MRI findings in two West Highland White Terrier dogs with hepatic encephalopathy secondary to portosystemic shunt

Abstract

A portosystemic shunt is an abnormal communication between the portal vascular system and the systemic circulation. A significant number of clinical signs associated with portosystemic shunting result from hepatic encephalopathy (HE); a syndrome encompassing neurological signs such as including changes in behaviour, ataxia, unresponsiveness, pacing, circling, blindness, seizures, coma and death. We present two West Highland White Terrier dogs diagnosed with HE based on clinical signs, bile acid stimulation test and imaging of the abnormal vessel communicating the portal and the systemic circulation. Magnetic resonance sequences of the brain revealed a poorly marginated and diffuse, bilateral and symmetric hyperintense lesions on T2-weighted, fluid attenuation inversion recovery and diffusion-weighted sequences relative to the brain parenchyma including the medial longitudinal fasciculus and reticular formation in the brainstem. No abnormalities were detected on T1-weighted sequences.

Brain MRI findings in a dog with late onset epileptic seizure after portosystemic shunt attenuation

“…CT angiography of the liver has recently become recognised as the diagnostic method of choice for dogs with congenital extrahepatic PSS 2. MRI findings of the brain in dogs with non‐surgically treated PSS have been previously reported,3–7 but brain changes after PSS ligation have not been described.…”

The link between neurology and behavior in veterinary medicine: A review

“…A: Chiari-like malformation and syringomyelia (Rusbridge et al, 2019;Sparks et al, 2018;Wrzosek et al, 2015), hydrocephalus (Horwitz, 2015), hydranencephaly (Davies et al, 2012), porencephaly (Davies et al, 2012). M: bromethalin toxicosis (Dorman et al, 1990), hepatic encephalopathy (Chrisman, 1994;Fernandes et al, 2019), hyperadrenocorticism (Bernardini, 2010), hyperthyroidism/hypothyroidism (Bernardini, 2010), hypocalcemia (Overall, 2003), hypomagnesemia (Bernardini, 2010), L-2-hydroxyglutaric aciduria (Abramson et al, 2003), lead poisoning (Bernardini, 2010), loperamide toxicity (Bernardini, 2010), lysosomal storage diseases (Skelly and Franklin, 2002). I:…”

“…A: hydrocephalus (Chrisman, 1994;Horwitz, 2015), Chiari-like malformation and syringomyelia (Rutherford et al, 2012). M: hepatic encephalopathy (Chrisman, 1994;Fernandes et al, 2019), hypocalcemia and hypomagnesemia (Falzone and Lowrie, 2011), L-2-hydroxyglutaric aciduria (Abramson et al, 2003), lead poisoning (Bernardini, 2010), thiamine and taurine deficiency (Falzone and Lowrie, 2011;Overall, 2003), uremic syndrome (Overall, 2003). I: idiopathic epilepsy (Packer et al, 2018(Packer et al, , 2016Watson et al, 2018).…”