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Concentrations of homovanillic acid (HVA), 5-hydroxyindoleacetic acid (5-HIAA) and 3-methoxy-4hydroxyphenylglycol (MHPG) were measured in lumbar CSF from 33 patients with affective illness and from 23 neurological controls. The group of patients with affective illness comprised 29 depressed and four manic patients. During illness, the concentration of HVA was higher in the depressed patients (P < 0.001) than in the controls. Both unipolar and bipolar depressed patients had increased HVA levels (P < 0.001 and P < 0.05, respectively). The concentration of MHPG was greater than control values in the unipolar (P < 0.01) and bipolar (P < 0.02) subgroups but did not differ from control values in the depressed group as a whole. The concentration of 5-HIAA in the depressed patients as a whole and in the unipolar and bipolar subgroups did not differ from control concentrations. During illness the manic patients had increased levels of HVA (P < 0.01) and normal levels of 5-HIAA and MHPG. Sixteen of the 29 depressed patients had a second lumbar puncture after they had r e covered. Compared with the pre-recovery values, the concentration of HVA was reduced in the unipolar depressives (P < 0.01) and the concentration of 5-HIAA lowered in the depressed group as a whole (P < 0.02).The present findings suggest involvement of catecholamines in affective disorders.

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In the presence of glucose (2 mg/ml), leucine (10 mM) noticeably increased islets' NADPH contents as well as the NADPH:NADP ratio; the changes occurred as soon as 1 min after its addition. NADH concentrations were also increased by leucine. The NADPH:NADP ratio as well as insulin release stimulated by glucose plus leucine were markedly decreased by methylene blue. The thiol oxidants diamide and tert-butyl hydroperoxide also inhibited insulin secretion in response to glucose plus leucine. Employing the perfused pancreas technique, the insulin-releasing action of p-chloromercuribenzoate was further enhanced by leucine. The combined effects were inhibited by tert-butyl hydroperoxide, however. Our data suggest that the insulin-releasing action of leucine depends on the islets' NADPH and reduced glutathione (GSH); in addition, leucine may contribute to insulin secretion by increasing the islet NADPH:NADP ratio and the NADH:NAD ratio. From the data, we assume that the observed increase of NADPH may lead via GSH to an increase in the number of such thiol groups in the beta-cell membrane, which are believed to be related to stimulation of insulin release and, thus, to increase the sensitivity of the beta-cell to stimulation by glucose and/or leucine.

The intraventricular pressure was compared with conductance to outflow of CSF (Cout) in 12 patients with high-pressure hydrocephalus of less than 3 months duration. Cout was measured by a lumbo-ventricular or a ventriculo-ventricular perfusion test. In all patients Cout was very low (median 0.016 ml mm Hg-1 minute-1). Thus high-pressure hydrocephalus may be considered to be the consequence of a greatly increased resistance to resorption of CSF. The level of the measured ICP (mean: ICP 23.5 mm Hg) corresponded to the theoretical level calculated from the measured Cout. B-waves were observed during most of the recording periods and episodes of plateau waves were seen in all patients but one. In this particular group of patients, the unsatisfactory results of ventriculo-atrial shunting emphasize the high risks associated conditions leading to high-pressure hydrocephalus.