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Abnormal thickening and thinning of the cerebral cortex in idiopathic normal‐pressure hydrocephalus
Author(s) -
Kang Kyunghun,
Han Jaehwan,
Yoon Uicheul,
Lee HoWon,
Lee SangWoo,
Jeong Shin Young
Publication year - 2020
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1002/alz.042212
Subject(s) - medicine , insula , middle frontal gyrus , cerebral cortex , gait disturbance , hydrocephalus , neuroscience , superior frontal gyrus , gyrus , psychology , magnetic resonance imaging , physical medicine and rehabilitation , radiology
Background We investigated differences in cortical thickness utilizing automated surface‐based cortical thickness analysis in 2 groups: idiopathic normal‐pressure hydrocephalus (INPH) patients who had a positive response to the cerebrospinal fluid tap test and healthy controls. We also explored whether a relationship exists between cortical thinning and gait disturbance in INPH patients. We hypothesized that INPH patients might show a characteristic pattern of cortical thickness change and that there may be unique relationships between cortical thinning and gait disturbance in INPH patients. Method Forty‐nine INPH patients and 26 healthy controls were imaged with MRI, including 3‐dimensional volumetric images, for automated surface‐based cortical thickness analysis across the entire brain. Gait disturbance features related to INPH were determined using the Gait Status Scale (GSS). Result Compared with age‐ and gender‐matched healthy controls, unexpectedly, INPH patients showed statistically significant cortical thickening mainly in areas located in the high convexity of the frontal, parietal, and occipital regions. Additionally, cortical thinning mainly in temporal and orbitofrontal regions was observed in the INPH group relative to the control group. The GSS scores were negatively correlated with cortical thickness in the medial orbital part of the superior frontal gyrus, gyrus rectus, superior temporal gyrus, temporal pole, and insula. Conclusion A distinctive pattern of cortical thickness changes was found in INPH patients. We cautiously suggest that cortical thickening in INPH can result from reactive gliosis. Further, our results support the hypothesis that cortical thinning in INPH can result from neuronal degeneration. In addition, cortical thinning can play an important role in gait disturbances in INPH patients.