Tennessee Medicine E-Journal


The term hepatic encephalopathy (HE) refers to a syndrome of potentially reversible cerebral dysfunction associated with hepatic insufficiency. Clinical features varied from slight behavioral changes to coma or even death. Although the pathogenesis of HE is not well understood, increased ammonia and manganese might play a role or lead to encephalopathy. Ammonia is assumed to affect brain metabolism and/or neurotransmission by either directly or indirectly. Acute ammonia intoxication affects different cerebral processes and leads to activation of the N–methyl–D–aspartate (NMDA) type of glutamate receptors in brain which is subsequently cause cell swelling and neuron degeneration due to influx of several ions. It has shown in animal studies that NMDA receptor antagonists have an effect to prevent or delay neuronal loss after hepatic failure. In this article we share our observations about efficacy and tolerability of amantadine sulfate in a patient who has parkinsonism secondary to chronic liver disease.

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Coronal and axial T1-weighted magnetic resonance images of the brain in a patient with chronic liver failure and parkinsonism. The bilateral and symmetric high T1 signal intensity changes involving the globus pallidus can be seen.

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Frontal intermittent rhythmic delta activity supports the diagnosis of toxic or metabolic encephalopathy.