The psychology of perserverative and stereotyped behaviour

Abstract

Many forms of psychopathology in higher animals and humans include the production of maladaptive, repetitive behaviour. Behaviour which is both repetitive and excessive in amount can be described as stereotyped whereas behaviour which represents a restriction of behavioural possibilities without excessive production can be described as perseverative. Both types of repetition can result from pathology in the neural mechanisms which control either the production of motor output or the organisation of behaviour at a higher level. A number of forms of repetitive behaviour can be induced environmentally. Confinement in adulthood results in a functional disorder which rapidly dissipates when normal conditions are restored but confinement in infancy may have a permanent effect on the organism's ability to interact in a flexible and creative way with its environment. The permanence of these disorders suggests that the environment can affect the way in which the nervous system develops. Repetitive behaviour is also a feature of mental illness including schizophrenia, autism, OCD, addiction and some neurological disorders including frontal lobe lesions, Tourette's syndrome and PD. In experimental studies in animals, stereotyped behaviour seems to be related mainly to excess dopaminergic activity in the basal ganglia while perserverative behaviour can be produced by lesions of the frontal lobes. It is supposed that the level of dopamine activity in the basal ganglia affects the baseline level of behavioural activation such that excess activation results in the excessive execution of the most probable response to the environment to the exclusion of other possibilities (i.e. stereotypy) while deficient activation results in the production of only a few responses which can exceed the necessary activation level (i.e. perseveration). In either case behaviour is 'stimulus-bound', being driven by only the most salient feature of the environment. The symptoms of PD result from inadequate levels of dopamine in the basal ganglia while the stimulant psychoses result from excessive availability of dopamine. The frontal lobes have a modulating effect on (i) the activation of motor activity by the basal ganglia, (ii) in the generation of self-initiated behaviour, i.e. volition, and (iii) in the neural mechanisms which permit different modes of neural function (e.g. perceiving, remembering or thinking) to be identified. Failures in these three functions could result in excessive and repetitive motor activity, stimulus-bound behaviour, the paucity of volitional and creative behaviour, and the perceptual and experiential symptoms of psychosis.