Inhibitory control is a component of executive function that governs the suppression of interference from irrelevant stimuli. Individuals diagnosed with many neuropsychiatric disorders, including many neurodevelopmental disorders such as ADHD (attention deficit hyperactivity disorder) and OCD (obsessive compulsive disorder), share neural dysfunction of inhibitory control.1
Although individuals diagnosed with OCD or ADHD share impairments in inhibitory control, they present with disorder-specific functional and structural brain abnormalities in frontostriatal region, according to new findings of a meta-analysis performed by investigators affiliated with King’s College London and Karolinska Institute in Stockholm, Sweden. The findings were published in JAMA Psychiatry.2
While the role of frontostriatal circuits is not completely elucidated, aberrant connectivity in frontostriatal circuits is known to impact cognitive processing, including specific components of executive function such as inhibitory control. Abnormalities of the frontal cortex and striatum have also been reported in many other neuropsychiatric disorders, including schizophrenia and depression.
In the current meta-analysis, researchers assessed structural abnormalities by analyzing the voxel-based morphometry (VBM) data of whole-brain gray matter (GMV) volume, and they assessed brain activation patterns by analyzing functional magnetic resonance imaging (fMRI) data. They compared structural and functional imaging data of patients diagnosed with ADHD (VBM, n=931 and fMRI, n=489) or OCD (VBM, n=928 and fMRI, n=287) with data collected on age-matched, typically-developing individuals that served as controls in the same ADHD (VBM, n=822 and fMRI, n=591) and OCD (VBM, n=822 and fMRI, n=284) studies.
Data indicate that patients with ADHD show decreased GMV (left z = 1.904, P < .001; right z = 1.738, P < .001) and function (left z = 1.447, P < .001; right z = 1.229, P < .001) in bilateral basal ganglia/insula, when compared to patients with OCD (and controls). Patients with OCD, on contrary, show increased GMV and function in bilateral ganglia/insula, relative to control participants.
Patients with OCD show reduced GMV (z = 1.622, P < .001) and function (z = 2.133, P < .001) in rostral and dorsal anterior cingulate/medial prefrontal cortex. Patients with ADHD, on contrary, show reduced function predominantly in the right ventrolateral prefrontal cortex (z = 1.229, P < .001).
Deficits in cognitive (and motor) inhibitory control are observed in various neuropsychiatric and neurodevelopmental disorders. For example, the aberrant function of the corticostriatal circuitry (eg, basal ganglia and prefrontal cortex) is involved in reduced inhibitory control over involuntary impulses in disorders such as Tourette’s Syndrome. Also, increased activation of the insula, for example, is hypothesized to indicate an increased effort to inhibit responses in individuals diagnosed with autism. And, reduced activation of the anterior cingulate, for example, has been reported in patients with schizophrenia, another disorder that involves executive dysfunction, including poor inhibitory control.
Taken together, although patients with ADHD or OCD share behavioral impairments in inhibitory control, they present with distinctive striatal and frontal functional and structural biomarkers. “Disorder-specific neurofunctional biomarkers … provide useful targets for treatment with drugs that target these regions, or for nonpharmacological therapies such as fMRI-based neurofeedback, brain stimulation, or cognitive training of functions mediated by these regions,” the investigators concluded in their publication.
1. Brem S, Grünblatt E, Drechsler R, et al. The neurobiological link between OCD and ADHD. Atten Defic Hyperact Disord. 2014;6(3):175-202.
2. Norman LJ, Carlisi C, Lukito S, et al. Structural and functional brain abnormalities in attention-defiict/hyperactivity disorder and obsessive-compulsive disorder: a comparative meta-analysis. JAMA Psychiatry. 2016. doi: 10.1001/jamapsychiatry.2016.0700. [Epub ahead of print]