A model of the neuropsychology of anxiety is proposed. The model is based in the first instance upon an analysis of the behavioural effects of the antianxiety drugs in animals. From such psychopharmacologi-cal experiments the concept of a “behavioural inhibition system” has been developed. This system responds to novel stimuli or to those associated with punishment or nonreward by inhibiting ongoing behaviour and increasing arousal and attention to the environment. It is activity in the BIS that constitutes anxiety and that (...) is reduced by antianxiety drugs. The effects of the antianxiety drugs in the brain also suggest hypotheses concerning the neural substrate of anxiety. Although the benzodiazepines and barbiturates facilitate the effects of γ-aminobutyrate, this is insufficient to explain their highly specific behavioural effects. Because of similarities between the behavioural effects of certain lesions and those of the antianxiety drugs, it is proposed that these drugs reduce anxiety by impairing the functioning of a widespread neural system including the septo-hippocampal system, the Papez circuit, the prefrontal cortex, and ascending monoaminergic and cholinergic pathways which innervate these forebrain structures. Analysis of the functions of this system suggests that it acts as a comparator: it compares predicted to actual sensory events and activates the outputs of the BIS when there is a mismatch or when the predicted event is aversive. Suggestions are made as to the functions of particular pathways within this overall brain system. The resulting theory is applied to the symptoms and treatment of anxiety in man, its relations to depression, and the personality of individuals who are susceptible to anxiety or depression. (shrink)

Pavlovian cues predict the occurrence of motivationally salient outcomes, thus serving as an important trigger of approach and avoidance behavior. The amygdala is a key substrate of Pavlovian conditioning, and the nature of its contribution varies by the motivational valence of unconditioned stimuli. The literature on aversive Pavlovian learning supports a serial-processing model of amygdalar function, while appetitive studies suggest that Pavlovian associations are processed through parallel circuits in the amygdala. It is proposed that serial and parallel forms of information (...) processing can be attributed to differential recruitment of amygdalar nuclei, with emphasis placed on the lateral amygdala. (shrink)

There is disagreement in the literature about the exact nature of the phenomenon of empathy. There are emotional, cognitive, and conditioning views, applying in varying degrees across species. An adequate description of the ultimate and proximate mechanism can integrate these views. Proximately, the perception of an object's state activates the subject's corresponding representations, which in turn activate somatic and autonomic responses. This mechanism supports basic behaviors that are crucial for the reproductive success of animals living in groups. The Perception-Action Model, (...) together with an understanding of how representations change with experience, can explain the major empirical effects in the literature. It can also predict a variety of empathy disorders. The interaction between the PAM and prefrontal functioning can also explain different levels of empathy across species and age groups. This view can advance our evolutionary understanding of empathy beyond inclusive fitness and reciprocal altruism and can explain different levels of empathy across individuals, species, stages of development, and situations. Key Words: altruism; cognitive empathy ; comparative; emotion; emotional contagion; empathy ; evolution; human; perception-action; perspective taking. (shrink)

Preston & de Waal are understandably cautious in applying their model to autism. They emphasise multiple cognitive impairments in autism, including prefrontal-executive, cerebellar-attention, and amygdala-emotion recognition deficits. Further empirical examination of imitation ability in autism may reveal deficits in the neural and cognitive basis of perception-action mapping that have a specific relation to the empathic deficit.

ArgumentThe article retraces the shifting conceptualizations of psychological trauma in experimental psychopathological research in the middle decades of the twentieth century in the United States. Among researchers studying so-called experimental neuroses in animal laboratories, trauma was an often-invoked category used to denote the clash of conflicting forces believed to lead to neurotic suffering. Experimental psychologists, however, soon grew skeptical of the traumatogenic model and ultimately came to reject neurosis as a disease entity. Both theoretical differences and practical circumstances, such as (...) the technical challenge of stabilizing neurotic symptoms in rats, led to this demise. Yet, despite their reservations, experimental psychologists continued to employ traumatic stimuli to produce psychopathological syndromes. In the 1960s, a new understanding of trauma evolved, which emphasized the loss of control experienced by traumatized animal subjects. These shifting ideas about trauma, I argue, reflect both varying experimental cultures, epistemic norms as well as changing societal concerns. (shrink)