Breaking up with your drug can be hard to do, but is it mainly because compulsive behavior involves specific brain regions?
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Advances in genetic research have led to an increased understanding of genotype-phenotype relationships. Excessive eating and weight gain characteristic of Prader-Willi syndrome (PWS) have been the understandable focus of much of the research. The intense preoccupation with food, lack of satiation, and incessant food seeking are among the most striking features of PWS. It has become increasingly clear that the behavioral phenotype of PWS also includes symptoms similar to obsessive compulsive disorder, which in all probability interact with the incessant hunger and lack of satiation to engender the intense preoccupation and food seeking behavior that is characteristic of this disorder. Several lines of evidence suggest that genetic material on chromosome 15 may alter synthesis, release, metabolism, binding, intrinsic activity, or reuptake of specific neurotransmitters, or alter the receptor numbers and/or distribution involved in modulating feeding. Among the likely candidates are GABAnergic, serotonergic, and neuropeptidergic mechanisms. This review summarizes what is known about the appetitive behavior and compulsivity in PWS and discusses the possible mechanisms underlying these behaviors. MRDD Research Reviews 2000;6:125-130.
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An exaggerated sense of responsibility is currently considered as the ground for the obsessive-compulsive disorder. Obsessive-like behaviors, such as hesitations and checks, may be induced in non-clinical subjects by increasing perceived responsibility (i.e., perceived personal influence on negative outcomes). In line with Salkovskis' proposal [The cognitive approach to anxiety: threat beliefs, safety-seeking behavior, and the special case of health anxiety and obsessions, in: P.M. Salkovskis (Ed.), Frontiers of Cognitive Therapy, Guilford, New York], we tested the hypothesis that reduced coping abilities (i.e., an exaggerated expectation of failure) are another effectual factor contributing to obsessive-like behaviors. We examined 47 normal volunteers in a visuo-spatial memory task, and manipulated their perceived personal influence and expectation of failure by giving differential instructions and feedback about their performance. Increase of perceived personal influence induced slowness, hesitations and checks without enhancing performance. Expectation of failure exacerbated obsessive-like behaviors, again without affecting performance. These results confirm the role of responsibility in obsessive-like behavior and indicate that reduced coping abilities may contribute to worsen dysfunctional strategies.
Prader-Willi syndrome (PWS) is a genetic disorder characterized by hyperphagia and food preoccupations. Researchers indicate that individuals with PWS, including young children, exhibit food and non-food-related compulsions. Normative rituals are also often present among typically developing preschoolers. However, it is unclear how these behaviors affect the child. Although preschoolers with PWS exhibit more types of rituals than other populations, it is uncertain if the severity of these behaviors differs from the rituals experienced during normative development. Thus, the purpose of this research was to determine whether the ritualistic behaviors exhibited by preschoolers with PWS differ in severity from those exhibited during normative development. We also sought to identify whether non-food ritualistic behavior was related to the hyperphagia in PWS. Parents of 68 children with PWS, 86 typically developing children, and 57 children with developmental delays completed questionnaires on rituals and eating behavior. Children with PWS exhibited more severe ritualistic behavior than typically developing children but not other children with developmental delays. However, the severity of non-food-related rituals was related to the severity of eating behavior in PWS. We hypothesize that this link between hyperphagia and non-food-related compulsivity may share a common underlying neurobiological mechanism.
Several studies indicate a serotonergic dysfunction in patients with obsessive-compulsive disorder (OCD). We examined serotonergic function in OCD by determining platelet 3H-impiramine binding sites in patients with OCD during a drug-free baseline period as well as normal control volunteers. The maximum number of binding sites (Bmax) and apparent dissociation constant (Kd) was determined using 3H-imipramine (IMI) as the binding ligand. We observed that the mean 3H-IMI binding Bmax (fmol/mg protein) determined in 24 patients with OCD was not significantly different from that in 23 normal control subjects. There were no significant differences in the Kd between patients with OCD and normal control subjects. Our results are thus similar to those reported by Insel et al (1985) and Black et al (1990), who observed no significant differences in platelet 3H-IMI binding between OCD patients and controls; but different from those reported by Weizmann et al (1986), who observed decreased 3H-IMI Bmax in OCD patients. The discrepancy in the results is not clear, but may be related to several factors. Our results thus indicate that any abnormality in serotonergic function present in patients with OCD is not related to imipramine binding sites in the platelets. However, the possibility that there may be an abnormal platelet serotonin uptake or other serotonergic function in OCD cannot be ruled out.
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A 34 year old woman with AIDS presented with adynamia and obsessive-compulsive behaviour. CT scan revealed bilateral toxoplasmic lesions involving basal ganglia. The neuropsychological picture resolved under specific antitoxoplasmic treatment. However, relapse of toxoplasmosis occurred in associating with the same behavioral changes. This is the first case of such a syndrome due to infectious lesions, and in which improvement through transient, was observed.
A case of progressive supranuclear palsy characterized by a loss of self-activation and a compulsive behaviour of the obsessive type is reported. The pathological examination was remarkable for the intensity of pallidal lesions and their diffusion to both the external and internal segments. While the loss of self-activation seemed to result from a damaged cortico-subcortical circuit forming a limbic loop, the compulsive behaviour of the obsessive type may have resulted from the interruption of a frontal-caudal-pallidal-luysian circuit.
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Another case of obsessive behaviour as the consequence of lentiform nuclei lesions is reported. All the aspects of an obsessive neurosis were present: irresistible compulsiveness, acute anxiety in case of non accomplishment, magic-like clues. The symptoms appeared after a carbon monoxide poisoning, in a 31-years-old woman who had previously a pathological personality, of the psychopathic type, but without obsessive features. The onset of compulsions was paralleled by frontal-like psychological changes, but there was no reduction of intellectual or mnesic functions. A previous depressive state continued after the poisoning, so that the patient did not show an empty mind as did the other patients; the loss of "self-psychic activation" was only partial. All these case-reports emphasize the fact that the neuropsychological testing must not be limited to the behaviour and must investigate the "mental content" as well. They also lead us to emphasize similitudes between psychic disorders related to lenticular lesions and those related to frontal lobe lesions, including obsessive-like activities. Such case-reports provide a model in which some components of the obsessive neurosis, hebephrenia and depression are the consequence of an identified brain damage. It can be suggested that the neural circuits involving frontal lobes and parts of the neostriatum and of the pallidum are implicated in the mechanisms of these three types of psychoses.