The previous chapter dealt with peripheral physiological arousal mechanisms. Although indices of peripheral arousal are not perfectly correlated (e.g. the phasic arousal associated with an orienting response produces an increase in skin conductance but a decrease in heart-rate), a com bination of pituitary-adrenal cortex activation with general sym pathetic arousal does serve to define our peripheral arousal pattern. The physiological state may correspond with behaviour, particularly during physical exercise and during the expression of intense emotion, or it may be behaviourally undetectable, as in some psychologically stressful or arousing situations in which responding is impossible or inappropriate. So our concept of ‘arousal’ has, even at this stage, to distinguish between ‘behavioural’ and ‘peripheral physiological’ components.Psychologists also use ‘arousal’ as a theoretical construct, to help explain relationships between dependent and independent variables. This usage is epitomized in the inverted-U-shaped curve relating performance on a given task to the subject’s level of arousal (Fig. 10.1); performance is poor at relatively low and high levels, and optimal at a m oderate arousal level.It should be emphasized that the inverted-U-shaped function is hypothetical, not a law of nature. It has to be empirically dem onstrated for any given task, an endeavour fraught with many problems of which the most pressing is to systematically vary ‘arousal’ level. To do this we need to operationalize our theoretical construct, to choose a m anipulation which directly 268
Figure 10.1 Inverted-U-shaped curve o f arousal and performance influences our subject’s ‘arousal’ level.At the extremes of a behavioural arousal dimension lie sleep and hysterical overactivity. It seems likely, even in the absence of experimental data, that task performance will be poorer in either of these states than during normal, alert waking, i.e. an inverted U could describe the function relating performance to these arousal states. So it is the range between these extremes that the experimental psychologist concentrates upon in the attem pt to discover if, for instance, performance on a vigilance task can be improved with mildly arousing stimuli and impaired with very arousing ones.The stimuli used tend to be stressors, such as white noise played through headphones, sleep deprivation, or incentives (i.e. where reward is proportional to performance). It is usually assumed that the intensity of the stressor is linearly related to
the degree of the subject’s arousal. The obtained relationship between stressor intensity and performance then represents the function relating arousal level and performance, and can be com pared with the predicted inverted U-shaped curve.It is perfectly legitimate for the psychologist concerned to deal only with his particular stressor, and to make no inferences beyond his own experim ental paradigm . However, this narrow approach would not help to link the many studies of stressors and performance; it also makes sense to treat together experiments on, for instance, white noise and incentives when the interpretation of results refers in both cases to something called ‘arousal’.Even when widely used as an explanatory device, ‘arousal’ need not involve the experimental psychologist in an appeal to possible physiological mechanisms; it can remain a valuable theoretical construct for integrating a range of experimental data, rather like ‘attention’ or ‘m otivation’. In fact, the introduction of the probable physiological substrates of arousal can lead to great confusion. It is clear that different stressors have differential effects on performance, and their combined effects may be additive, independent, or even antagonistic (e.g. sleep deprivation and white noise). If they acted upon a common substrate o f‘arousal’, then their actions on behaviour should be similar and additive.Cognitive performance depends, as we shall see, on central physiological arousal mechanisms. These are complex and interactive, not simple and independent. The notion of a single central ‘arousal’ system is now outmoded, and along with it any ideas that experimental psychologists may have about a common ‘arousal’ substrate m ediating the effects of stressors on performance. This latter hypothesis was a fruit of the early work on the behavioural functions of the brainstem reticular formation, which dem onstrated conclusively its major role in the control of sleep and waking behaviour. Before analysing this work in more detail, I shall first discuss in more general terms the phenom ena of sleep and waking.We spend around 30 per cent of our lives asleep, far more time than we give to eating, drinking, or, in most cases, learning. For centuries, the question of the function or func-
tions of sleep has been discussed, and we still have no answer; or, more precisely, we have many suggestions, but no consensus. The basic phenom ena are undisputed. Mammals, birds, reptiles, and fish sleep. Even molluscs and insects show behaviour indistinguishable from sleep. Some rare subjects manage on an hour or less per night; otherwise hum ans need, or think they need, between five and ten hours sleep in every twenty-four. If we are deprived of sleep, we feel tired, and tend to make up some of the deficit on subsequent nights.These simple observations raise complex questions. The ubiquity of sleep across the phylogenetic scale implies that it has a necessary function, but does not distinguish between physiological hypotheses (e.g. tissue restoration), psychological hypotheses (e.g. processing of the previous day’s experiences), or ecological hypotheses (e.g. safety from predation). The regularity of sleep patterns within the circadian cycle needs explanation. Is sleep actively triggered by the brain in response to darkness or to some intrinsic biological rhythm such as tem perature; or perhaps by the daily build-up of some ‘need for sleep’ represented by, for instance, a drop in synaptic transm itter levels? Alternatively, sleep might be a passive process; the natural state, as it were, into which the brain falls unless incoming environmental stimulation is sufficient to arouse it.No single chapter can deal with all the questions. I shall present some hypotheses relating to many of them, and then review the current status of the reticular formation as the physiological substrate of central arousal.