A psychological and neuroanatomical model of obsessive-compulsive disorder - PubMed (original) (raw)
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A psychological and neuroanatomical model of obsessive-compulsive disorder
Edward D Huey et al. J Neuropsychiatry Clin Neurosci. 2008 Fall.
Abstract
Imaging, surgical, and lesion studies suggest that the prefrontal cortex (orbitofrontal and anterior cingulate cortexes), basal ganglia, and thalamus are involved in the pathogenesis of obsessive-compulsive disorder (OCD). On the basis of these findings several models of OCD have been developed, but have had difficulty fully integrating the psychological and neuroanatomical findings of OCD. Recent research in the field of cognitive neuroscience on the normal function of these brain areas demonstrates the role of the orbitofrontal cortex in reward, the anterior cingulate cortex in error detection, the basal ganglia in affecting the threshold for activation of motor and behavioral programs, and the prefrontal cortex in storing memories of behavioral sequences (called "structured event complexes" or SECs). The authors propose that the initiation of these SECs can be accompanied by anxiety that is relieved with completion of the SEC, and that a deficit in this process could be responsible for many of the symptoms of OCD. Specifically, the anxiety can form the basis of an obsession, and a compulsion can be an attempt to receive relief from the anxiety by repeating parts of, or an entire, SEC. The authors discuss empiric support for, and specific experimental predictions of, this model. The authors believe that this model explains the specific symptoms, and integrates the psychology and neuroanatomy of OCD better than previous models.
Figures
FIGURE 1. The Key Brain Structures Implicated in Reward and Emotion
The position of the amygdala, orbitofrontal cortex and cingulate cortex are shown on a midsagittal view (top), and on a ventral view (bottom) of the human brain. Reproduced with permission from Luxenberg et al. 1988 (114)
FIGURE 2. Model of Interaction of Basal Ganglia with Other Brain Structures
GPi = internal segment of globus pallidus; GPe = external segment of globus pallidus; SNc = substantia nigra pars compacta; SNr = substantia nigra pars reticulata; VTA = ventral tegmental area; ABL = basolateral amygdala. Reproduced with permission from Frank et al. 2006 (54)
FIGURE 3. Reward Values Associated with Active SECs at a Given Time
This figure shows a hypothesized schematic representation of the changes in a few active motivational/reward states. The overall reward state at a given time of an animal will be the summation of the component reward states, and the emotional “flavor” of the reward state is provided through interactions with limbic structures. SECs = structured event complexes
FIGURE 4. The Standard Model of OCD
OCD = obsessive-compulsive disorder. Excitatory connections are labeled +; inhibitory connections are labeled −. Reproduced with Permission from Rauch et al. 2006 (94)
FIGURE 5. A Neuroanatomical Model That Incorporates Direct and Indirect Striatal Pathways
GPi = globus pallidus interna; SNr = substantia nigra pars reticulata In OCD, the direct pathway is strongly activated in relation to the indirect pathway resulting in OFC-subcortical hyperactivity. Large arrows represent inputs that are strengthened in patients with OCD. Reproduced with permission from Stein 2006 (96)
FIGURE 6. Schematic Representation of the SEC/OCD Model
Brain areas are listed with summary of function. In healthy people, initiation of an SEC can generate motivational anxiety. Completion of such an SEC results in a reward signal and a reduction in anxiety. People with OCD do not receive the full reward signal and reduction of anxiety upon completion of an SEC, giving them the sensation of leaving a task undone, which they attempt to remove by repeatedly performing an SEC or segments of an SEC. Symptoms of OCD can be acquired by damage to the basal ganglia, OFC, or ACC. OCD = obsessive-compulsive disorder; SEC = structured event complex; OFC = orbitofrontal cortex; ACC = anterior cingulate cortex;
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