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Neurobiological underpinnings of personality disorders

Introduction: Modern psychiatry favours a multifactorial model of personality and personality disorder stressing close interactions of neurobiological and psychosocial influences. Currently, categorical and dimensional models are being passionately discussed for revisions of diagnostics of personality disorders in future systems of classification. This revision may have important consequences. A traditional categorical approach to study neurobiological factors in the aetiopathogenesis of personality disorder has been meeting many difficulties so far. To conceptually and methodologically differentiate character as the result of a complex process of social learning, and temperament as the neurobiological fundament of any personality may be considered a first step out of this dilemma. The well-known psychobiological model of personality by Cloninger et al. (1) conceptualise temperament according to four basic dimensions of personality, novelty seeking, harm avoidance, reward dependence, and persistence. Individual tendencies in various dimensions may form the neurobiological underpinnings of typical personality and personality disorder. A major system of neurotransmitter has been linked to each dimension of temperament in theoretical terms leading to differential psychopharmacological hypotheses in the case of a discrete personality disorder. Although some empirical findings support some clinical utility of this model, the neurobiological hypotheses have not been empirically validated (5). Another methodological approach is about to identify some endophenotypes in major dimensions of personality being linked to underlying genotypes that influence the traits and dimensions of personality disorders, as well as susceptibility to major psychiatric illnesses. Clinical dimensions of personality disorders that lend themselves to the study of corresponding endophenotypes include affective instability, impulsivity, aggression, emotional information processing, cognitive disorganisation, social deficits, and proneness to psychosis (4). Research data on the neurobiology of personality disorders: For the time being, research data on the neurobiology of personality disorders may best be presented within the framework of DSM-IV clusters of personality disorders (2). Each cluster may be conceptualised in terms of discrete dimensions that might turn out as promising endophenotypes (Table 1). Cluster A Neurobiological research in cluster A first and foremost refers to schizotypal personality disorder within a concept of schizophrenia spectrum disorders. Here it focuses on pathological alterations within the cognitive–perceptive organisation and underlines typical socio–affective deficits, neurocognitive dysfunctions, psychotic-like disturbances of perception and thinking. 1) Patients with schizotypal personality disorders are basically hampered in the processing of important social information that essentially forms a theory of mind. Deficits in social perception can be reliably measured by neuropsychological tests. The deficits seem to be more subtle than in schizophrenic patients, but importantly contribute to the clinically well-known eccentricity and profound interpersonal difficulties of schizotypal patients. In various neuropsychological performances combined with neuroimaging methods (PET, SPECT, fMRI), schizotypal patients take a medium position between normal control persons and schizophrenic patients. In tests measuring executive functions, learning or working memory, they less activate dorsolateral prefrontal cortex than control persons, but significantly stronger than schizophrenic patients, and in addition activate other areas of the anterior frontal cortex (BA 10) for compensation. They show structural reductions in the temporal lobe in an amount as schizophrenic patients do, but less pronounced reductions in the frontal cortex, whereas schizophrenic patients demonstrate major volume reductions in both cerebral regions. 2) Dopamine system may play a decisive role in the susceptibility to psychotic-like symptoms of perceptions and thoughts. Measures of HVA, the end-metabolite of dopamine in CSF positively correlate with psychometric scores of perceptual and cognitive distortions. In pharmacologic challenges, e.g. with amphetamine, schizotypal patients show a stronger response than control persons, but a less pronounced response than schizophrenic patients do. Their mitigated response may be in line with neuroimaging findings of reduced striatal volumes that are considered a protective factor against full-blown state of psychosis. Molecular–genetic investigations hint to a probably important polymorphism of COMT underlining the basic influence of dopamine system on the one hand, linking to major neurocognitive functions as working memory on the other that quite likely are regulated, however, by various other neurotransmitter systems as e.g. norepinephrine. Cluster B Essential characteristics of this cluster of personality disorders affect impulsivity, aggression, emotional regulation and emotional information processing. Neurobiological research is more or less exclusively based on borderline personality disorder. Affective instability and impulsivity turned out to be as basic personality dimensions in BPD demonstrating a relative stability in time. In addition, a tendency to dissociation under psychosocial stress and trauma is considered another typical personality dimension marking a special mode of emotional and cognitive information processing. Affective instability comprises an increased general emotional responsivity with reduced thresholds for emotional stimuli on the one hand, and high intensity of emotional expression and heavily reduced recovery to initial levels of affectivity on the other. Affective instability in DSM-IV Cluster Dimensions