The dog was hit by a car and had external head wounds but was neurologically normal. The head wound was superficial and was debrided. The debridment did not result in entry into the frontal sinus. However, an underlying comminuted right frontal bone fracture was detected and several small bone fragments were removed. Three weeks later, the dog developed what the owners perceived to be back pain. Within 2 days, the perceived pain progressed to inability to rise, leaning to the left, circling to the left, leftsided head tilt, and behavioral change. The dog was then referred for further evaluation. At this time, the dog had loss of menace response in the left eye, loss of corneal reflex in the left eye, head tilt to the left, tongue deviation to the left, positional nystagmus, and severe vestibular ataxia. The pupillary light responses and palpebral reflexes were normal. The proprioceptive reactions and myotatic reflexes were normal and no back pain was elicited. Clinical signs and neurologic examination suggested a multifocal CNS lesion. Because of the dog's clinical signs and history, the major considerations were meningoencephalitis, intracranial hemorrhage, and tension pneumocephalus.The leukocyte count was elevated at 20,900 cells/ml. The leukogram was consistent with a glucocorticoid-induced leukocytosis with increased segmented neutrophils at 19,019 cells/ml, decreased lymphocytes at 627 cells/ml, and a normal band neutrophil count. There was increased blood glucose at 214 mg/dl, also consistent with a stress response. The coagulation profile was normal.

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Background Seizures in the early postoperative period after intracranial surgery may affect outcome in dogs. Objectives To determine the incidence of early postoperative seizures (EPS) in dogs with brain tumors, identify specific risk factors for EPS, and determine if EPS affects outcome. Animals Eighty‐eight dogs that underwent 125 intracranial surgeries for diagnosis and treatment of rostrotentorial brain tumors. Methods Retrospective cohort study. All patients with a diagnosis of rostrotentorial brain tumor from 2006 to 2020 were included. Early postoperative seizures were diagnosed by observation of seizure activity within 14 days of neurosurgery. Previously diagnosed structural epilepsy, perioperative anticonvulsant drug (ACD) use, magnetic resonance imaging (MRI), and tumor characteristics were evaluated. Outcome measures included neurologic and nonneurologic complications, duration of hospitalization, and survival to discharge. Results Dogs with rostrotentorial brain tumors had EPS after 16/125 (12.8%) neurosurgical procedures (95% confidence interval [CI], 7%‐19%). Presence of previous structural epilepsy was not associated with EPS risk (P = 1). Perioperative ACD use also was not associated with EPS (P = .06). Dogs with EPS had longer hospitalization (P < .001), were more likely to have neurologic complications postsurgery (P = .01), and were less likely to survive to discharge (P = .01). Conclusions and Clinical Importance It is difficult to predict which dogs are at risk of EPS because the presence of previous structural epilepsy and the use of perioperative ACDs was not associated with EPS. However, seizures in the early postoperative period are clinically important because affected dogs had prolonged hospitalization, more neurologic complications, and decreased short‐term survival.

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Three juvenile dogs presented with an acute onset of paraspinal hyperesthesia and/or neurologic deficits. These dogs underwent anesthesia for MRI and additional diagnostics. The thoracolumbar MRI in Dog 1 revealed an accumulation of T2-weighted (T2W) hyperintense, T1-weighted (T1W) iso- to hyperintense, contrast enhancing extradural material. The differential diagnoses were meningitis with secondary hemorrhage or empyema or late subacute hemorrhage. The initial cervical MRI in Dog 2 revealed T1W meningeal contrast enhancement suspected to be secondary to meningitis. A repeat MRI following neurologic decline after CSF sampling revealed a large area of T2W and T1W hyperintensity between fascial planes of the cervical musculature as well as T2W iso- to hyperintense and T1W iso- to hypointense extradural material at the level of C1 consistent with hemorrhage. The cervical MRI in Dog 3 revealed T2W hyperintense and T1W iso- to hypointense extradural compressive material consistent with hemorrhage. Dogs 1 and 2 underwent CSF sampling and developed complications, including subcutaneous hematoma and vertebral canal hemorrhage. Dog 3 underwent surgical decompression, which revealed a compressive extradural hematoma. In each case, a hemophilia panel including factor VIII concentration confirmed the diagnosis of hemophilia A. Dog 1 had a resolution of clinical signs for ~5 months before being euthanized from gastrointestinal hemorrhage. Dog 2 was euthanized due to neurologic decompensation following CSF sampling. Dog 3 did well for 2 weeks after surgery but was then lost to follow-up. This case series provides information on clinical signs, MRI findings, and outcome in 3 juvenile dogs with hemophilia A that developed neurologic deficits or paraspinal hyperesthesia secondary to spontaneous or iatrogenic vertebral canal hemorrhage. Hemophilia A should be considered as a differential in any young dog presenting with an acute onset of hyperesthesia with or without neurologic deficits. This diagnosis should be prioritized in young male dogs that have other evidence of hemorrhage on physical exam.