control dogs that spent at least some time outdoors, affected dogs were more likely to have access to pasture land, farm ponds, and cattle, and to have consumed wildlife, at least occasionally. The largest numbers of dogs with dysautonomia were identified during February and April, with relatively few dogs identified during the summer and early fall., Conclusion and Clinical Relevance: Although the cause of dysautonomia is unknown, results suggest that dogs with dysautonomia were significantly more likely to live in rural areas and spend > or =50% of their time outdoors than were control dogs examined for unrelated diseases.

A 2.5-year-old domestic shorthair cat was evaluated because of dysphagia and weight loss of 4 weeks' duration. MIld blepharospasm and conjunctival hyperemia were evident in both eyes, oral mucous membranes were tacky on palpation, and salivary glands were enlarged. Results of a Schirmer tear test were 0 mm/min for both eyes. Administration of atropine did not cause salivation or caused secretion fo thick rope-like saliva. Examination of biopsy specimens of salivary glands revealed a plasmacytic infiltrate. Sjögren's syndrome (SS) was diagnosed. Oral administration of prednisone was instituted but was discontinued after a minimal positive response was evident 6 weeks after initiation of treatment. Palliative treatment with a 6% solution of pilocarpine 4 to 5 times/d, cyclosporine, hylan A, and neomycin-polymyxin-bacitracin ophthalmic ointment resulted in clinical improvement in the cat. Although reported rarely in animals, SS may be more common than currently is recognized. Most treatment regimens for SS are aimed at alleviating clinical signs.

Objective: To determine whether anesthesia of the infraorbital and inferior alveolar nerves abolishes reflex-evoked muscle action potentials (REMP) during tooth-pulp stimulation in halothane-anesthetized cats., Animals: 8 healthy adult cats., Procedure: In halothane-anesthetized cats, an anodal electrode was attached to the tooth to be stimulated and a platinum needle cathodal electrode was inserted in adjacent gingival mucosa. Cathodal and anodal electrodes were moved to the upper and lower canine, upper fourth premolar, and lower first molar teeth for stimulation; baseline REMP was recorded. A 25-gauge 1-cm needle was inserted 0.5 cm into the infraorbital canal. A 25-gauge 1-cm needle was inserted 1 cm rostral to the angular process of the ramus, and advanced 0.5 cm along the medial aspect. Chloroprocaine was injected at each site. Each tooth was stimulated every 10 minutes for 90 minutes., Results: REMP was abolished within 10 minutes for all upper teeth, except for the upper canine tooth in 1 cat, and abolished within 10 minutes for lower teeth in 4 cats. In 1 cat, REMP was not abolished in the lower first molar tooth. In 3 cats, REMP was not abolished in the lower canine and first molar teeth. At 90 minutes, REMP was restored for all teeth except the lower canine tooth in 1 cat, for which REMP was restored at 120 minutes., Conclusions and Clinical Relevance: Regional anesthesia of the infraorbital and inferior alveolar nerves may provide dental analgesia in cats.

Objective: To evaluate efficacy and safety of the calcium channel antagonist nimodipine in dogs with idiopathic epilepsy., Design: Prospective clinical trial., Animals: 10 dogs with idiopathic epilepsy. Dogs were included if seizures were inadequately controlled despite treatment with barbiturates and serum phenobarbital concentrations were > 25 micrograms/ml, if dogs had intolerable adverse effects when treated with barbiturates, or if dogs had mild, inadequately treated seizures., Procedures: Dogs were treated with nimodipine (2.5 mg/kg [1.1 mg/lb] of body weight, PO, q 12 h), and other medications were slowly withdrawn. Dogs were monitored for seizure frequency and severity as well as any adverse effects to the medication., Results: Few adverse effects were reported. Seizure control, however, was generally inadequate. All but 2 dogs were withdrawn from the study because of poor seizure control. Plasma nimodipine concentrations were low, with a mean peak concentration of 105.3 ng/ml., Clinical Implications: Nimodipine was not successful in controlling seizures in dogs used in this study.

A 6-year-old cat that was laterally recumbent and panting was evaluated because of a 10-day history of progressive neurologic abnormalities. Despite aggressive treatment, the cat died on the day of admission. At necropsy, a 1.5-cm-diameter, fluid-filled cyst was found in the white matter of the left cerebrum. The cyst was identified as a coenurus of Taenia serialis, on the basis of the cyst wall, distribution of scolices, and the shape and dimensions of rostellar hooks. Scolices were found in varying stages of ontogeny, ranging from undifferentiated to nearly mature. Taenia serialis has a canid-lagomorph life cycle, with cats being accidental intermediate hosts. However, the potential exists for rare zoonotic transmission and subsequent serious disease in human beings and other accidental intermediate hosts.

A 4-year-old castrated mixed-breed dog had atypical signs of chronic distemper encephalomyelitis. The predominant signs were related to visceral rather than somatic dysfunction. The visceral dysfunction was largely attributable to distemper-associated inflammatory lesions in the spinal cord and resulted in fecal incontinence, urinary incontinence, and priapism. Empirical treatment of the dog resulted in transitory improvement prior to euthanasia performed because of the progressive nature of the encephalomyelitis.

Clinical signs of dysautonomia, including dilated pupils, dry mucous membranes, and megaesophagus, were observed in a cat. The diagnosis was confirmed by use of autonomic nervous system function testing including 0.1% pilocarpine and physostigmine ocular response tests, plasma catecholamine assays, and cardiovascular responses to various perturbations intended to elicit autonomic responses. The cause of the autonomic dysfunction was not ascertained, and the cat was euthanatized after 5 weeks of unsuccessful treatment with pilocarpine, metoclopramide, prochlorperazine, and parenteral nutrition.

Nerve sheath fibrosarcomas of the left 5th through 8th cranial nerve roots were diagnosed in 1 dog and of the left 4th through 8th cranial nerve roots in another dog. Clinical signs in both dogs included head tilt to the left, circling to the left, left hemiparesis and proprioception deficits, rotary nystagmus, left-sided atrophy of masticatory muscles, and cutaneous hypalgesia of the left side of the face. Cranial nerve roots from both dogs were incorporated in discrete, firm, encapsulated, lobulated, tan masses of various sizes that compressed adjacent brain stem and cranial nerves. There were no regional or distant metastases; however, there was enlargement of nerve roots adjacent to the masses. The masses were composed of bundles and sheets of anaplastic, polymorphic to spindle-shaped cells that infiltrated cranial nerves and ganglia and extended into the brain along nerve roots. Masses contained various amounts of collagen and reticulin fibers, but no mucopolysaccharide ground substance. There was no myelin or S-100 protein associated with neoplastic cells. The tumors appeared to have a multicentric origin from cranial nerve sheaths.

Spongy degeneration of the CNS was diagnosed in 2 female Labrador Retriever littermates. The dogs had histories of progressive cerebellar ataxia and episodes of extreme extensor rigidity beginning at 4 and 6 months of age. One had a history of hearing difficulties. When examined at 9 months of age, both dogs had moderate ataxia and dysmetria of the head, trunk, and limbs, hyperreflexia with clonus, and extensor rigidity with episodes of exaggerated rigidity and opisthotonos. One dog was euthanatized and the other was monitored for 2 months, during which time her signs progressed to severe dysmetria, weakness, muscle atrophy, and rigidity with marked hyperreflexia. Necropsy of both dogs revealed astrocytic abnormalities and spongy degeneration of the white matter of the CNS. The clinical signs and postmortem findings were similar to the juvenile form of spongy degeneration in man.