Cats undergoing excision of intracranial meningiomas had a low perioperative mortality and a long-term prognosis of more than 3 years.

The primary study objective was to determine whether clinical examination and magnetic resonance imaging (MRI) can underestimate canine gliomatosis cerebri (GC); we also investigated immunohistochemical features. Seven dogs with GC were studied; four recruited specifically because of minimal MRI changes. Neuroanatomic localization and the distribution of MRI, gross and sub-gross lesions were compared with the actual histological distribution of neoplastic cells. In six cases, clinical examination predicted focal disease and MRI demonstrated a single lesion or appeared normal. Neoplastic cells infiltrated many regions deemed normal by clinical examination and MRI, and were Olig2-positive and glial fibrillary acid protein-negative. Four dogs had concurrent gliomas. GC is a differential diagnosis for dogs with focal neurological deficits and a normal MRI or a focal MRI lesion. Canine GC is probably mainly oligodendrocytic. Type II GC, a solid glioma accompanying diffuse central nervous system neoplastic infiltration, occurs in dogs as in people.

Objective To describe the successful case management of an extradural hematoma secondary to anticoagulant rodenticide toxicity causing spinal compression and paraplegia. Case Summary A 3‐month‐old, female intact, mixed breed dog was presented for a 12‐hour history of paraplegia. CBC and biochemistry results were unremarkable, and a coagulation panel revealed prolonged prothrombin time with normal activated partial thromboplastin time. Magnetic resonance imaging revealed an extradural compressive lesion within the vertebral canal extending from T6 to T11, most consistent with an extradural hematoma. Further coagulation testing revealed a coagulopathy caused by vitamin K1 deficiency and confirmed exposure to the anticoagulant rodenticide, diphacinone. The dog was medically managed with fresh frozen plasma, aminocaproic acid, and oral vitamin K1 therapy. A right‐sided T6 to T11 hemilaminectomy was later performed for removal of the extradural hematoma and spinal decompression. The dog's neurological status gradually improved postoperatively and, at the time of discharge, was nonambulatory paraparetic with voluntary micturition. Four weeks postoperatively, the dog had normal prothrombin and activated partial thromboplastin times and was nonambulatory paraparetic with strong motor function. New or Unique Information Provided This is the first reported case of a dog with an extradural hematoma secondary to anticoagulant rodenticide causing spinal cord compression and neurological deficits. Surgical management of this case was successful and resulted in improvement of neurological signs. Extradural hematoma should be considered as a potential location of bleeding in rodenticide toxicity as well as a differential diagnosis in patients with neurological deficits.