Introduction

The caudate nucleus (Cd) is one of the structures that make up the corpus striatum, which is a component of the basal ganglia. This brain area is one of the brain structures which involved in the memory system and functions as part of the cortico–basal ganglia–thalamic loop. The patients with obsessive compulsive disorder (OCD) have shown cognitive defect and neurofunctional abnormality through various clinical and functional studies. It can be assumed that Cd may be dysfunctional in persons with OCD, in that it may perhaps be unable to properly regulate the transmission of information during memory processing between the thalamus and the prefrontal cortex. Therefore, for verifying how the OCD symptom affects to abnormal functional activity and connectivity at Cd during memory processing, and whether leading to brain volume changes in direct or indirect, we performed multi study combined with fMRI and VBM study.

Methods

Forty right-handed subjects included twenty patients with OCD (mean age, 29.4±9.9 years) who are diagnosed by a psychiatrist using the DSM-IV-TR and 20 healthy controls (mean age, 29.7±8.3 years) with no history of neurological or psychiatric illness. The duration of patient’s illness was 5.8±4.7 years. All the participants underwent the clinical interviewed by using Yale-Brown Obsessive-Compulsive Scale, Hamilton Depression Scale 17 and Hamilton Anxiety Scale. The difference of symptom severity in both groups was analyzed by Mann-Whitney U test. The activation paradigm for memory processing consisted of the following cycle: rest (14s), first encoding (18s), rest (14s), first retrieval (18s), rest (14s), second encoding (18s), rest (14s), second retrieval (18s), and rest (14s). MR scanning was performed on a 3 Tesla Magnetom Verio MR Scanner (Siemens Medical Solutions, Erlangen, Germany) with an 8-channel head coil. Anatomical T1-weighted images were acquired using a three-dimensional magnetization-prepared rapid acquisition gradient-echo sequence with repetition time (TR)/echo time (TE)= 1900/2.35 ms, field-of-view (FOV)= 22×22 cm2, matrix size= 256×256, number of excitation (NEX)= 1 and slice thickness= 1 mm. functional images were acquired from a total of 25 axial slices parallel to an anterior commissure to posterior commissure line using a gradient-echo echo planner image (GRE-EPI) with the follow parameters: TR/TE= 2000/30 ms, flip angle= 90°, FOV= 22×22 cm2, metrix size= 64×64, NEX= 1, and slice thickness= 5mm without a slice gap. The 3D T1 image data were processed by SPM8 with DARTEL tool. The fMRI data were processed by using SPM12 and CONN software.

Results

In fMRI results, patients with OCD showed higher activities in the right/left inferior temporal gyrus (ITG), medial prefrontal cortex (MPFC), dorsolateral prefrontal cortex (DLPFC) and anterior cingulate cortex (ACC) compare to healthy controls in memory encoding (uncorrected P<0.001) (figure 1a). The Cd, DLPFC and ITG had a positively connected each other in OCD patients. However, the Cd connected with ACC and right ITG connected with left ITG positively in healthy controls (uncorrected P<0.001) (figure 2a). In memory retrieval, Cd is observed as higher activity in OCD patients (uncorrected P<0.001) (figure 1b). This Cd has composed positive connectivity with DLPFC and vmPFC in OCD patients, but negative connectivity in healthy controls (uncorrected P<0.001) (figure 2b). In VBM, OCD patients showed a significant increase in gray matter (GM) volumes: cerebellum, DLPFC, orbitofrontal cortex (OFC), Hippocampus, Cd and TIG and white matter volumes: DLPFC (FWE P<0.05) (figure 3). The GM volume in Cd and OFC of patients with OCD showed positive correlation with HAMA and Y-BOCS (r=0.458, p=0.042; r=0.525, p=0.016) (figure 4). The BOLD signal changes in Cd of patients with OCD showed positive correlation with Y-BOCS (r=0.478, p=0.033) (figure 5). In summary, the lasting psychiatric symptoms with OCD more than five years may be closely associated with neurofunctional and morphological changes, give rise to abnormal explicit memory processing.

Conclusion

This finding will be helpful to understand the neuroanatomical and functional mechanism for explicit memory processing in relation to OCD symptoms. In particular, it puts forward a possibility that focal functional connectivity and brain volume changes may be affected by lasting OCD symptoms, and leading to memory dysfunction. The functional and morphological profiles of Cd could be emphasized to abnormal processing of explicit memory by OCD symptoms. Furthermore, it will be enhancing the diagnostic accuracy for OCD as additional information on the brain functional and cerebral volume charges.

References

1. Yager LM, et al, Neuroscience. 2015;301:529-41. 2. Jang IS, et al. Neuroreport. 2017;28:1-9.