Neurodynamic Mechanisms in the Cognitive-Behavioral Treatment of Obsessive-Compulsive Disorder
Neurodynamic Mechanisms in the Cognitive-Behavioral Treatment of Obsessive-Compulsive Disorder
Issue Date
2000
Authors
Dal Corso, Daniel
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Abstract
A model of obsessive-compulsive disorder (OCD) is proposed that accounts for a broader range of symptoms and psychotherapeutic efficacy than previous biological and cognitive models. The present model synthesizes aspects of Salkovskis' (1985) cognitive model with Saxena, Brody, Schwartz, and Baxter's (1998 ) neurodynamic model. OCD is described as conditioned fear modified by factors that render it pathological. These include environmental and genetic influences leading to the kindling of the amygdala and bed nucleus of the stria terminalis (BNST). Kindling leads to a hyperactive BNST and hyperexcitable amygdala (Rosen & Schulkin, 1998). Kindling produces asynchronous neural activity (ASyA), as seen in epilepsy, and has value for modeling some forms of psychopathology as "limbic seizure" activity (Adamec, 1990). The present model suggests that stimuli that induce BNST hyperactivity stimulate the medial hypothalamus and depress striatal dopamine levels that, in turn, generate escape behaviors. Stimulus-response associations in the striatum form nondeclarative memories linking stimuli to cognitive, behavioral, and visceral response macros (Graybiel, 1998). These responses are not causally linked to the source of aversive stimulation. Although the striatum attempts to learn a more adaptive response, it is flooded with irrelevant stimulation (i.e., ASyA). This weakens the signal-to-noise ratio for meaningful associations, learning fails to occur, and old responses are repeated (i.e., obsessions and compulsions). Neurodynamic mechanisms of psychotherapeutic treatment focus on altering specific declarative and nondeclarative memories and engaging dorsolateral "executive" processes to alter striatal response macros. Testable hypotheses are generated based on the model. The generality of the model and its implications for other anxiety disorders are discussed.