Research has documented abnormal inhibition-related brain activity as well as impaired
behavioral performance of RI in OCRD. Despite the growing evidence suggesting a RI
deficit as a fundamental process in OCRD, no validated treatment exists that can directly
alter RI deficits and in turn ameliorate OCRD symptoms. It is vital to develop a highly
specific intervention that precisely engages a theoretically and empirically
well-grounded target such as RI deficits, to significantly improve the efficacy of our
intervention efforts. The overarching goal of this study is to examine whether the
computerized cognitive training program can improve the neural indicators of the ability
to inhibit inappropriate responses, and produce a clinically meaningful level of
reduction in obsessive-compulsive disorder and related symptoms. Our central hypothesis
is that cognitive training designed to enhance RI will improve neural indices:
fronto-basal ganglia circuitry, especially right inferior frontal cortex of RI among
individuals with OCRDs. We also hypothesize that the change in the RI neural circuit will
mediate the consequent clinical improvements in OCRD symptomatology.
Phase I (R61) will aim to examine change in neural RI indices via the RIT intervention,
Adults diagnosed with OCRD problems (OCD, TTM, or SPD) will be randomly assigned to the
RIT or placebo control (PLT) condition. At pre- and post-training, neurobehavioral
measures of RI will be taken, including the Stop-Signal Task (SST) assessing SSRT and
fMRI task assessing rIFC activation. Each RIT participant will continue with the training
within the range of 8 to 16 sessions until the criterion-level change in SSRT is attained
(based on the ongoing SSRT estimation), with the PLT group receiving comparable levels of
training. We will also collect 1-month follow-up data on functional outcomes in order to
obtain information on the effect of the intervention on the OCRD symptom indices.
Phase II (R33) is identical to Phase I in the overall study procedures. Adults diagnosed
with OCRD problems will be assigned to RIT or PLT. Analytic focus will be on the
reduction in OCRD symptoms and their potential mediational pathway (rather than the
change in the neural RI indices, which is the primary analytic focus in Phase I). Other
than these differences, the overall flow and procedures of the study will be identical
between Phases I and II.
The key assessments will include the fMRI tasks of the RI processes and
clinician-administered measures of OCRD symptoms. There are other self-reported,
computerized, and clinician-administered measures that will be administered across
various points over the course of the study.