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Hepatic encephalopathy (HE) is an extremely rare cause of focal seizures and is usually a diagnosis of exclusion when more commoner causes such as infection, autoimmune and malignancy have been discounted. The literature reports patients with generalised cerebral oedema and rarely status
Hepatic encephalopathy is a serious complication of cirrhosis that presents with a variety of neuropsychiatric abnormalities, including disorientation, asterixis, and coma. Seizures are an uncommon and potentially dangerous complication of hepatic encephalopathy. We present a unique Hepatic encephalopathy represents a reversible decrease in neurological function caused by liver disease. Overall incidence of seizures in hepatic encephalopathy varies between 2% and 33%. Non-convulsive status epilepticus may be particularly common in these patients. Psychiatric disturbances
OBJECTIVE
To determine if a model of hepatic encephalopathy (HE) exhibits decreased sensitivity to the neuronal effects of a drug that induces seizures as a consequence of decreasing GABA-mediated inhibitory neurotransmission.
METHODS
3-Mercaptopropionic Acid (MPA) is an inhibitor of L-glutamate
Seizure is the second most common neurologic complication after liver transplantation and may be caused by metabolic abnormalities, electrolyte imbalance, infection, and immunosuppressant toxicity. A 61-year-old male patient underwent liver transplantation due to hepatitis B virus-related liver
To assess neuronal mechanisms of potential importance in the pathogenesis of hepatic encephalopathy, visual evoked potentials were recorded in rabbits with acute hyperammonemic encephalopathy, postictal coma, and toxin-induced coma resulting from the administration of a combination of subcoma doses
OBJECTIVE
It is known that patients with convulsion often present hyperammonemia. The elevation of ammonia levels in convulsion is considered to occur along with extensive muscle contractions, but the details remain unclear. In emergency pathologies, such as cardiopulmonary arrest or hemorrhagic
Between 1999 and 2012, 11 cases of congenital portosystemic shunts (cPSS) resulting in hepatic encephalopathy were diagnosed in goat kids necropsied at the California Animal Health and Food Safety Laboratory System and at the Department of Pathology, Immunology & Microbiology, School of Veterinary
A previous study of the patterns of visual evoked responses (VERs) in rats was interpreted as providing support for the synergistic neurotoxins hypothesis of the pathogenesis of hepatic encephalopathy (HE) due to fulminant hepatic failure (FHF). In contrast, other studies of the patterns of VERs in
Increased intracranial pressure is present in more than 80% of patients with fulminant hepatic failure. However, patients with encephalopathy secondary to chronic liver disease are thought not to develop elevated intracranial pressure. We report two patients with chronic liver disease in hepatic
OBJECTIVE
Transient hyperammonemia can occur after episodes of seizure. To verify that transient hyperammonemia is a unique finding in seizure patients, we compared the change in blood ammonia concentration during the postictal period with that of other patients who suffered consciousness
A 45-year-old man with alcohol-related decompensated cirrhosis presented with jaundice, fever, headache and altered sensorium. At presentation, he had tachycardia, disorientation to time and place, asterixis, icterus and upgoing plantar response. Investigations showed anaemia, thrombocytopenia,
The definition of hepatic coma has been used for the most severe course of hepatic insufficiency, independent from the pathogenesis. This means, that from the psychiatric point of view the hole survey of the exogen reaction type was subdivided. The neurologic symptomatology was rather neglected. In
Patients with epilepsy may suffer from renal or hepatic diseases that interfere with their antiepileptic drug (AED) treatment. Furthermore, such diseases may themselves cause seizures. Reduced renal function and hypoalbuminemia lead to accumulation of renally excreted AEDs, such as gabapentin,
A 6-year-old ShihTzu presented with tonic-clonic cluster seizure. T2-weighted magnetic resonance (MR) images showed bilateral diffuse hyperintense lesions at the cerebral cortex with enlarged sulci. Computed tomography revealed a portosystemic shunt (PSS) and azygos continuation. Based on the