Aberrant Resting-State Corticostriatal Functional Connectivity in Cirrhotic Patients with Hyperintense Globus Pallidus on T1-Weighted MR Imaging

Xi-Qi Zhu,Ying Cui,Gao-Jun Teng,Hua-Jun Chen,Yu Wang,Wang Zhan

doi:10.1371/journal.pone.0048886

Xi-Qi Zhu, Ying Cui + Show 4 more

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https://doi.org/10.1371/journal.pone.0048886

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Abstract

Neurobiological and neuroimaging studies have emphasized the structural and functional alterations in the striatum of cirrhotic patients, but alterations in the functional connections between the striatum and other brain regions have not yet been explored. Of note, manganese accumulation in the nervous system, frequently reflected by hyperintensity at the bilateral globus pallidus (GP) on T1-weighted imaging, has been considered a factor affecting the striatal and cortical functions in hepatic decompensation. We employed resting-state functional magnetic resonance imaging to analyze the temporal correlation between the striatum and the remaining brain regions using seed-based correlation analyses. The two-sample t-test was conducted to detect the differences in corticostriatal connectivity between 44 cirrhotic patients with hyperintensity at the bilateral GP and 20 healthy controls. Decreased connectivity of the caudate was detected in the anterior/middle cingulate gyrus, and increased connectivity of the caudate was found in the left motor cortex. A reduction in functional connectivity was found between the putamen and several regions, including the anterior cingulate gyrus, right insular lobe, inferior frontal gyrus, left parahippocampal gyrus, and anterior lobe of the right cerebellum; increased connectivity was detected between the putamen and right middle temporal gyrus. There were significant correlations between the corticostriatal connectivity and neuropsychological performances in the patient group, but not between the striatal connectivity and GP signal intensity. These alterations in the corticostriatal functional connectivity suggested the abnormalities in the intrinsic brain functional organiztion among the cirrhotic patients with manganese deposition, and may be associated with development of metabolic encephalopathy. The manganese deposition in nervous system, however, can not be an independent factor predicting the resting-state brain dysfunction in real time.

Highlights

Metabolic encephalopathy caused by liver cirrhosis includes a wide spectrum of neurological dysfunction, such as progressive deficits in neuromotor function, cognition, and intellect
An increased expression of peripheral benzodiazepine binding sites was observed in the striatum and prefrontal regions of cirrhotic patients with minimal hepatic encephalopathy (MHE) [6]
We aimed to test whether the temporal correlation of neuronal activity between the striatum and other brain regions changes in the cirrhotic patients with manganese accumulation in their nervous systems, and whether the altered functional connectivity of the striatum correlates with neurocognitive dysfunction in these patients

Summary

Introduction

Metabolic encephalopathy caused by liver cirrhosis includes a wide spectrum of neurological dysfunction, such as progressive deficits in neuromotor function, cognition, and intellect. Subcortical structures, the basal ganglia in particular, are implicated in brain dysfunction induced by hepatic dysmetabolism. Previous studies have demonstrated that lesions of the striatum are involved in chronic acquired hepatocerebral degeneration [1,2,3]. Finlayson and Supeville [4] investigated the neuronal cell loss in basal ganglia samples obtained at autopsy from cirrhotic patients. Guevara and colleagues [5] showed a remarkable decrease in the gray matter density of the putamen coupled with atrophy of the cerebral cortex. An increased expression of peripheral benzodiazepine binding sites was observed in the striatum and prefrontal regions of cirrhotic patients with minimal hepatic encephalopathy (MHE) [6]

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