Pharmakopsychiatrie, Neuro-Psychopharmakologie最新文献

The antidepressive effect of viloxazine (300 mg/d) was investigated during three weeks in 41 patients with depressive syndromes requiring drug-treatment against amitriptyline (150 mg/d), using a controlled double-blind design. Viloxazine differs from amitriptyline by selective inhibition of norepinephrine re-uptake, whereas amitriptyline acts also on serotonin re-uptake. Psychopathological changes were documented by means of the Hamilton Depression Rating Scale, the Bf-S (v. Zerssen), the AMDP-System, and videotaped recordings. Besides routine clinical-chemical tests, the serum concentrations of viloxazine and partly of amitriptyline were determined. Repeated EEG-recordings were evaluated by spectral analysis. The number of global responders and non-responders -- defined according to the final HDRS-scores -- was equally distributed between the two drug-groups. The AMDP-evaluation suggests that viloxazin has a somewhat more marked and more rapid effect on symptoms of retardation, whereas amitriptyline acts predominantly on depressive mood, disturbances of sleep and vital feelings. The EEG-profile of both drugs was similar to the spectral changes seen under tricyclic antidepressants, through only the viloxazine-induced changes reached statistical significance on the 10th and 20th day, the variability of the EEG-recordings being greater in the amitriptyline group. The viloxazine blood levels showed a remarkably low inter- and intraindividual variance. Steady state was reached at day 5 at the latest. Amitriptyline serum concentrations still increased between the 10th and the 21st day. The average blood concentration of viloxazine was higher in the responder- than in the non-responder-group.

Only about 1/4 of the statements made by the patients or accompanying persons regarding preclinical medication proved to be true. In about 66% of the cases 1--5 drugs were not stated during the first interview, while in 10% of the cases more drugs were stated than had actually been taken. Among the substances which had remained anonymous, the main shares are represented by benzodiazepines (28%), narcotic drugs (19%), neuroleptics (15%) and alcohol (15%). If one relates the number of false statements to the individual patients grouped according to diagnoses, the relatively highest quota of defaulters is found among the addicts, namely, 100%. This means that all the addicts had made false statements. The second rank is occupied by the alcoholic group who made 66% false statements, followed by the patients suffering from psychoses with 52% false statement, and the depressive patients with 47% false statements.

Two case reports and data from literature on the subject are used by the authors to describe characteristics of pathogenetic importance of neuroleptic induced stupor (NIS). The origin of NIS is outlined briefly and some fundamental clinical and experimental facts are presented, all of which stress the importance of the acute blockade of postsynaptic DA-ergic receptors. Emphasis is placed on the significance of the possible relationship and similarity between NIS and catatonic stupor, and on the theoretical possibilities which this offers.

A sample of 8 young and 8 elderly subjects was examined in a 2x2x2 factorial design, whether and how promazine interacts with pentobarbital as a hypnotic agent. Analyses of self-reports led to the following conclusions: 1. Young subjects and not experience any significant effects from either the single components (pentobarbital, promazine) and/or their combination. 2. Elderly subjects experienced positive effects in sleep and hangover parameters under the single components as well as under the combination. Consequences for research in clincal psychopharmacology are discussed.

Amitriptyline (AMI) was studied in rats snd mice in order to find out whether it had a central antiserotonin activity, previously demonstrated for doxepin - a compound chemically related to AMI. It was observed that AMI at low doses antagonized the head twitch response to L-5-hydroxytryptophan or 5-methoxytryptamine, as well as tryptamine-induced convulsions. In the hind limb flexor reflex preparation of the spinal rat AMI acted as a serotonin antagonist: when administered alone, it did not change the flexor reflex but prevented its stimulation induced by serotoninmimetics (LSD, quipazine, fenfluramine) not affecting that one evoked by noradrenalinemimetics (clinidine). At higher doses, AMI revealed a noradrenolytic activity. The results indicate that AMI, similarly as doxepin, has a central antiserotonin activity.

In the search for the biochemical basis of the action of Piracetam, the effects of this encephalotropic substance on the neuronal and glial phospholipid metabolism was investigated. Piracetam increases the incorporation of 32P into phosphatidylinositol and phosphatidyl choline of both glia and neuronal cell bodies (Figs. 1 and 2). When taking the important role of phosphatidylinositol in the processes of synaptic transmission and axonal conduction into consideration, the data obtained in the present work suggest that piracetam may stimulate excitatory neurons and may be involved in the process of synaptic transmission. The stimulatory effect of piracetam on the incorporation of 32P into phosphatidylinositol and phosphatidyl choline appears to be mediated by noerpinephrine or another neurotransmitter. Glial cells, isolated from the cerebral cortex of a rabbit, contained approximately one-third more phospholipids per uint protein than the neuronal cell bodies. The distribution and pattern of phospholipid relative to the total amount, was rather similar in both cell types. The incorporation of 32P into phosphatidylinositol and phosphatidyl choline was somewhat faster in neurons than in glial cells. Compared to glial cells the neuronal cell fraction had a higher phospholipid turnover.

Measurements of beta-endorphin-like immunoreactivity have been performed in CSF and plasma of patients with schizophrenia and other neuropsychiatric disorders. The detection limit of the RIA was between 20--50 pg/ml (6--15 fmole/ml). In CSF the quantity of beta-endorphin-like immunoreactivity ranges up to 65 pg/ml. The data from schizophrenics and other neuropsychiatric patients show no obvious deviation from the results in a control group of medical patients with normal CSF findings. In plasma the immunoreactive beta-endorphin-like material ranges up to 250 pg/ml. There is only a small tendency to higher values in schizophrenic patients, if compared with different types of neuroses and affective and organic psychoses. In a second series of experiments also this tendency could not be reproduced. In 9 electroconvulsive treatments an increase of blood beta-endorphin-like immunoreactivity was observed 7 times. A possible endorphinergic mechanism in the mode of action of electroconvulsion is hypothesized.