Altered regional and circuit resting-state activity associated with unilateral hearing loss.
The deprivation of sensory input after hearing damage results in functional reorganization of the brain including cross-modal plasticity in the sensory cortex and changes in cognitive processing. However, it remains unclear whether partial deprivation from unilateral auditory loss (UHL) would similarly affect the neural circuitry of cognitive processes in addition to the functional organization of sensory cortex. Here, we used resting-state functional magnetic resonance imaging to investigate intrinsic activity in 34 participants with UHL from acoustic neuroma in comparison with 22 matched normal controls. In sensory regions, we found decreased regional homogeneity (ReHo) in the bilateral calcarine cortices in UHL. However, there was an increase of ReHo in the right anterior insular cortex (rAI), the key node of cognitive control network (CCN) and multimodal sensory integration, as well as in the left parahippocampal cortex (lPHC), a key node in the default mode network (DMN). Moreover, seed-based resting-state functional connectivity analysis showed an enhanced relationship between rAI and several key regions of the DMN. Meanwhile, lPHC showed more negative relationship with components in the CCN and greater positive relationship in the DMN. Such reorganizations of functional connectivity within the DMN and between the DMN and CCN were confirmed by a graph theory analysis. These results suggest that unilateral sensory input damage not only alters the activity of the sensory areas but also reshapes the regional and circuit functional organization of the cognitive control network.
Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, China.
Xingchao
X
Wang
MRI Research Center and Beijing City Key Lab for Medical Physics and Engineering, Peking University, Beijing, China.
Yang
Y
Fan
Department of Neural reconstruction, Beijing Neurosurgery Institute, Capital Medical University, Beijing, China.
Fu
F
Zhao
Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, China.
Zhenmin
Z
Wang
MRI Research Center and Beijing City Key Lab for Medical Physics and Engineering, Peking University, Beijing, China.
Jianqiao
J
Ge
Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, China.
Kai
K
Zhang
Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, China.
Zhixian
Z
Gao
MRI Research Center and Beijing City Key Lab for Medical Physics and Engineering, Peking University, Beijing, China; McGovern Institute for Brain Research, Peking University, Beijing, China.
Jia-Hong
JH
Gao
Neuroimaging Research Branch, National Institute on Drug Abuse, National Institutes of Health, Baltimore, Maryland, United States of America.
Yihong
Y
Yang
Department of Psychology, Queens College, The City University of New York, Flushing, New York, United States of America; Department of Psychiatry, Mount Sinai School of Medicine, New York, New York, United States of America; Friedman Brain Institute, Mount Sinai School of Medicine, New York, New York, United States of America; Fishberg Department of Neuroscience, Mount Sinai School of Medicine, New York, New York, United States of America.
Jin
J
Fan
MRI Research Center and Beijing City Key Lab for Medical Physics and Engineering, Peking University, Beijing, China.
Qihong
Q
Zou
Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, China; Department of Neural reconstruction, Beijing Neurosurgery Institute, Capital Medical University, Beijing, China.
Pinan
P
Liu
D000328:Adult; D016022:Case-Control Studies; D002540:Cerebral Cortex / Q000503:physiopathology*; D005260:Female; D046088:Hearing Loss, Unilateral / Q000503:physiopathology*; D006624:Hippocampus / Q000503:physiopathology*; D006801:Humans; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D009434:Neural Pathways / Q000503:physiopathology*