A Subset of Dogs with Presumptive Idiopathic Epilepsy Show Hippocampal Asymmetry: A Volumetric Comparison with Non-Epileptic Dogs Using MRI.

MRI-acquired volumetric measurements from 100 dogs with presumptive idiopathic epilepsy (IE) and 41 non-epileptic (non-IE) dogs were used to determine if hippocampal asymmetry exists in the IE as compared to the non-IE dogs. MRI databases from three institutions were searched for dogs that underwent MRI of the brain and were determined to have IE and those that were considered non-IE dogs. Volumes of the right and left hippocampi were measured using Mimics® software. Median hippocampal volumes of IE and non-IE dogs were 0.47 and 0.53 cm3, respectively. There was no significant difference in overall hippocampal volume between IE and non-IE dogs; however, IE dogs had greater hippocampal asymmetry than non-IE dogs (P < 0.012). A threshold value of 1.16 from the hippocampal ratio had an 85% specificity for identifying IE-associated asymmetry. Thirty five percent of IE dogs had a hippocampal ratio >1.16. Asymmetry was not associated with any particular hemisphere (P = 0.67). Our study indicates that hippocampal asymmetry occurs in a subset of dogs with presumptive idiopathic/genetic epilepsy, suggesting a structural etiology to some cases of IE.

Congenital Hydrocephalus.

There are several types of hydrocephalus, which are characterized based on the location of the cerebrospinal fluid (CSF) accumulation. Physical features of animals with congenital hydrocephalus may include a dome-shaped skull, persistent fontanelle, and bilateral ventrolateral strabismus. Medical therapy involves decreasing the production of CSF. The most common surgical treatment is placement of a ventriculoperitoneal shunt. Postoperative complications may include infection, blockage, drainage abnormalities, and mechanical failure.

Cholesteatoma and meningoencephalitis in a dog with chronic otitis externa.

A 10-year-old female spayed German Shepherd dog, with a year-long history of recurrent left ear infections, was presented for progressive ataxia, head tilt, and pain on opening of the mouth. On physical examination, a large amount of ceruminous debris was present in the left ear and multiple neurologic defects localizing to the cerebellum and vestibular system were identified. Magnetic resonance imaging (MRI) demonstrated a minimally contrast-enhancing mass within the left bulla, an intracranial space-occupying, heterogeneously contrast-enhancing lesion at the level of the left cerebello-medullary junction, and contrast enhancement of the ipsilateral meninges. Cerebrospinal fluid analysis revealed a marked mixed cell pleocytosis (nucleated cell count 655 cells/µL). The mass was visualized within the horizontal ear canal by otoscopic examination and a biopsy was taken. Impression smears of the biopsy contained many anucleate keratinized squamous epithelial cells, mild mixed inflammation, and few presumptive fibroblasts. With the provided clinical history and MRI findings, a cytologic diagnosis of cholesteatoma was made. A ventral bulla osteotomy was performed, and histopathologic examination of resected tissue confirmed the cytologic diagnosis of cholesteatoma. The dog's clinical symptoms improved postoperatively, but the dog died of unrelated causes, 3.5 months later. To our knowledge, this is the first description of the cytologic features of a cholesteatoma, which is a nonneoplastic, but locally invasive epidermoid cyst, in the middle ear of dogs.

Necrotizing meningoencephalitis in a large mixed-breed dog.

CASE DESCRIPTION: A 4-year-old 26-kg (57.2-lb) spayed female Staffordshire Bull Terrier mix was evaluated because of a 24-hour history of cluster seizures. CLINICAL FINDINGS: Neurologic examination revealed altered mentation and multifocal intracranial signs; MRI was performed. The MRI findings included multifocal, asymmetric forebrain lesions affecting both the gray and white matter, an area suggestive of focal necrosis, and loss of corticomedullary distinction. A midline shift and caudal transtentorial herniation were noted, suggestive of greater than normal intracranial pressure. TREATMENT AND OUTCOME: Because the dog's clinical signs worsened despite medical treatment and additional evidence of increased intracranial pressure, bilateral craniectomy and durectomy were performed. Histologic evaluation of a brain biopsy specimen revealed bilateral and asymmetric areas of necrosis in the subcortical white matter and adjacent gray matter. At the periphery of the necrotic areas, there was increased expression of glial fibrillary acidic protein and Virchow-Robin spaces were expanded by CD3+ lymphocytes. Results of immunohistochemical analysis of brain tissue were negative for canine distemper virus, Neospora canis, and Toxoplasma gondii. These clinical, imaging, and histopathologic findings were compatible with necrotizing meningoencephalitis. The dog's neurologic status continued to worsen following surgery. Repeated MRI revealed ongoing signs of increased intracranial pressure, despite the bilateral craniectomy. The owners elected euthanasia. CLINICAL RELEVANCE: To the author's knowledge, this is the first report of necrotizing meningoencephalitis in a large mixed-breed dog. Necrotizing meningoencephalitis should be considered as a differential diagnosis in dogs other than small or toy breeds that have signs suggestive of inflammatory disease.