Abstract
The understanding of obsessive-compulsive disorder (OCD) has evolved with the knowledge of behavior, the brain, and their relationship. Modern views of OCD as a neuropsychiatric disorder originated from early lesion studies, with more recent models incorporating detailed neuropsychological findings, such as perseveration in set-shifting tasks, and findings of altered brain structure and function, namely of orbitofrontal corticostriatal circuits and their limbic connections. Interestingly, as neurobiological models of OCD evolved from cortical and cognitive to sub-cortical and behavioral, the focus of OCD phenomenology also moved from thought control and contents to new concepts rooted in animal models of action control. Most recently, the proposed analogy between habitual action control and compulsive behavior has led to the hypothesis that individuals suffering from OCD may be predisposed to rely excessively on habitual rather than on goal-directed behavioral strategies. Alternatively, compulsions have been proposed to result either from hyper-valuation of certain actions and/or their outcomes, or from excessive uncertainty in the monitoring of action performance, both leading to perseveration in prepotent actions such as washing or checking. In short, the last decades have witnessed a formidable renovation in the pathophysiology, phenomenology, and even semantics, of OCD. Nevertheless, such progress is challenged by several caveats, not least psychopathological oversimplification and overgeneralization of animal to human extrapolations. Here we present an historical overview of the understanding of OCD, highlighting converging studies and trends in neuroscience, psychiatry and neuropsychology, and how they influenced current perspectives on the nosology and phenomenology of this disorder.
Highlights
Obsessive-compulsive Disorder (OCD) is known to Western medicine at least since the Middle Ages (Berrios, 1996)
In functional brainimaging studies comparing the pattern of cortical activation between obsessive-compulsive disorder (OCD) patients and healthy individuals, cognitive deficits are associated both with decreases and increases of cortical blood-oxygenlevel dependent (BOLD) signal or glucose metabolism over the orbitofrontal cortex (OFC), dorsolateral prefrontal cortex (dlPFC), and temporo-parietal cortices (Balleine and O’Doherty, 2010; Banca et al, 2015)
In a rat model of pharmacologically-induced compulsivity, evidence was presented that the inability to change between two actions is related to the occurrence of an abnormal phasic dip in VTA dopamine neuron burst firing at the completion of a compulsive-like action sequence, leading to the recurrent activation of the same action, rather than the expected transition to a new action sequence (Joel and Doljansky, 2003)
Summary
Obsessive-compulsive Disorder (OCD) is known to Western medicine at least since the Middle Ages (Berrios, 1996). The term obsession derives from the Latin word obsidere, meaning to be possessed, occupied or preoccupied by something (Denys, 2011). It describes the occurrence of formal elements of thought (ideas, images, fears, doubts, ruminations) in a recurrent and persistent manner. Obsessive thoughts are accompanied by repetitive stereotyped behaviors, i.e., compulsions, from the Latin term compellere, meaning to be forced to something (Denys, 2011). Compulsions are not in themselves pleasurable or gratifying to the patient In most cases they are performed in order to reduce the anxiety evoked by obsessions, and are recognized by the subject as disproportionate or unrealistically related to the harm they are intended to avoid (Hollander et al, 2008). We briefly review the current state of the art with regard to the neurobiology of OCD, and how neurobiological models have opened new perspectives on the phenomenology of this disorder
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