Multifocal Ischemic Brain Infarctions Secondary to Spontaneous Basilar Artery Occlusion in a Dog with Systemic Thromboembolic Disease

A 6-year-old, male intact Chihuahua was presented to the Veterinary Teaching Hospital of the University of Bern after experiencing a single generalized seizure. The dog was hypothermic (rectal temperature, 36.1°C), obtunded and had a non-ambulatory tetraparesis. Postural reactions were reduced in all 4 limbs and a right-sided head tilt, a severely reduced menace response, delayed direct and consensual pupillary light reflexes, and bilaterally absent nasal sensation and corneal reflexes were present. Other cranial nerve reflexes and segmental spinal reflexes were considered normal, and no pain response was elicited on spinal palpation or by passive movement of the head and neck. The clinical findings were consistent with multifocal intracranial disease with involvement of the forebrain and brainstem. There was regenerative anemia (hematocrit 0.33 L/L; reference range, 0.39–0.57 L/L, reticulocytes 209.6 9 10/ L; reference range, 10.9–111.0 9 10/L), a neutrophilic left shift (band neutrophils 0.55 9 10/L; reference range, 0.0–0.3 9 10/L) without neutrophilia (8.31 9 10/L; reference range, 3.0–11.5 9 10/L) and lymphopenia (0.6 9 10/L; reference range, 1.0–4.8 9 10/L). Hypokalemia (3.71 mmol/L; reference range, 4.22–5.43 mmol/L), hypocalcemia (2.15 mmol/L; reference range, 2.42– 2.85 mmol/L), hypocholesterolemia (2.89 mmol/L; reference range, 3.47–10.03 mmol/L), hypoproteinemia (48.4 g/L; reference range, 56.0–73.0 g/L), hypoalbuminemia (24.1 g/L; reference range, 30.0–40.5 g/L), a low serum creatinine concentration (29 lmol/L; reference range, 52–117 lmol/L), hyperbilirubinemia (21.3 lmol/L; reference range, 0.5–3.9 lmol/L), and increased activity of alanine aminotransferase (661 IU/L; reference range, 26–126 IU/L), alkaline phosphatase (251 IU/L; reference range, 9–132 IU/L), aspartate aminotransferase (343 IU/ L; reference range, 22–76 IU/L), creatine kinase (781 IU/ L; reference range, 64–400 IU/L), gamma-glutamyl transferase (19 IU/L; reference range, 1–7 IU/L), and glutamate dehydrogenase (45 IU/L; reference range, 2–10 IU/ L) were present. Abnormalities were not noted on urinalysis and oscillometric blood pressure measurements were within normal limits. Right and left lateral thoracic radiographs revealed mild generalized cardiomegaly without evidence of congestive heart failure, minimal pleural effusion, and reduced abdominal detail. Abdominal ultrasound revealed mild anechoic fluid with signs of peritonitis and steatitis of the abdominal fat, hepatomegaly and mild bilateral pyelectasis. Abdominocentesis revealed a clear fluid with low total protein concentration (12 g/L), consistent with transudate. Magnetic resonance imaging (MRI) of the brain revealed multifocal intra-axial, sharply delineated lesions, mainly affecting the gray matter in the cerebellar vermis, right brainstem, left thalamus, right caudate nucleus, and dorsolaterally in the area of the right parietal and occipital lobes without mass effect. These lesions were hyperintense on T2-weighted (T2W) and fluid attenuation recovery (FLAIR) sequences, and hypointense on T1-weighted (T1W) sequences with no contrast enhancement after intravenous administration of 0.15 mmol/kg gadodiamide and no evidence of hemorrhage on T2*-weighted (T2*W) gradient echo sequences (Figs 1A, 2A). The lesions were hyperintense on diffusion weighted images (DWI), and hypointense on the apparent diffusion coefficient (ADC) map, indicating restriction of diffusion (Figs 1B, 2B). No abnormality of the basilar artery was observed on conventional T1W and T2W spin echo, FLAIR, T2*W, and DWI MRI sequences, however, MR angiography was not performed. MRI findings were compatible with multifocal, acute, ischemic infarction. Cerebrospinal fluid, collected from the cerebellomedullary cistern, contained 27 white blood cells per From the Division of Neurological Sciences, (Salger, Vandevelde, Henke); the Division of Clinical Neurology, (Salger, Vandevelde, Henke); the Department of Clinical Veterinary Medicine, (Salger, Stahl, Vandevelde, Henke); the Division of Clinical Radiology, (Stahl); and the Department of Veterinary Pathology, Vetsuisse Faculty, University of Bern, Bern, Switzerland (Piersigilli). Corresponding author: F. Salger, Division of Neurological Sciences, Vetsuisse Faculty, University of Bern, 3012 Bern, Switzerland; e-mail: [email protected]. Submitted March 28, 2014; Revised June 9, 2014; Accepted July 30, 2014. Copyright © 2014 by the American College of Veterinary Internal Medicine DOI: 10.1111/jvim.12447 Abbreviations: