Guidelines for reducing the risk of disease transmission in the psychophysiology laboratory. SPR Ad Hoc Committee on the Prevention of Disease Transmission.

The acquired immunodeficiency syndrome (AIDS) pandemic has highlighted the need for safeguards against the inadvertent transmission of infectious disease in the psychophysiology laboratory. These Guidelines identify factors contributing to the risk of bloodborne disease transmission to subjects or technicians, and recommend procedures to minimize such risk, given current knowledge and techniques. The lowest risk is associated with the application of devices, such as surface electrodes, to nonabraded, intact skin. Such devices should be clean, but do not require disinfection. The potential risk of infection is higher when surface electrodes are applied to non-intact skin. Abrasion, or other breaks in the skin, can allow seepage of blood products carrying such pathogens as hepatitis B virus and the human immunodeficiency virus that causes AIDS. Thus electrodes require high-level disinfection before reuse on non-intact skin. In addition, technicians should wear gloves during skin preparation and should abrade the skin no more than necessary, using only sterile, preferably non-sharp materials. The highest risk is that associated with items that enter sterile tissue, such as subdermal electrodes and the needles and lancets sometimes used in skin preparation. Such items must be sterile at the time of use and must be handled with extreme caution.

Effects of stimulus repetition, duration, and rise time on startle blink and automatically elicited P300.

Intense auditory stimuli of sudden onset evoke not only startle blinks but also an event-related potential component resembling classic P300, even when subjects have no assigned task. To more closely examine the relationship of this P300 to startle, event-related potentials and eyeblink were recorded from 16 young adults in three paradigms designed to produce wide variation in startle amplitude: an Habituation series of 30-ms, 105dBA white noise bursts, a Duration paradigm which presented 105dB noise bursts for 3, 10, 30, or 90 ms, and a Rise Time paradigm which varied the rise/fall times (3, 15, 30, and 45 ms) of 110dBA, 1000-Hz tone bursts. Subjects received two runs of each paradigm. Only on the final Duration and Rise Time runs were stimuli explicitly task relevant; on those runs subjects rated verbally, midway in each 8.4-s interstimulus interval, the disturbingness of the prior sound. Although even the briefest noise bursts evoked parietal P300 as well as startle blink, P300 did not behave like startle. P300 habituated more slowly than did blink amplitude, was more responsive to sustained noise than were blink, N110, and P190, and most importantly, did not show the sensitivity to stimulus rise time manifested by these measures. These findings suggest that the amplitude of automatically elicited P300 is not governed by the same mechanisms as startle amplitude, but behaves more like a defense response.

Lead-stimulation effects of human cardiac orienting and blink reflexes.

Innocuous prestimulation can inhibit or facilitate a startle reflex in lower animals, depending on its lead time and on whether it is dircrete or continues throughout the lead interval. Similar effects of lead stimulation on the unconditioned blink reflex were found in human subjects, but human subjects also showed an effect not seen in lower animals. Under conditions of temporal and stimulus uncertainty, the presentation of discrete stimuli at lead times that have no effect in rats produced blink facilitation as well as pronounced cardiac decelerations during the lead interval in man. The article suggests that this effect might be mediated by an attentional process and that it could be dissociated from effects produced by a classical arousal mechanism.