Biomedical subjects
Publications and source records attributed to W M Herrmann.
Explore the source record for details and available documents.
Investigations of the psychotropic effects of progestogens employing the technique of quantitative pharmaco-EEG indicated that progestogens produce a profile similar to that of the minor tranquillizers. Healthy volunteers received single oral doses in a double-blind controlled study. A short review of the clinical literature adds support to the suggestion that progestogens have sedative properties.
Employing the technique of quantitative pharmaco-EEG investigations on the psychotropic effects of progestogens indicated that progestogens produce a profile similar to that of minor tranquilizers. A short review of the clinical literautre adds support to the suggestion that progestogens may have sedative/tranqulizing properties.
In a controlled double-blind trial 2X12 healthy male volunteers were tested during treatment with lithium sulphate (24--36 mval/d) or placebo. Volunteers were tested after one and two weeks' drug intake using the following tests: Quantitative pharmaco EEG, psychological performance and mood scales. In comparison to pacebo, lithium shows increased mistake duration of the pursuit rotor (MLS), decreased flicker fusion threshold and an impairment of mood. The EEG effects (decrease 7--9 cps, increase 20--50 cps) require further clarification.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
In a review article, clinical literature concerned with the psychotropic effects of androgens is presented, and the results of experimental clinical work from biochemistry, electrophysiology and psychoexperimental tests are reported. The conclusion that androgens do have psychotropic properties similar to those of well known psychotropic substances is based on evidence from a number of sources: Clinical observations of patients with androgen deficiency or excess, observations of the effect of androgen therapy, and lastly experimental work with methods developed especially for testing psychotropic substances.
Explore the source record for details and available documents.
Based on "quantitative pharmaco-EEG" using computer-analyzed EEG (CEEG) measurements, unknown CNS effects of lisuride hydrogen maleate (LHM) were established. CEEG profiles of LHM in low dosages (less than or equal to 10 mcg) are similar to CNS "inhibitory" compounds, while in higher dosages (25 mcg to 100 mcg) they resemble "psychostimulant" compounds. By measuring the brain function using computer period analysis of cerebral biopotentials, dose-efficacy relations were found (in the range of 25-75 mcg) which suggest the bioavailability of LHM at the CNS level. By comparing the CEEG profiles of LHM with the previously studied compounds, five different clinical uses of LHM were predicted. The pilot trials suggest that LHM may have therapeutic potentials in patients with "aging" and/or organic brain syndromes, and in children with behavioral disturbances.
The somatosensory evoked potential (SEP) of physically and mentally healthy male subjects was recorded before as well as 4 hours after administration of one single dose of placebo, cyproterone acetate (an antiandrogen), and mesterolone (an androgen). Quantitative evaluation of drug-induced changes in SEP latencies and amplitudes, which, when plotted in terms of t-values, result in the so-called "SEP profiles", did not demonstrate any significant alterations after placebo. Contrary to this, cyproterone acetate induced systematic and significant changes characterized by a latency increase in the early peaks and latency decrease in the late peaks of the SEP. Apart from the non-significant amplitude changes, such alterations were previously described by us as typical for drugs of the anxiolytic class. Mesterolone on the other hand, produced a significant latency decrease in the early part and a latency increase in the late part of the evoked response which was found to be typical for the SEP profiles of tricyclic antidepressants. The amplitude did not show any systematic changes. Based on step-wise discriminant analysis of these data we could significantly differentiate both hormones from placebo as well as from each other. A comparative analysis of low and high doses did not yield any significant differences between the two levels. It was concluded that both test substances have psychoactive properties; whereas cyproterone acetate reveals anxiolytic qualities, mesterolone exhibits antidepressant ones. These findings are discussed from the clinical as well as from the neurophysiological point of view.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
There is convincing evidence that the functions of sleep include restoration of brain energy storage and memory consolidation. The circadian timing system (CTS) is involved in the daily variation of almost any physiological and psychological variable evaluated thus far. Disturbances of the CTS can be clinically observed by their influence on the sleep-wake cycle, hormones, body temperature, and locomotor activity. This article reviews the basic mechanisms of circadian rhythm sleep disturbances, names the applicable diagnostic tools and specific therapeutic strategies, and thereby hints at the impact of circadian rhythm sleep disturbance on psychiatric disorders, especially disorders of affect and cognition. In light of the preventive, diagnostic, and therapeutic tools now available, a new round of chronobiological studies in psychiatry seems justified, promising, and necessary.
Explore the source record for details and available documents.
A 6-month double-blind, randomized, placebo-controlled clinical trial preceded by a 3-week single-blind, washout/run-in placebo phase was performed in male and female patients, 55-85 years of age with a clinical diagnosis of mild to moderate multi-infarct dementia according to DSM-III to evaluate the therapeutic efficacy and safety of nicergoline 30 mg b.i.d. Primary endpoints for efficacy were the changes in the Sandoz Clinical Assessment Geriatric Scale (SCAG) and Mini-Mental State Examination (MMSE) scores at the end of the treatment with respect to baseline. Secondary endpoints were Clinical Global Impression, 3 subtests of the Weschsler Adult Intelligence Scale and Blessed A scale for activities of daily living, and all endpoints in 2-month intervals. A total of 252 patients were screened, 136 patients entered the double-blind phase and were evaluated as intent-to-treat (ITT) patients. Fifteen patients were excluded from the efficacy analyses of valid cases (VC) due to protocol violations or because they dropped out of the study prematurely. Confirmatory efficacy analysis after 6 months of treatment revealed superiority of nicergoline treatment with p < 0.01 for both SCAG and MMSE scores (ITT and VC). Subsequent descriptive efficacy analysis resulted in significant differences in favor of nicergoline, in the majority of cases as early as 2 months after start of treatment. Nicergoline was well tolerated and a similar number of adverse events were observed in both the placebo and the nicergoline group.
In a pilot double-blind trial in 21 patients with learned or idiopathic insomnia (DSM-IIIR), patients received placebo for 1 week (nights 1-7), either active (zolpidem, 10 mg) or placebo treatment for 2 weeks (nights 8-21) and then placebo for a further week (nights 22-28). Variables to measure efficacy, rebound and withdrawal were assessed daily from day 1 to day 28. Polysomnographic recordings together with sleep cycle analysis were performed on nights 7, 21 and 28. Patients treated with 10 mg zolpidem for 2 weeks had significantly improved sleep efficiency at the end of the randomised double-blind phase compared with the placebo group. Fractionated sleep-cycle analysis showed an increase in slow-wave sleep during the first 2-hour cycle after sleep onset. During the withdrawal placebo week, most of the main sleep variables remained relatively stable in the zolpidem group (nights 22-28), and deteriorated further in the placebo group. At the end of the withdrawal phase, there was a statistically significant difference between groups, in favour of the zolpidem treatment, in sleep efficiency, total sleep time, absolute and percentage of time awake, and percentage of REM sleep. REM sleep, which was normal in both groups at baseline, decreased significantly in the placebo group between nights 22 and 28 (during the withdrawal placebo week) compared with the zolpidem treatment group, and the number of periods of time awake increased. Minor subjective complaints were recorded under zolpidem and were comparable with those under placebo. Zolpidem seemed to improve some important sleep variables, when assessed both objectively and subjectively. The sleep cycle analysis suggested a possible shift of slow-wave sleep to an earlier period of the night, with a more physiological sleep structure. There was no evidence for withdrawal or rebound after stopping the 2 weeks of zolpidem treatment, but rather signs that the effect of zolpidem outlasted active treatment. The present pilot study justifies a prospective confirmatory comparison of zolpidem with benzodiazepines in an adequate number of patients and withdrawal after 6-8 weeks of treatment.
A placebo-controlled, randomized double-blind study conducted at a general practitioner's surgery was designed to investigate the efficacy of bencyclane in 120 outpatients with cerebral dysfunctions based on organic brain syndrome. The study started with a 4-week placebo washout phase and then continued with a 12-week treatment phase. 200 mg Bencyclane-hydrogenfumarate was administered b.i.d. Efficacy was assessed by a doctor's symptom rating (SCAG) and a study nurse's rating (BGP) as well as by two performance tests (CFF and ZVT-G). Data from 106 patients (52 under bencyclane and 54 under placebo) were statistically analysed. More side effects were seen under bencyclane than under placebo, in particular insomnia, headache, akathisia, nausea and vomiting. As an a priori hypothesis, it was stated that after alpha-adjustment there should be a statistically significant difference in symptomatology (SCAG, BGP) and performance (CFF, ZVT-G). With regard to performance, the zero hypothesis could be rejected on the 5% level, and on the 1% level with respect to symptomatology. The experimental error on both the performance and the symptom level was below 6%. The drug effects were significant on a confirmatory level and are considered to be also of clinical relevance.