White matter lesions associated with the reemergence of grasp reflexes in patients with idiopathic normal pressure hydrocephalus

特发性正常压力脑积水患者抓握反射恢复相关的白质病变

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Abstract

BACKGROUND: The white matter damage inducing the reemergence of grasp reflexes and their potential lateralization remains unstudied. Idiopathic normal pressure hydrocephalus (iNPH), a subcortical dementia, is an ideal model for these investigations. We aim to understand the contributions of white matter to the inhibition of grasp reflexes in patients with iNPH. METHODS: A total of 48 patients (mean age at admission: 77.8 ± 5.2 years; 56% male) with probable iNPH were retrospectively enrolled in this study. The intensity of grasp reflexes was assessed using a four-category classification. A voxel-based morphometric analysis of the fractional anisotropy (FA) maps was conducted to identify responsible regions related to the grasp reflex. The white matter fibers passing through these regions were tracked using fiber-tracking data from fifty age-/sex-matched healthy subjects from the Lifespan Human Connectome Project Aging Study. Fibers with an inter-subject overlap rate > 50% were defined as reliable tracts for further discussion. RESULTS: Positive grasp reflex was identified in 60% (29/48) of probable iNPH cases. The voxel-based multiple regression analysis revealed that the reflex intensity scores were negatively correlated with FA values in the right frontal subcortical white matter near the anterior horn of the right lateral ventricle. The white matter fibers project through this structure mainly to the posterior parts of the right superior, middle, and inferior frontal gyri; the bilateral presupplementary motor areas; the right dorsal anterior cingulate cortex; the ventral lateral nuclei of the bilateral thalami; the pulvinar inferior nucleus of the right thalamus; the lateral part of the right putamen; and the right subthalamic nucleus. CONCLUSION: The inhibition of grasp reflexes is achieved via a right-lateralized prefrontal cortex-basal ganglia-thalamocortical 'stopping' network.

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