On a retrospective basis, the response to adding chronic oral bromide (BR) to phenobarbital (PB) administration in 23 refractory canine idiopathic epileptics between 1986 and 1991 was studied. The mean age for an observed first seizure was 24 months (range 7 to 72) for all dogs. Thirteen (57%) dogs were males with no breed predisposition observed. All dogs were diagnosed as having idiopathic epilepsy based on normal metabolic and neurologic diagnostic evaluations. Dogs were evaluated before BR therapy for a mean time of 22 months (range 5 to 75 months). Seventeen dogs (74%) received multiple antiepileptic drugs (AEDs) before BR therapy. All animals were maintained on PB at least 4 months before the onset of BR therapy, with a mean trough serum concentration of 37.8 mcg/mL and no improvement in seizure severity or recurrence. Twelve dogs presented with generalized isolated seizures and 11 with generalized cluster seizures (two or more seizures within 24 hours) as their first seizure. The effects of BR therapy were evaluated for a mean time of 15 months (range 4 to 33), with 17 dogs (74%) followed for I2 or more months. The mean BR serum concentration for the 0 to 4 months time period was I17 mg/dL compared with 161 mg/dL for the greater than 4 months period. Overall, response to BR therapy was associated with a reduction in the total number of seizures in 83% of the dogs when compared with their respective pre-BR period. For those followed for 1 year after BR, there was a 53% reduction in the number of seizures compared with the previous 12 months. Furthermore, owners reported a decrease in seizure intensity (65% of dogs) and change to a less severe seizure type (22% of dogs) in those dogs that continued to have seizures. Seizure-free status was obtained in 26% of the dogs with protection continuing up to 31 months in one dog. No correlations could be determined between response to BR and either age of onset of the first seizure or interval from the first AED therapy to BR therapy.Adverse effects of concomitant BR and PB therapy were polydipsia (56% of dogs), polyphagia (30% of dogs), excessive sedation (30% of dogs), and generalized ataxia (17% of dogs). As a result of BR treatment, the P B dosage was reduced in eight dogs (35%). In conclusion, concomitant BR and PB was well tolerated in dogs of this study and was effective in treating refractory canine idiopathic epilepsy, regardless of prior interval of seizure activity or previous treatment.
This study is the first attempt to classify seizures and to characterise epilepsy in a referral-based equine population. Predictive factors of epilepsy in horses were similar to those reported in other species and may assist the clinician with the early diagnosis of epilepsy.
Cavernous sinus syndrome (CSS) is characterized by deficits in more than one of the cranial nerves (CN) that traverse the cavernous sinus at the base of the cranial vault: CN 111 (oculomotor), IV (trochlear), VI (abducens), and the first two branches of CN V (trigeminal). Records from 4 dogs and 8 cats with CSS diagnosed over a 14-year period were reviewed. The most common clinical signs were ophthalmoparesis or ophthalmoplegia, mydriasis with no direct or consensual pupillary light reflexes, ptosis, decreased corneal sensation, and decreased retractor oculi reflex. All cats had initial signs referable to a left CSS lesion (one had bilateral CSS), whereas in all dogs the lesions were localized to the right cavernous sinus. Median ages at diagnosis were 9 and 10 years of age for dogs and cats, respectively. Cerebel lomedullary cisternae cerebrospinal fluid analysis in 6 aniavernous sinus syndrome (CSS) is a recognized syn-C drome in people characterized by variable impairment of multiple cranial nerves (CN) including the oculomotor (III), trochlear (IV), abducens (VI), and the first two branches of the trigeminal nerve (CN V)." The cavernous sinus is a paired venous sinus that lies on each side of the floor in the middle cranial fossa and runs from the orbital fissure to the petro-occipital canal! CN 111, IV, VI, and the ophthalmic branch of V exit the skull through the orbital fissure on their way to innervation of the muscles of the eye.4 The maxillary branch of CN V passes in the dura mater of the lateral wall of the cavernous sinus and exits through the round f~r a m e n .~ This intimate association of CN 111, IV, VI, and the ophthalmic and maxillary branches of CN V is the reason for multiple cranial nerve deficits due to inflammatory or mass lesions in this area.In people, CSS is associated with several disease processes. Neoplasia accounted for approximately 70% of the cases in one study.5 Other causes include infectious and noninfectious inflammatory:,' v a~c u l a r ?~,~ and traumatic lesions.' Only sporadic individual cases of CSS have been described in animals . *-' * This retrospective study describes CSS in 4 dogs and 8 cats. The purpose of this article is to familiarize the clinician with the common clinical signs, diagnostic tests, clinical outcome, and review of applicable neuro-ophthalmology associated with CSS in these species. Materials and Methods Criteria for EnrollmentMedical records from The Ohio State University Veterinary Teaching Hospital were reviewed for all small animals diagnosed with CSS from 1979 to 1993. The criterion for a diagnosis of CSS was a deficit in more than one cranial nerve closely associated with the cavernous sinus: CN 111, IV, VI, and the maxillary and ophthalmic branches of CN V. Diagnostic EvaluationThe diagnostic evaluation of each animal varied. All animals had complete physical, ophthalmologic, and neurological examinations. Serological, biochemical, and hematologic evaluation performed on one or more animals included CBC, serum chemistry profile, feline Provoca...
Pseudolymphoma and anticonvulsant hypersensitivity syndrome are recognized potential sequelae to anticonvulsant administration in humans. However, a pseudolymphoma-like reaction to anticonvulsants in veterinary species has not previously been reported. This case highlighted a potentially serious yet reversible sequela to phenobarbital treatment that may have been mistaken for more severe illness such as neoplasia.
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