In this time series study, the temporal sequences of postmortem changes in brains kept at different temperatures were investigated in different areas of mouse brains. Fixation of tissues kept at different storage temperatures (4 °C, 22 °C, 37 °C) was delayed for four time points (24, 120, 168, 336 h). Histological and immunohistochemical investigations were carried out to determine how postmortem autolysis may affect the cellular morphology and the expression of neural cell epitopes. Results showed that the autolytic changes started earlier in brains at 22 °C and 37 °C and in the grey matter compared to the white matter, with the cerebellum and hippocampus showing the earliest postmortem changes. The cellular antigens were differently affected by the autolytic process overtime: NeuN and Olig2 immunoreactivity was gradually lost at the nuclear site and diffused into the cytoplasm; increased background staining was observed with SMI-32; GFAP showed an increase in immunolabeling, whereas 2F11 immunoreactivity decreased. This study suggests that the morphological analysis and immunohistochemical investigation of the brain tissue could be satisfactorily applied to forensic cases, providing useful data for the estimation of the postmortem interval.

A 13-month-old, neutered, male, domestic shorthair cat was referred with a history of progressive paraparesis, proprioceptive ataxia, and lumbar spinal pain. Neurological examination revealed non-ambulatory paraparesis consistent with L4-S1 myelopathy. Magnetic resonance of the thoracolumbar spinal cord identified a dorsal intradural extramedullary space-occupying lesion extending from L5 to L6. It was homogeneously hyperintense in T2-weighted imaging and isointense in T1-weighted imaging and exhibited marked and homogeneous contrast enhancement in the T1-weighted post-contrast imaging. The removed tissue was composed of neoplastic cells arranged as pseudostratified or multilayered trabecular and tubular structures, supported by internal and external limiting PAS-positive membranes. The neoplastic cells were immunoreactive for vimentin and NSE and negative for GFAP, Olig2, synaptophysin, PCK, S-100, NeuN, and nestin. The Ki-67 nuclear labeling index was up to 90%. The tumor was consistent with the diagnosis of medulloepithelioma, which is most frequently reported as an intraocular tumor. The morphological and immunohistochemical features of the tumor showed remarkable concordance with most human medulloepitheliomas. This is the first spinal cord medullopethelioma report in a cat, with the clinical, neuroradiological, histological, and immunohistochemical findings being described.

Human hemangioblastoma is a benign, slow-growing, highly vascular neoplasm. The tumor most commonly arises in the cerebral hemispheres and cerebellum, where it is more frequently observed in patients with von Hippel–Lindau disease. In veterinary medicine, hemangioblastoma has only been described in the central nervous system of dogs and in the skin of lambs. Our study aimed to characterize the clinical and neuropathological features of five cases of canine spinal cord hemangioblastoma and one case of sciatic nerve localization, and to compare these results with those reported in the veterinary literature. Diagnoses were achieved by neurological examination, neuroimaging, surgery or post-mortem examination, histopathology, and immunohistochemistry. All tumors were composed of numerous, haphazardly arranged capillaries lined by plump endothelium and interstitial fusiform to stellate stromal cells. Immunohistochemically, the stromal cells were strongly immunolabeled with NSE and carbonic anhydrase IX and were negative for von Willebrand factor VIII and inhibin-α. Canine hemangioblastoma exhibits morphological and immunohistochemical features comparable to the human counterpart, although the latter is mostly positive for inhibin-α. Surgery may be effective in cases of intradural-extramedullary and peripheral nerve locations, as in humans. This is the first report of peripheral nerve hemangioblastoma in animals.

A 7-month-old spayed female mixed-breed dog was evaluated for a subacute, progressive, cerebellar syndrome characterized by ataxia and intention tremors. Brain magnetic resonance imaging (MRI) revealed moderate cerebellar atrophy and mild bilateral symmetrical intra-axial lesions at the level of the caudate nuclei. A neurodegenerative disorder was suspected. Over a 2-year period, signs of neurologic disease worsened with suspected myoclonic epileptic seizures and severe cerebellar ataxia. Follow-up MRI showed progressive cerebellar and cerebral atrophy, as well as well-defined, bilateral, and symmetrical lesions affecting the caudate nuclei. Histopathology revealed severe cerebellar degeneration with a loss of Purkinje cells and depletion of the granular and molecular layers. Malacic areas at the level of the caudate nuclei characterized by extensive necrosis were observed. Genetic testing identified a clear top candidate variant in the SERAC1 gene on chromosome 1. These findings are consistent with multiple system degeneration, a rare inherited neurodegenerative disorder resembling MEGD(H)EL syndrome (3-methylglutaconic aciduria with deafness-dystonia, [hepatopathy], encephalopathy, and Leigh-like syndrome) in humans.