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A Neurodevelopmental Model of Obsessive-Compulsive Disorder?

A Neurodevelopmental Model of Obsessive-Compulsive Disorder?
Rosenberg and Keshavan recently tried to draw together these various literatures into a neurodevelopmental model of OCD. First, they noted that several lines of evidence suggest that OCD may result from a neurodevelopmental rather than a degenerative process: (1) a number of cases of OCD begin in childhood; (2) there is a similarity between many OCD rituals and ‘‘developmentally normal’’ childhood rituals; and (3) neurological soft signs present at the onset of the disorder do not show any exacerbation, even when OCD symptoms progress and increase in severity. Second, as noted from the data presented earlier, if there is a region of the brain involved in OCD, it is probably part of the ventral prefrontal cortical region (VPFC). Recall that this region has been identified from psychosurgery and functional neuroimaging studies, as well as treatment response studies. This zone is also connected to limbic structures in the cingulate and anterior lobes.
Importantly, developmental brain morphology studies indicate that there is substantial maturation in the brain cortex from birth up to about 20 years of age. To test their hypothesis, Rosenberg and Keshavan conducted an MRI study of twenty-one treatment-naive pediatric outpatients with OCD and twenty-one normal control subjects. Those with OCD had significantly larger anterior cingulate volumes than normal control subjects but did not have differences in posterior cingulate, dorsolateral prefrontal cortex, amygdala, hippocampal, superior temporal gyral, or whole temporal lobe volumes. Additionally, there was a significant positive correlation between anterior cingulate volume and severity of obsessional, but not compulsive symptoms. Furthermore, there was a trend (p = .055) for a significant correlation between age and cingulate volumes among the control patients (r = .45), but not among the patients with OCD (r = .12). Rosenberg and Keshavan suggested that the lack of correlation between age and anterior cingulate volumes in patients with OCD may represent a delay in the normal neuronal ‘‘pruning’’ process (i.e., the normal developmental reduction in the number of neuronal circuits), leading to larger caudate volumes and more neuronal circuits. Because these circuits are involved in regulating purposive behaviors, abnormality in these circuits (as evidenced by dysplasia) could manifest itself clinically as an inability to regulate behavior or conversely, the production of excessive behaviors such as excessive washing or checking behaviors. Although this is an interesting model, as the authors noted, it is not without its limitations. First, again the study is based on a small number of patients, and it is one of the few studies to date with a pediatric population.
Second, the relationship between age and anterior cingulate volume was a statistically significant trend but did not meet the traditional criterion for significance. One or two additional subjects could substantially affect the correlation coefficient. Thus, replicative studies are necessary before one can draw firm conclusions. Third, more sophisticated neuroimaging techniques such as PET are necessary to delineate the relationship more clearly between developmental neurochemical changes in serotonin and the neurobehavioral and functional neuroanatomic development in OCD.

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