A 36 year-old female patient with schizophrenia and Tourette syndrome is described. Clinical course, present neurological and psychopathological state, results of psychological testing, computed tomography and MR tomography of the skull, EEG and evoked potentials are reported. Results of neurochemical analysis of CSF and plasma are presented. Possible relationships between Tourette syndrome and schizophrenia are discussed with particular reference to neurochemical findings.

In an open trial, 15 patients with PD (mostly stage V) were treated with the partial DA agonist, terguride, a derivative of lisuride. To the basic therapy, consisting of L-dopa plus benserazide and amantadine, a slowly increasing dosage of TDHL up to a maximum of 1.5 mg/day t.i.d. was added. There were 3 drop-outs; 12 patients completed the trial which lasted for 12 weeks. At this time a significant improvement in total score, bradykinesia, and functional score was seen, as well as a marked improvement in tremors score in the patients who showed this symptom (Columbia Rating Scale). As side-effects, dyskinesias occurred in two patients, psychotic symptoms in one, and marked orthostatic symptoms in one patient. No significant differences before and after 12 weeks TDHL treatment were found in the concentrations of noradrenaline, adrenaline, serotonin, and 5-hydroxy-indole-acetic-acid in plasma. It is concluded that TDHL is effective even in advanced stages of PD, and it is speculated that partial DA agonists may become important in the treatment of PD and might possibly have an advantage over "classical" DA agonists.

The discovery that MAO can be differentiated biochemically and pharmacologically into two forms, types A and B, with different substrate specificities and inhibitor sensitivities has renewed the interest in MAO inhibiting as a therapeutic agent. L-Deprenyl, a selective inhibitor of MAO-B, was introduced by us into clinical use as an adjunct to L-DOPA some years ago. This drug has found therapeutic importance in that it can potentiate the pharmacological action of L-DOPA. The mechanism underlying the action of L-deprenyl is thought to be related to its inhibition of MAO-B and thus increased levels of PEA and DA, as measured in the striatal and limbic region of human brain. Animal studies have indicated the MAO-A is mainly, but not exclusively, located in brain neurons, while MAO-B is preferentially placed in glia and astrocytes. In general human and primate brain studies show similar MAO distribution. The observation that MAO-B activity could not be located in the catecholaminergic neurons of human brain by the use of monoclonal antibody studies seriously questions the validity of this technique. The exact locations of MAO-A and -B in human brain are important to understand the mechanism of L-deprenyl action as an antiparkinson drug. If there is an absence of MAO-B from dopaminergic neurons, one may now consider that MAO-B activity within glia plays a far more important role than hitherto considered. This, however, is questionable.

Comparing the pattern of serotonin, 5-hydroxyindole acetic acid, 3,4-dihydroxyphenyl acetic acid and homovanillic acid in five brain areas of one dysphoric patient to those of 3 depressed patients it seems that dysphoria biochemically is a state between depression and mania. Dynamically, dysphoria may possibly be seen as a behavioral correlate of a switch process between high and low turnover of neurotransmitters (rather high frequency in comparison to bipolar disorder with very low frequency). However, the biochemical data are obviously in agreement with psychiatric findings, i.e. that dysphoria in any case is an extremely labile state.