An eight-year-old female spayed boxer was presented in acute convulsive status epilepticus (SE). Blood gas analysis and serum biochemistry revealed mild metabolic acidosis [pH 7·3, reference interval (RI) 7·35 to 7·45, bicarbonate 13 mmol/L, RI 18 to 24] and mild azotaemia (creatinine 203 µmol/L, RI 35 to 106). The complete blood count and the cerebrospinal fluid analysis were unremarkable. Brain magnetic resonance imaging (MRI) showed bilateral T2 and FLAIR hyperintensity of both temporal lobes, more severely on the left side, and mildly enlarged lateral ventricles (Fig 1). There was no contrast enhancement present. According to the World Health Organisation animal grading system (Koestner and others 1999) histopathological examination revealed oligodendroglioma (Fig 2A) in the left temporal and piriform lobes accompanied by status spongiosus, capillary proliferation, disseminated microbleeding, gliosis and neuronal necroses in adjacent structures. Moderate oedema and gliosis was evident in the right hippocampus and temporal lobe (Fig 2B).


Figure 1. Transverse FLAIR MRI image of the brain. Both lateral ventricles are mildly enlarged. Severe hyperintensity (asterisks) is visible along both temporal and piriform lobes, obscuring white and grey matter. The hyperintensities approached the mildly enlarged lateral ventricles, offering a broader contact at the left side. The left piriform lobe is bigger and more hyperintense than the right one. No contrast enhancement could be observed on T1-W images

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Figure 2. Haematoxylin and eosin-stained sections of the brain. (A) Left temporal lobe with diffuse infiltrations of an oligodendroglioma. Note indistinct tumour margins and neuronal necroses (arrows). Bar = 150 µm. (B) Right temporal lobe with moderate edema (asterisks) and mild gliosis including gemistocytes (arrows) and microglia (arrowhead). Bar = 80 µm

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According to Young and others (2011), cortical thickening and peripheral localisation may be suggestive for oligodendrogliomas; however, the main MRI-diagnosis in the present case was suggestive of bilateral temporal lobe oedema.

MRI and histopathological examination of canine and feline patients with acute seizures have produced similar findings in the piriform and temporal lobes (Melemma and others 1999, Mariani and others 2001, Vanhaesebrouck and others 2012). SE may cause brain damage through a variety of mechanisms such as excitotoxic effects, hypoxia, lactic acidosis and ischaemia. Some neurons of the temporal lobe are known to be highly vulnerable to SE (Sommer 1880). With the present case, the authors would like to emphasise that seizure-induced temporal lobe changes can mask the primary pathology even when high-field (1·5 T) MRI is used. For better diagnosis it is recommended to repeat the imaging after the decrease of seizure-induced changes.

  • A. Pakozdy, D. Thaller*, M. Gumpenberger, M. Leschnik,

  • A. Galler, S. Shibly and A. Klang*

  • Clinical Department for Companion Animals and Horses,

  • Clinic for Small Animals Internal Medicine, University of

  • Veterinary Medicine Vienna, Austria

  • *Institute of Pathology and Forensic Veterinary Medicine,

  • University of Veterinary Medicine Vienna, Austria

  • Clinic of Diagnostic Imaging, University of Veterinary

  • Medicine Vienna, Austria


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  2. References
  • Koestner, A., Bilzer, T., Fatzer, R., Schulman, F. Y., Summers, B. A. & Van Winkle, T. J. (1999) Oligodendroglial tumors. In: Histological Classification of Tumors of the Nervous System of Domestic Animals. 2nd edn. Armed Forces Institute of Pathology, Washington, DC, USA. pp 19-20
  • Mariani, C. L., Platt, S. R., Newell, S. M., Terrell, S. P., Chrisman, C. L. & Clemmons, R. M. (2001) Magnetic resonance imaging of cerebral cortical necrosis (Polioencephalomalacia) in a dog. Veterinary Radiology and Ultrasound 42, 524-531
  • Melemma, L. M., Koblik, P. D., Kortz, G. D., Lecouteur, R. A., Chechowitz, M. A. & Dickinson, P. J. (1999) Reversible magnetic resonance imaging abnormalities in dogs following seizures. Veterinary Radiology and Ultrasound 40, 588-595
  • Sommer, W. (1880) Erkrankung des Ammonhorns als aetiologisches Moment der Epilepsie. Archiv für Psychiatrie und Nervenkrankheiten 10, 631-75
  • Vanhaesebrouck, A. E., Posch, B., Pleassas, I. N., Palmer, A. C. & Constantino-Casas, F. (2012) Temporal lobe neoplasia: a new cause of feline hippocampal necrosis? Proceedings of the 25th ECVN/ESVN Congress, Ghent, Belgium, September 14–15, 2012. p 80
  • Young, B. D., Levine, J. M., Porter, B. F., Chen-Allen, A. V., Rossmeisl, J. H., Platt, S. R., Kent, M., Fosgate, G. T. & Schatzberg, S. J. (2011) Magnetic resonance imaging features of intracranial astrocytomas and oligodendrogliomas in dogs. Veterinary Radiology and Ultrasound 52, 132-141