Seizure etiologic classification and long-term outcome for cats with juvenile-onset seizures.

OBJECTIVE To identify seizure etiologic classification for cats that developed seizures at < 12 months of age and describe the long-term outcome of affected cats. DESIGN Retrospective cohort study. ANIMALS 15 client-owned cats with seizures that began at < 12 months of age. PROCEDURES Information on each cat was obtained from the medical records, veterinarians, and owners. Inclusion required an onset of seizures before 12 months of age and a complete medical record, including a final diagnosis. RESULTS 7 of the 15 cats had structural epilepsy, 4 had idiopathic epilepsy, and 4 had reactive seizures. Median age at seizure onset was 27 weeks (range, 0.4 to 41 weeks). Cluster seizures were reported in 6 cats, and status epilepticus was reported in 2. Age at the onset of seizures, presence of cluster seizures, and seizure semiology (ie, generalized vs focal seizures) were not significantly associated with seizure etiologic classification. CONCLUSIONS AND CLINICAL RELEVANCE Results suggested that cats that developed seizures at < 12 months of age were more likely to have structural epilepsy than idiopathic epilepsy or reactive seizures. Therefore, advanced diagnostic imaging is recommended in cats with juvenile-onset seizures if metabolic and toxic causes are excluded.

Prevalence, clinical presentation, prognosis, and outcome of 17 dogs with spinal shock and acute thoracolumbar spinal cord disease.

OBJECTIVE: To describe the prevalence, signalment, clinical features, etiology, and outcome in dogs with acute thoracolumbar disease and suspected spinal shock. DESIGN: Retrospective clinical case study (2005-2010). SETTING: Private specialty practice. ANIMALS: Medical records of 263 dogs with thoracolumbar spinal magnetic resonance imaging were reviewed. If decreased or absent withdrawal reflexes were present in 1 or both pelvic limbs, in the absence of a spinal lesion in the lumbosacral intumescence, dogs were diagnosed with spinal shock. Dogs with suspected or confirmed spinal neoplasia, myelomalacia, or meningomyelitis were excluded. Seventeen of 263 dogs (6%) met inclusion criteria. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Thoracic lesions were significantly more likely to result in spinal shock when compared to lumbar lesions (P = 0.03). Fibrocartilaginous embolism was the most commonly diagnosed etiology (7 of 17 dogs), and was more common in the thoracic spine compared to in the lumbar spine (P = 0.10). Six of 17 dogs (35%) were diagnosed with intervertebral disk herniation; 4 of 17 dogs (24%) with suspected acute noncompressive nucleus pulposus extrusion. Two dogs were lost to follow-up. Fourteen of 15 (93%) dogs had improved or normal reflexes by 60 days post injury. CONCLUSIONS: Although the prevalence of spinal shock was low, it should be considered in any dog presenting with an acute history of thoracolumbar spinal injury with reduced or absent reflexes in the pelvic limbs. The presence of spinal shock should not dissuade a veterinarian from pursuing appropriate diagnostic testing and therapy for the underlying etiology.

Imaging diagnosis--hyperostosis associated with meningioma in a dog.

A 5-year-old neutered male Beagle mix dog had a 5-day history of generalized tonic-clonic seizures. Before the seizures, the dog had a 1-2-month history of progressive right hemiparesis. In computed tomography images, a presumed extraaxial mass with hyperostosis and destruction of the skull covering the mass were identified. Surgical excision was performed and the histopathologic diagnosis was meningioma. Hyperostosis is frequently associated with feline meningioma, but this report documents that hyperostosis may also occur secondary to meningioma in the dog.

Medical management of Toxoplasma meningitis in a white-throated capuchin (Cebus capucinus).

A 32-yr-old white-throated capuchin monkey (Cebus capucinus) was presented for paraparesis. A diagnosis of protozoal meningitis was made on the basis of a lymphocytic pleocytosis with elevated protein in cerebrospinal fluid and a positive serum titer to Toxoplasma gondii of 131,072 using an indirect hemagglutination test. Treatment with clindamycin and trimethaprim-sulfamethoxazole resulted in improvement within 3 days and complete clinical resolution within 2 wk.