Gait deficits in liver disease: Hepatic encephalopathy and hepatic myelopathy

Abstract

Summary In this issue, the unusual clinical presentation of a horse diagnosed is described with severe liver cirrhosis and hepatic encephalopathy. The horse initially presented for thoracic and pelvic limb ataxia and weakness, and signs of forebrain disease were not apparent until later in the disease process. The typical pathology of central nervous system disease associated with liver disease is related to encephalopathy and forebrain disease; however, the spinal cord is occasionally also involved. Hepatic myelopathy is a rare syndrome usually associated with surgical or acquired portosystemic shunts, liver cirrhosis and/or portal hypertension in man. Where a gliopathy is the most prominent pathological feature seen in hepatic encephalopathy, in hepatic myelopathy the most remarkable feature is demyelination of the corticospinal tracts of the distal cervical and thoracic spinal cord with occasional axon loss. The clinical signs of hepatic myelopathy are spastic paresis/paralysis with normal sensory findings and preserved sphincter function. The prognosis for hepatic myelopathy is generally poor. In summary, in severe liver disease, motor deficits can occur secondary to the encephalopathy, but motor deficits can also occur as a result of spinal cord pathology such as seen in hepatic myelopathy. In examination of horses with myelopathies, liver disease as a cause of myelopathy should be included in our list of differentials.

Multisystemic bovine mycobacteriosis in a pony with neurological signs and weight loss

“…A diagnosis of HE was made on the basis of extreme elevations in hepatobiliary enzymes in conjunction with clinical signs of weight loss, obtunded demeanour, anorexia, hypersalivation and ataxia. These nonspecific signs are frequently reported in cases of severe hepatic impairment (West ; Nout ). An objective diagnosis of HE can be established by demonstrating hyperammonaemia, elevated serum bile acids, γ‐glutamyl transferase, aspartate transaminase and sorbitol dehydrogenase enzymes (Mair ); however, other studies have concluded that hyperammonaemia is not consistently a feature of HE (McGorum et al .…”