Twenty-eight surgical procedures were performed in 23 dogs with atlantoaxial subluxation. Dorsal stabilization in seven dogs resulted in two recoveries and five failures of fixation. Ventral decompression and stabilization in 18 dogs resulted in eight recoveries and four failures of fixation. Six dogs died or were euthanatized within 7 days of ventral stabilization. Using either technique, four of seven nonambulatory dogs recovered.

Nerve-sheath tumor was diagnosed in 10 dogs with clinical signs of unilateral trigeminal nerve dysfunction. Unilateral temporalis and masseter muscle atrophy were present in all cases. An enlarged foramen and distorted rostral petrous temporal bone were seen with computed tomography imaging in one case. Magnetic resonance imaging was used to identify the lesion accurately in seven cases. Surgery was performed for biopsy and lesion removal in three cases. Cases not treated had a progressive course eventually resulting in euthanasia or death. Of the cases treated surgically, one case is alive without disease progression 27 months after surgery. Survival times of the nontreated cases ranged from five to 21 months.

Magnetic resonance imaging was performed in seven dogs with histopathologically‐confirmed brain infarcts. The infarcts were non‐hemorrhagic in four dogs and hemorrhagic in three dogs. Six dogs had single infarcts involving the cerebrum and one dog had multiple infarcts involving the cerebrum and brain stem. Non‐hemorrhagic infarcts were typically wedge‐shaped, hypointense on T1‐weighted images, hyperintense on T2‐weighted images, and did not enhance with gadolinium‐DTPA. Hemorrhagic infarcts had mixed intensity on T1‐ and T2‐weighted images, with variable patterns of enhancement.

GM1 gangliosidosis is a fatal neurodegenerative disease that affects individuals of all ages. Favorable outcomes using adeno-associated viral (AAV) gene therapy in GM1 mice and cats have prompted consideration of human clinical trials, yet there remains a paucity of objective biomarkers to track disease status. We developed a panel of biomarkers using blood, urine, cerebrospinal fluid (CSF), electrodiagnostics, 7 T MRI, and magnetic resonance spectroscopy in GM1 cats-either untreated or AAV treated for more than 5 years-and compared them to markers in human GM1 patients where possible. Significant alterations were noted in CSF and blood of GM1 humans and cats, with partial or full normalization after gene therapy in cats. Gene therapy improved the rhythmic slowing of electroencephalograms (EEGs) in GM1 cats, a phenomenon present also in GM1 patients, but nonetheless the epileptiform activity persisted. After gene therapy, MR-based analyses revealed remarkable preservation of brain architecture and correction of brain metabolites associated with microgliosis, neuroaxonal loss, and demyelination. Therapeutic benefit of AAV gene therapy in GM1 cats, many of which maintain near-normal function >5 years post-treatment, supports the strong consideration of human clinical trials, for which the biomarkers described herein will be essential for outcome assessment.

Premortem magnetic resonance imaging (MRI) was performed in two cats with brain stem abscessation confirmed post mortem by histology and recovery of multiple bacterial species. The MRI features of the abscesses were distinctive and included a thick and marked enhancement of the abscess capsule and extension of the lesion from a tympanic bulla in one cat. A focal area of increased signal intensity was present on T2-weighted images. A circumscribed area of decreased signal intensity was surrounded by a ring of increased signal intensity on precontrast T1-weighted images. A center of decreased signal intensity with a thick, markedly enhanced abscess capsule was observed on post contrast T1-weighted images. These findings are compared to the current experimental and clinical literature of brain abscess. The underlying pathogenesis of MRI features is reviewed.