European radiology · 2017
Retrosplenial cortical thinning as a possible major contributor for cognitive impairment in HIV patients.
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Shin Na-Young, Hong Jinwoo, Choi Jun Yong, Lee Seung-Koo, Lim Soo Mee, Yoon Uicheul
Аннотация
OBJECTIVES: To identify brain cortical regions relevant to HIV-associated neurocognitive disorder (HAND) in HIV patients.
METHODS: HIV patients with HAND (n = 10), those with intact cognition (HIV-IC; n = 12), and age-matched, seronegative controls (n = 11) were recruited. All participants were male and underwent 3-dimensional T1-weighted imaging. Both vertex-wise and region of interest (ROI) analyses were performed to analyse cortical thickness.
RESULTS: Compared to controls, both HIV-IC and HAND showed decreased cortical thickness mainly in the bilateral primary sensorimotor areas, extending to the prefrontal and parietal cortices. When directly comparing HIV-IC and HAND, HAND showed cortical thinning in the left retrosplenial cortex, left dorsolateral prefrontal cortex, left inferior parietal lobule, bilateral superior medial prefrontal cortices, right temporoparietal junction and left hippocampus, and cortical thickening in the left middle occipital cortex. Left retrosplenial cortical thinning showed significant correlation with slower information processing, declined verbal memory and executive function, and impaired fine motor skills.
CONCLUSIONS: This study supports previous research suggesting the selective vulnerability of the primary sensorimotor cortices and associations between cortical thinning in the prefrontal and parietal cortices and cognitive impairment in HIV-infected patients. Furthermore, for the first time, we propose retrosplenial cortical thinning as a possible major contributor to HIV-associated cognitive impairment.
KEY POINTS: • Primary sensorimotor and supplementary motor cortices were selectively vulnerable to HIV infection • Prefrontal and parietal cortical thinning was associated with HIV-associated cognitive impairment • Retrosplenial cortical thinning might be a major contributor to HIV-associated cognitive impairment.
METHODS: HIV patients with HAND (n = 10), those with intact cognition (HIV-IC; n = 12), and age-matched, seronegative controls (n = 11) were recruited. All participants were male and underwent 3-dimensional T1-weighted imaging. Both vertex-wise and region of interest (ROI) analyses were performed to analyse cortical thickness.
RESULTS: Compared to controls, both HIV-IC and HAND showed decreased cortical thickness mainly in the bilateral primary sensorimotor areas, extending to the prefrontal and parietal cortices. When directly comparing HIV-IC and HAND, HAND showed cortical thinning in the left retrosplenial cortex, left dorsolateral prefrontal cortex, left inferior parietal lobule, bilateral superior medial prefrontal cortices, right temporoparietal junction and left hippocampus, and cortical thickening in the left middle occipital cortex. Left retrosplenial cortical thinning showed significant correlation with slower information processing, declined verbal memory and executive function, and impaired fine motor skills.
CONCLUSIONS: This study supports previous research suggesting the selective vulnerability of the primary sensorimotor cortices and associations between cortical thinning in the prefrontal and parietal cortices and cognitive impairment in HIV-infected patients. Furthermore, for the first time, we propose retrosplenial cortical thinning as a possible major contributor to HIV-associated cognitive impairment.
KEY POINTS: • Primary sensorimotor and supplementary motor cortices were selectively vulnerable to HIV infection • Prefrontal and parietal cortical thinning was associated with HIV-associated cognitive impairment • Retrosplenial cortical thinning might be a major contributor to HIV-associated cognitive impairment.