ABSTRACT. -Exposure of 20 subjects to negative ionisation was monitored by EEG. Negative ionisation was supplied by an Ionotron apparatus (Amcor-Amron, Herzlia-Israel) with an output of 3.5 x 105 ions/(cm3, sec) at 1 m distance. Objective findings in ten normal subjects showed reduction of the frequency of the alpha-waves from 10 or 11 down to 9 or 8 Hz, increase of the amplitude by up to 20%, advance of the alpha rhythm pattern from the occipital to the frontal area and general synchronisation of the EEG records of both hemispheres. These reactions were suppressed in 10 subjects by tranquillisers. Subjective findings included relaxation, alertness, improved working capacity and relief from the Serotonin Irritation Syndrome produced by the positive ionisation of hot, dry desert winds. INTRODUCTIONSulman e t al. (1970) have shown that about 30% of a normal population are sensitive to the electrical charges of the weather front. The positive air ions which are taken up by the lungs affect these subjects by being transferred to the thrombocytes which release their serotonin content and produce the "Serotonin Irritation Syndrome" . This is characterised by insomnia, tension, migraine, oedemuta, palpitations, dyspnoea, flushes, hyperperistalsis or pollakisuria (Sulman et al., 1970). Increase in positive air ionisation produces the above complaints as a prodromal syndrome of the hot dry Sharav wind which appears 1-2 days before arrival of the wind itself . lautients suffering from the Serotonin Irritation Syndrome can be cured either by antiserotonin drugs (Sulman, 1969) or by applying artificial negative air ionisation which gives relief to 75% of the suffering pgtients (Sulman et al., 1974). We have studied the rationale of negative ionising treatment on neurohormone excretion (Sulman et al., 1970). The present paper is devoted to its effect on the EEG. Preliminary investigations on this subject have been reported by Silverman and Kornblueh (1957). MATERIALS AND METHODSExperiments were carried out in the summer when the weather in Israel is stable and there are thus practically no fluctuations of external ionisation. Ten This paper is devoted to the m e m o r y of Dr Igho H.Kornblueh, the pioneer of ion therapy, who passed away in 1973 in Philadelphia. Working on this project in 1957 he concluded "that further r e s e a r c h on the effects of ionisation on the EEG is warranted".

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The antimuscarinic potency of dibenzepin (Noveril) was estimated by measuring (a) central in vivo effects in mice (antihypothermia and antitremor, both induced by oxotremorine), (b) peripheral in vivo activity (mydriasis caused by systemic administration of the drug), (c) the effects of dibenzepin on isolated smooth muscle from guinea pig ileum, and (d) in vitro determination of the affinity constant of dibezepine toward the muscarinic binding sites in whole mouse-brain homogenate. The data allowed the construction of a normalized antimuscarinic potency scale for some of the common tricyclic antidepressants. With a value of 1 for scopolamine, the following relative anticholinergic potencies were calculated: dibenzepin--1/600, nortriptylne--1/300, imipramine - 1/200, and amitriptyline - 1/75. These values suggest an explanation for the absence of clinically detectable anticholinergic side effects during treatment of depression with high doses of dibenzepin. Structural and spatial interrelations among various tricyclic antidepressants and scopolamine are discussed.

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Dibenzapine (720 mg, Noveril) was infused intravenously to 16 depressed patients during a period of 3 h. Serum prolactin levels were determined by radioimmunoassay and changes in clinical condition were evaluated according to the Hamilton Equation. The two variables were correlated to each other. In most of the patients Noveril caused a dramatic but short-lived improvement in depressive symptoms. There was much variability in the prolactin response to the drug. Serum prolactin levels showed a great elevation in 9 patients. In all patients the hormonal levels returned to their former normal levels after termination of the infusions. The treatment was then continued with Noveril per os. There was no significant correlation between serum prolactin levels and clinical condition or its change. The elevation of serum prolactin levels as a reaction to Noveril treatment may be explained by the prominent serotonergic action of Noveril. A time lag between serotonergic and dopaminergic actions of the drug when given in higher doses may be an additional explanation. Other possible hypotheses are discussed.