Kyushu University · Psychology
Professor Tomohiro Nakao's research lab focuses on the neurobiological underpinnings of obsessive-compulsive disorder (OCD) and attention-deficit/hyperactivity disorder (ADHD), with a particular emphasis on brain network dysfunctions, structural and functional neuroimaging, and their relationships to cognitive control and symptom progression. The lab investigates how abnormalities in key brain regions—such as the pre-SMA, IFG, dorsal caudate, and salience network—contribute to impaired response inhibition and cognitive flexibility in OCD. Longitudinal and resting-state fMRI studies are central to understanding disease progression and the impact of pharmacological and psychological interventions.
Figures are computed from collected data and may differ slightly.
These findings confirm that the most prominent and replicable structural abnormalities in ADHD are in the basal ganglia. They furthermore suggest that ADHD patients may progressively catch up with their developmental delay with advancing age and that use of stimulant medication may be associated with normalization of structural abnormalities in ADHD, although longitudinal studies are needed to confirm both observations.
Obsessive-compulsive disorder (OCD) was previously considered refractory to most types of therapeutic intervention. There is now, however, ample evidence that selective serotonin reuptake inhibitors and behavior therapy are highly effective methods for treatment of OCD. Furthermore, recent neurobiological studies of OCD have found a close correlation between clinical symptoms, cognitive function, and brain function. A large number of previous neuroimaging studies using positron emission tomograp
Recent evidence suggests that presupplementary motor area (pre-SMA) and inferior frontal gyrus (IFG) play an important role in response inhibition. However, no study has investigated the relationship between these brain networks at resting-state and response inhibition in obsessive-compulsive disorder (OCD). We performed resting-state functional magnetic resonance imaging scans and then measured the response inhibition of 41 medication-free OCD patients and 49 healthy control (HC) participants b
These results provide evidence that the impaired cognitive flexibility of OCD may be associated with dysfunctions of the brain network from the dorsal caudate (DC) to important nodes of the salience network. Our results extend the neuropsychological model of OCD by showing intrinsically different associations between OCD and HC in functional network and cognitive flexibility.
Not a few patients with obsessive-compulsive disorder (OCD) have experienced events that affected the onset. The onset of OCD is not limited to the original meaning of trauma; rather, traumatic experiences such as unexpected exposure to contaminants or various stressful life events often cause the onset of OCD. It would be useful to understand the experiences surrounding the onset, including stressful life events and traumatic experiences, for comprehension of the pathophysiology of OCD. In the
The results suggested that abnormal brain activation occurs in the early phase of OCD and that the long-term persistence of OCD might involve a decline in cognitive function.
Hoarding disorder (HD) is a newly listed disease in the new category of Obsessive-Compulsive and Related Disorders in the DSM-5. Patients with HD find it difficult to discard possessions regardless of their actual value and to organize those things. As a result, the possessions overflow the living space and hinder living functions. Though the hoarding symptom had been regarded as a subtype of obsessive-compulsive disorder (OCD) to date, recent studies have revealed many differences in clinical c
The results might help to explain the inconsistency of previous studies. As with OCD, HD is considered to have cognitive dysfunction as its basis. This result is convincing after considering the clinical features of HD and suggested that structural abnormalities in the prefrontal regions might relate to the pathophysiology of HD.
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