[Hepatic encephalopathy]. / Hepatische Enzephalopathie.

Hepatic encephalopathy (HE) is a neuropsychiatric complication of acute and chronic liver disease. Its etiology and pathogenesis are thought to be a complex, metabolically induced, and therefore potentially reversible disturbance in brain functions. The diagnosis is based on demonstrating both a disorder of the central nervous system and a concomitant liver disease as well as the exclusion of any neurological or psychiatric disorder of other etiology. The diagnosis of HE is clinical and displays a wide spectrum of neuropsychiatric symptoms in different degrees of severity. Ancillary diagnostic workup includes laboratory tests, neuroimaging, and neurophysiological exams such as electroencephalography and evoked potentials. The therapy of HE mainly consists of treatment and avoidance of any precipitating conditions such as high protein intake, infections, and gastrointestinal bleeding. Other therapeutic approaches modulate metabolic processes such as ammonium synthesis and excretion, formation of neurotransmitters, and as a last resort liver transplantation. The prognosis depends ultimately on the course of the liver disease.

Short-term effects of CHO, fat and protein loads on total tryptophan/tyrosine levels in plasma as related to %REM sleep.

The effect on plasma amino acid levels and sleep parameters of three experimental diet conditions was investigated in 12 healthy young men. A total of 71 sleep records and 715 plasma samples were analysed for %REM (TDT) and total plasma tryptophan and tyrosine respectively. The ratio of tryptophan to tyrosine was virtually the same under the fat supplement as under the nosupplement conditions. The ratio associated with the CHO load was found to be 14 per cent higher, however. A 29 per cent higher value found with the Protein load may be misleading due to the nature of the supplement used. %REM (TDT) was not found to be significantly related to any of the above conditions.

Weight gain and the sleeping electroencephalogram: study of 10 patients with anorexia nervosa.

The relation between reduced nutritional intake, with consequent weight loss, and sleep disturbance was studied by comparing certain sleep encephalogram patterns in a group of inpatients with anorexia nervosa before, during, and after a regimen of refeeding with a normal diet to a matched population mean weight. At low body weights patients had less sleep and more restlessness, especially in the last four hours of the night. During refeeding and weight gain slow-wave sleep initially increased and then tended to decrease during the final stage of restoration of weight back to matched population mean levels. With the overall weight gain, however, there was a significant increase in length of sleep and rapid eye movement sleep, the latter increasing especially during the later stages of weight gain. These results reaffirm that insomnia, and especially early morning waking, is associated with low body weight in anorexia nervosa, and their implications are discussed with particular reference to a hypothetical association between various anabolic profiles and the need for differing components of sleep.

Plasma tryptophan and sheep.

Free, bound, and total plasma tryptophan (F.P.T., B.P.T., and T.P.T.) levels have been measured throughout the night in six young female volunteers. All-night polygraphic sleep recordings were also made. No direct temporal relationship was found between plasma tryptophan levels and specific sleep stages. The mean F.P.T. levels, however, were found to have a positive correlation with rapid-eye-movement (R.E.M.) sleep and a negative correlation with non-R.E.M. sleep. An inverse relationship existed between the F.P.T. and B.P.T. levels. There appeared to be a diurnal variation in F.P.T. levels, with high readings in the first half of the night.