No abstract

Psychosomatic factors, sympathoneural and sympathoadrenal as well as cardiovascular mechanisms, were studied in 24 patients 18-24 years of age with borderline hypertension, 50 age-matched nonnotensive offspring of hypertensive parents, and 49 controls with no family history of hypertension. They were compared by projective and questionnaire-based psychological tests and their circulatory and neurohormonal reactivity to mental (Stroop color-word conflict test and arithmetic test) and physical stressors (orthostasis and bicycle ergometry test) were measured. Borderline hypertensive subjects externalized aggression less (p<0.05) but internalized it more (/?<0.05) and were more submissive (p<0.05) when compared with controls. Offspring of hypertensive parents showed a similar but weaker pattern. Both risk groups reported more positive interactions with their parents (genetic risk subjects versus controls, p<0.05; borderline hypertensive patients versus controls, p=0.08) and had higher state-anxiety levels (p<0.05). There were more subjective symptoms of £-adrenergic receptormediated functions (e.g., tachycardia, tremor) in borderline hypertensive subjects and offspring of hypertensive parents, elevated heart rates (analysis of repeated measures, p< 0.001), and enhanced plasma norepinephrine concentrations (p<0.05) when compared with controls. These findings in subjects at risk for the development of hypertension suggest that psychosomatic factors and sympathetic overactivity are involved in the early phase of hypertension. Neurogenically mediated excessive responsiveness to stressful stimuli has been proposed as a pathophysiological mechanism. More frequent, larger, and longer-lasting pressor responses result in a pressurerelated impairment of baroreceptor reflexes followed by a resetting, 4 or lead to structural adaptive changes in the resistance vessels. 5 In addition, enhanced sympathetic nervous system activity may result in increases in cardiac output, vascular resistance, and sodium and water retention and thereby elevated levels of blood pressure. 6 In accepting a psychosomatic approach to the pathogenesis of hypertension, the psychosomatic factor must be present well before the development of high blood pressure. We therefore investigated risk groups (i.e., patients with borderline hypertension 7 and nonnotensive subjects with a family history of hypertension 8 ) rather than established hypertensive patients. Psychological characteristics were assessed by projective and questionnaire-based psychological tests in an endeavour to differentiate the above risk groups from a control population with a low risk of hypertension. Responses to stressors (i.e., cognitive tasks and physical exercise) were compared by measuring cardiovascular and biochemical stress markers. Methods SubjectsOf the 123 subjects, 18-24 years old and of both sexes, all were Caucasian: Twenty-four were consecutive untreated outpatients with borderline hypertension (15 with and nine without a family history of by guest on May 9, 2018 http://hy...

In a double-blind study, fifty-five healthy, male medical students received a tranquilizer (bromazepam, 'Lexotanil') or placebo according to dosage group (placebo, 1.5 mg and 3 mg bromazepam). The subjects were randomly allocated to three groups (placebo: n = 19; 1.5 mg: n = 19; and 3 mg: n = 17). Dependent variables tested were the subjective assessment of performance and the level of activation (self-rating), and aspects of psychomotor function were assessed using the standard testing devices. The medication was administered for a total of 14 days. The testing times reported here were: before start, and after 7 and 14 days of administration of serum or placebo. The subjective evaluation (self-rating) such as performance assessment and level of activation demonstrated no changes related to either the medication or the length of time elapsed. The objective measures of performance revealed two main effects: lengthening of time of reaction to optical stimuli during the course of the study, especially in the higher bromazepam dosage group (sedative effect). This sedative effect was, however, relatively weak since, despite this observation, there was a significant training effect in the 3 mg group with regard to attentiveness and alertness testing. The results were also evaluated for a possible effect on driving ability. In the group studied here and at the relatively low dosage administered, any possible negative influence can be disregarded.

The effects of short-term (acute) doses of bromazepam were studied in a double-blind trial with the aid of three dosage groups comprising a total of fifty-five healthy male medical students (who received placebo, and 1.5 mg or 3.0 mg bromazepam, respectively). Subjective well-being was recorded through self-ratings by the volunteers, and the variables of psychomotor function by standard testing instruments. In terms of subjective well-being, fatigue and decreased performance (statistically confirmed throughout) were reported by the probands in all three dosage groups after they were administered either the drug or placebo. None of the dose-effect relationships were statistically significant, although this trend was more pronounced, purely in quantitative terms, in the group that received 3 mg bromazepam than in either the placebo or the 1.5 mg bromazepam group. In the reaction time and in critical flicker-frequency (CFF) testing, the trend mentioned above was confirmed. In the attentiveness and memory span test, learning effects were statistically confirmed in equally uniform fashion. The action of the substance was again not statistically significant. It may be concluded from this that subjective, and also in part objective, fatigue and decreased performance were related to the type of trial design employed, and not, generally speaking, to the action of the substance. However, again independently of the drug's activity, statistical confirmation was obtained of improved performance and/or learning activity in three variables of the alertness testing apparatus. Variables of driving ability were not adversely affected, but--if anything--stabilized. Our investigation studied the single-dose schedules of bromazepam--viz. 1.5 mg and 3 mg--that are most commonly prescribed for patients. The subacute and personality-related effects of the drug will be the subject of a later report.

In contrast to the usual type of drug studies it is not our intention to single out specific drug effects, but we are interested in cognitive-psychomotor functioning of psychiatric patients across various periods of therapy, whether due to drug treatment or to underlying mental-affective disorders. 3 groups of psychiatric male patients (7 anxious/inhibited depressives, 7 schizophrenics, 6 patients with psychotic episodes) matched for age (mean = 30 years) and education (no academic trainig) with a group of healthy controls (n = 7) were examined three times during the first 6–8 weeks of their ordinary clinical therapy. The major criterion for the inclusion of a patient next to these diagnostic categories was an initial favorable response to the specified drugs (amitriptyline for the depressives, haloperidol for the schizophrenics, and thioridazine for the patients with psychotic episodes). Each subject was tested in an experimental laboratory with respect to cognitive-psychomotor performance (vigilance, divided attention, choice reaction time), mood, subjective fitness for driving, depression, and paranoia. All groups of patients improved significantly between the acute and the chronic phase. However, healthy controls showed a sharper increase of achievement. While the depressives and the patients with psychotic episodes function on a level of questionable fitness for driving, schizophrenics vary greatly intra- and interindividually, generally on a lower level.