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Hepatic encephalopathy AbstractHepatic encephalopathy (HE) is a neuropsychiatric disorder which can appear as a complication of acute or chronic liver disorders. Pathophysiologically the disorder is a clinical manifestation of a low-grade chronic cerebral edema, which leads to changes in astrocytic function with disturbances of glioneuronal communication. The findings point to a disturbance of cerebral oscillatory networks in HE that is triggered by possible neurotoxic- and hydration-sensitive, thalamic structures and results in an abnormally low-frequency and rigid thalamocortical and corticomuscular coupling. While the diagnosis of high-grade HE will be done exclusively by the clinical picture, psychometric and neurophysiological tests are necessary to diagnose the low-grade forms. Yet, the analysis of the critical flicker frequency (CFF) has been shown to be an easy and simple semi-quantitative test procedure for the quantification and follow-up of neuropsychiatric deficits in HE. The recognition and consequent treatment of the precipitating factors are the most important therapeutic measures. These are complemented by dietetic and pharmaceutical treatment.
The case of a patient with largely preserved intelligence, but severe and persistent memory impairments is reported. FA, a 46-year-old patient with the diagnosis of prolonged depression was investigated repeatedly over a two year period with neuroradiological, neuropsychological, neuromonitoring and other methods. While no brain damage was detectable in FA, he manifested continued and severe anterograde and retrograde memory disorders together with an inhibition in his thinking processes. Otherwise, his intellectual capabilities were in the normal range, that is he was not pseudo-demented. Various approaches with drug treatment and psychotherapy failed to improve his condition.
The condition is interpreted as ‘mnestic block syndrome’ and is considered to be related to an altered brain metabolism which may include changes in various transmitter and hormonal systems (GABA-agonists, glucocorticoids, acetylcholine). Whether depression contributes to this syndrome is uncertain from FA's cognitive performance, but may be a possibility.
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