Children with obsessive-compulsive disorder: are they just "little adults"?

Abstract

Childhood-onset obsessive-compulsive disorder (OCD) affects 1%-2% of children and adolescents. It is characterized by recurrent obsessions and compulsions that create distress and interfere with daily life. The symptoms reported by children are similar to those seen among individuals who develop OCD in adulthood, and the two groups of patients are treated with similar symptom-relieving behavior therapies and medications. However, there are differences in sex ratios, patterns of comorbidity, and the results of neuroimaging studies that might be important. Here we review the diagnosis and treatment of childhood-onset OCD in light of pediatric and adult studies. We also discuss current knowledge of the pathophysiology of the disorder. Despite advances in this area, further research is needed to understand better the etiopathogenesis of the disorder and to develop new, more effective therapeutic options.

Figure 1. Model for the cortico-striato-thalamo-cortical circuit dysfunction in individuals with OCD.

This model outlines the hypothesis that the cortico-striato-thalamo-cortical circuit is dysfunctional in individuals with OCD. Increased glutamatergic signals from the frontal cortex are hypothesized to increase excitation in the striatum, which increases inhibitory GABA signals to the GPi and SNr. (A) One possibility is that this then decreases the inhibitory output via GABA from the GPi and SNr to the thalamus, resulting in thalamic excitatory glutamatergic output to the frontal cortex. This positive feedback loop leads to repetitive thoughts (obsessions) and behaviors (compulsions). An indirect external loop composed of the GPe and subthalamic nucleus (STN) is postulated to contribute to a steady state of excitation/inhibition in this model. (B) A second possibility is that there is an unknown dysfunction at the striatum and GPe. Decreased inhibition on the GPe leads to increased inhibition of the STN, which decreases its excitation of the GPi/SNr. The GPi/SNr then decreases its inhibitory output on the thalamus, resulting in excitatory output to the frontal cortex (adapted from ref. 67).

Figure 2. The cortico-striato-thalamo-cortical circuit in a healthy individual.

In the normally functioning cortico-striato-thalamo-cortical circuit, glutamatergic signals from the frontal cortex lead to excitation in the striatum, which increases inhibitory GABA signals to the GPi and the SNr. This then decreases the inhibitory output via GABA from the GPi and SNr to the thalamus, resulting in thalamic excitatory glutamatergic output to the frontal cortex. This is a positive feedback loop. An indirect external loop composed of the GPe and subthalamic nucleus (STN) is postulated to contribute to a steady state of excitation/inhibition. The striatum inhibits the GPe, which decreases its inhibition on the STN. The STN is then free to excite the GPi/SNr and therefore inhibit the thalamus (adapted from ref. 67).

Figure 3. Serial T1-weighted brain MRIs of a 14-year-old male patient with severe worsening of OCD symptoms after an infection with GABHS.

MRI was performed before and after treatment with plasma exchange. Note the decreased caudate size after treatment (outlined with dotted and solid lines). This provides further support for basal ganglia–mediated dysfunction in OCD and the potential for immunological treatments for PANDAS. Adapted with permission from Oxford University Press (124).