Biomedical subjects
Publications and source records attributed to M Velden.
Sleep onset latency was substantially reduced in an experiment for 9 adults when short acoustic stimuli were given in synchrony with the heartbeat compared to a control condition in which the same stimuli were given asynchronously. By the same stimulation technique sleep quality was ameliorated in a group of 10 patients with primary insomnia.
The interpretation of the 'cardiac cycle time effect', also named 'time-dependent primary bradycardia' by the Laceys, who first observed it, has been controversial in psychophysiology. Unconfounded evidence for the dependence of a vagal effect of psychological stimuli on time of stimulation within the cardiac cycle has been missing to date. An experiment in which the subjects could not anticipate the occurrence of the stimuli (short tones of a specific frequency that had to be counted) was performed. The data reduction procedure secured unambiguous interpretation of the data with respect to time-dependency or no time-dependency. No indication of any kind of cycle time dependency of the vagal effect was found.
Since the now classical experiments by Brown and Eccles in 1934, the effect of a stimulation of the vagus nerve on the heart has been derived from changes in the length of cardiac periods. Based on a simple model for the genesis of heartbeats, it is shown that the procedure employed by Brown and Eccles gives a distorted picture of the actual vagal effect. A corrected procedure for inferring the vagal effect from changes in heart period length is proposed. This new procedure is applied to empirical data from animal experiments with direct stimulation of the vagus nerve. It is shown that, if the vagal effect depends on time of stimulation within the cardiac cycle (cycle time-dependency), single vagal effect curves for each time of stimulation within the cycle have to be constructed. Other data reduction procedures are reviewed with respect to their appropriateness for demonstrating cycle time-dependency.
Since a valid non-invasive method for continuously measuring blood pressure is available for the psychophysiological laboratory, a procedure must be found for depicting blood pressure characteristics (systolic, diastolic, pulse pressure) on a real time scale, that is not simply from one heartbeat to the next. Values for blood pressure characteristics are actualized by heartbeats and thus occur at discrete points in time only, quite like values for heart rate. It is being assumed that the conditions for the blood pressure characteristics vary continuously, however, and that a value, actualized by a heartbeat, is representative for a time interval extending halfway before and after the point in time where it occurs. For computing a value for a real time interval it is proposed to weight the blood pressure values according to the amount of time their respective time intervals extend within the real time interval.
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Time-dependent bradycardia, a term introduced by the Laceys (Lacey and Lacey, 1980), refers to the fact that the duration of a cardiac cycle is related to when in that cycle, or the just preceding cycle, certain stimuli occur. Since stimulus effects on heart activity with very short latencies have been known for a long time, the question arises whether the effect is one in its own right, or whether it is simply a result of the new way of data reduction introduced by the Laceys. Theoretically, the effect can be explained without assuming anything beyond the well-known short latency bradycardia often observed upon stimulation. Derivation of the effect from an empirical curve of cardiac activity not related to cycle phase shows that we are not dealing with a new effect.
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The effect of experimentally induced anxiety on pain perception was examined using a signal detection discrimination experiment. The experimental condition consisted in unsignalled application of very painful stimuli which substantially raised state anxiety. The discrimination task included the total range of painful stimuli. The results indicated a range-specific effect of anxiety on pain, particularly on increased sensitivity in the upper range of intensities. The importance of testing the effect of anxiety over the whole range of intensities is stressed. That prior work considered only one intensity level may be the main reason why previous signal detection studies about pain and anxiety showed contradictory results.
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