Lecture
Etiology and Pathogenesis
Clear conceptions of the phenomenology of borderline mental disorders are lacking, and their characteristic symptoms often appear vague, bizarre, indeterminate, and virtually resistant to objectification. In this connection, coherent concepts of the origin of neurotic experiences have been proposed only by psychoanalysts. Freud held three theories of anxiety. According to the first, anxiety is a manifestation of repressed libido; the second viewed it as a repeated reliving of the trauma of birth; the third, which can be regarded as the definitive psychoanalytic theory of anxiety, posits the existence of two types of anxiety - primary and signal anxiety. Signal anxiety represents a sentinel defense mechanism that warns the "ego" of an impending threat to its equilibrium, while primary anxiety is the emotion accompanying the disintegration of the "ego." Primary anxiety signifies a failure of defense and manifests itself in nightmares.
Biological theories of the etiopathogenesis of neurotic disorders are based on the identification of biological markers of brain mechanisms that correlate with the corresponding symptomatology. Despite the separation of anxiety and depressive disorders into distinct diagnostic categories in modern classifications, the high prevalence of cases with combined manifestation of anxiety and depression symptoms has provided grounds for reviving the concept of a single symptomatic continuum underlying these disorders. Genetic and neurobiological evidence has been obtained showing that the link between anxiety and depressive disorders is realized not only at the clinical level but also at the pathophysiological level. A so-called neurotic factor has been identified, encompassing feelings of inferiority and rejection, demoralization, shyness, and general affective distress.
Research into the neurobiology of borderline mental disorders has been directed primarily at studying the noradrenergic, GABAergic, and serotonergic neurotransmitter systems. The latter plays a particular role as a common substrate in the pathophysiology of neurotic manifestations. Another neurotransmitter implicated in the etiopathogenesis of anxiety in particular may be adenosine, since it is possibly linked to the anxiogenic effect of caffeine. A similar effect is produced by sodium lactate and by carbon dioxide when its concentration in the air is raised to 5%. Although the mechanism of this effect is not fully understood, it is thought to be related to hyperstimulation of the subcortical nuclei of the pons.
+Borderline mental disorders also have a serious genetic basis: among patients with agoraphobia, up to 20% of relatives suffer from similar disorders, and generalized anxiety disorders are characterized by concordance in 50% of monozygotic and 15% of dizygotic twins.
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