Intravascular lymphoma (IVL) is characterized by the proliferation of large malignant lymphocytes within the lumen of blood vessels. This retrospective, multi-center, case series study aimed to describe the MRI features of confirmed central nervous system IVL in dogs and compare them with histopathological findings. Medical record databases from seven veterinary centers were searched for cases of histologically confirmed IVL. Dogs were included if an MRI was performed. The MRI studies and histopathology samples were reviewed to compare the MRI changes with the histopathological findings. Twelve dogs met the inclusion criteria (12 brains and three spinal cords). Imaging of the brains revealed multifocal T2-weighted/FLAIR hyperintense and T1-weighted iso-hypointense lesions, with variable contrast enhancement; areas of abnormal diffusion both in arterial and venous territories in diffusionweighted imaging; and meningeal enhancement. On gradient echo images (GRE), the changes comprised tubular susceptibility artifacts, consistent with the "susceptibility vessel sign", and additional variably sized/shaped intraparenchymal susceptibility 294

Backround The endolymphatic sac is an organ devoid of sensory receptors. It is connected with the endolymphatic compartment and contains endolymph. Endolymphatic sac tumor is a rare neoplasm involving the middle and inner ear described in humans and dogs, does not show cellular characteristics of malignancy, but can be locally invasive and involve destruction of the temporal bone and adjacent structures. Case description: An 8 months old female cat was referred because of sudden onset of vestibular signs starting 3 days prior to referral. On clinical examination the patient showed depression, right head-tilt, left sided facial paralysis, horizontal nystagmus with fast phase to the left. The magnetic resonance images showed a voluminous extra axial lesion, with irregular morphology and well defined margins, with intracranial extension in the region of the pons, rostral medulla oblongata, cerebellar vermis, floccule and left cerebellar hemisphere. Due to the progressive clinical deterioration, the cat was euthanized two weeks later. A necropsy was then performed and histological samples taken. The necropsy revealed the presence of a voluminous dark red irregular mass extending from the tympanic bulla to the posterior cranial fossa following the left glossopharyngeal nerve. The histopathologic exam of the extra-axial lesion featured a non-encapsulated, moderately cellular, rather loose, proliferation of cuboidal to columnar epithelium breaching through chunks of an otherwise normal appearing dura mater and invading some cranial nerves.
 Sections of the cerebellum and brainstem revealed moderate, focal, impingement of the parenchyma with very mild extension of the proliferating cells into the ventral left side of the medulla oblongata.
 Based on these histological characteristics, the lesion was defined as endolymphatic sac tumor, a rare neoplasm described in human beings and with 2 reports in dogs.

 Conclusion To our knowledge, this is the first report describing an endolymphatic sac tumor in a cat.

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A 9.5-year-old labrador presented with signs of progressive C1-C5 myelopathy. Magnetic resonance imaging of the cervical spine revealed a broad-based, jagged and partially ill-defined intradural mass lesion at the level of C3-C4 cervical vertebra. Decompressive spinal surgery was performed and the removed mass was sent for histopathological examination that identified an intradural extraosseous osteosarcoma. This very rare canine spinal tumour appears to arise predominantly in the cervical spine and occurs with no predisposing factors. It should be considered as a differential diagnosis for spinal tumours. CASE PRESENTATIONA 9.5-year-old, female, entire labrador was presented to the Department of Neurology and Neurosurgery with progressive deteriorating neurological deficits over a period of 2 months and a background history of laryngeal paralysis treated withThis is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

We investigated the clinical, genetic, and pathological characteristics of a previously unknown severe juvenile brain disorder in several litters of Parson Russel Terriers. The disease started with epileptic seizures at 6 to 12 weeks of age and progressed rapidly to status epilepticus and death or euthanasia. Histopathological changes at autopsy were restricted to the brain. There was severe acute neuronal degeneration and necrosis diffusely affecting the grey matter throughout the brain with extensive intraneuronal mitochondrial crowding and accumulation of amyloid-β (Aβ). Combined homozygosity mapping and genome sequencing revealed an in-frame 6-bp deletion in the nuclear-encoded pitrilysin metallopeptidase 1 (PITRM1) encoding for a mitochondrial protease involved in mitochondrial targeting sequence processing and degradation. The 6-bp deletion results in the loss of two amino acid residues in the N-terminal part of PITRM1, potentially affecting protein folding and function. Assessment of the mitochondrial function in the affected brain tissue showed a significant deficiency in respiratory chain function. The functional consequences of the mutation were modeled in yeast and showed impaired growth in permissive conditions and an impaired respiration capacity. Loss-of-function variants in human PITRM1 result in a childhood-onset progressive amyloidotic neurological syndrome characterized by spinocerebellar ataxia with behavioral, psychiatric and cognitive abnormalities. Homozygous Pitrm1-knockout mice are embryonic lethal, while heterozygotes show a progressive, neurodegenerative phenotype characterized by impairment in motor coordination and Aβ deposits. Our study describes a novel early-onset PITRM1-related neurodegenerative canine brain disorder with mitochondrial dysfunction, Aβ accumulation, and lethal epilepsy. The findings highlight the essential role of PITRM1 in neuronal survival and strengthen the connection between mitochondrial dysfunction and neurodegeneration.