Increased interhemispheric resting-state functional connectivity in paroxysmal kinesigenic dyskinesia: A resting-state fMRI study

Ren, Jiechuan; Lei, Du; Yang, Tianhua; An, Dongmei; Xiao, Fenglai; Li, Lei; Huang, Xiaoqi; Gong, Qiyong; Zhou, Dong

doi:10.1016/j.jns.2015.02.046

Cited by 22 publications

(30 citation statements)

References 53 publications

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“…Analysis of functional neuroimaging in patients with PKD has failed to define the distinct neural characteristics of PKD-D and PKD-C. 9,10,13,15,17,31 Consequently, diagnosis remains based on clinical symptoms that are diverse and vary between individuals. 5 To this end, we investigated the distinct neural characteristics of PKD-D and PKD-C.…”

Section: Discussionmentioning

confidence: 99%

“…32 Resting-state fMRI (in the absence of movement) presented evidence of hyperconnectivity in the PKD and provided theoretical explanations for movement-related fMRI findings. 17 …”

Section: Discussionmentioning

confidence: 99%

“…Detailed and comprehensive investigations are therefore required to establish the pathology of the disorder. 9,10,17 …”

Section: Discussionmentioning

confidence: 99%

“…10,12 Earlier structural 12,15 and functional 10,17 studies suggested bilateral abnormality in cortical-basal ganglia-thalamus circuitry regions, including thalamus and putamen, a common pathophysiology in PKD. From the relatively detailed clinical information, we concluded that attacks were predominantly left-sided in 12 patients, including unilateral, bilateral, and alternating cases, and right-sided in 10 patients.…”

Section: Discussionmentioning

confidence: 99%

“…Resting-state functional magnetic resonance imaging (RS-fMRI) studies have revealed increased intrinsic activity in the bilateral putamen and cortical-basal ganglia circuitry in PKD patients. 9,10 More recently, increased resting-state interhemispheric functional connectivity in the basal ganglia-thalamo-cortical circuitry has been demonstrated in PKD patients, 17 suggesting that PKD can be considered a circuit disorder and not restricted to localized structural or functional abnormalities. 18,19 Regional homogeneity (ReHo) is an effective measure of local connectivity, which quantifies the functional communication between a center voxel and its neighbors in 3 dimensions.…”

Section: Introductionmentioning

confidence: 99%

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Frequency-Specific Local Synchronization Changes in Paroxysmal Kinesigenic Dyskinesia

Liu

Miao

et al. 2016

Medicine

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The neurobiological basis of paroxysmal kinesigenic dyskinesia (PKD) is poorly defined due to the lack of reliable neuroimaging differences that can distinguish PKD with dystonia (PKD-D) from PKD with chorea (PKD-C). Consequently, diagnosis of PKD remains largely based on the clinical phenotype. Understanding the pathophysiology of PKD may facilitate discrimination between PKD-D and PKD-C, potentially contributing to more accurate diagnosis.We conducted resting-state functional magnetic resonance imaging on patients with PKD-D (n = 22), PKD-C (n = 10), and healthy controls (n = 32). Local synchronization was measured in all 3 groups via regional homogeneity (ReHo) and evaluated using receiver operator characteristic analysis to distinguish between PKD-C and PKD-D.Cortical-basal ganglia circuitry differed significantly between the 2 groups at a specific frequency. Furthermore, the PKD-D and PKD-C patients were observed to show different spontaneous brain activity in the right precuneus, right putamen, and right angular gyrus at the slow-5 frequency band (0.01–0.027 Hz).The frequency-specific abnormal local synchronization between the 2 types of PKD offers new insights into the pathophysiology of this disorder to some extent.

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Section: Discussionmentioning

confidence: 99%

“…32 Resting-state fMRI (in the absence of movement) presented evidence of hyperconnectivity in the PKD and provided theoretical explanations for movement-related fMRI findings. 17 …”

Section: Discussionmentioning

confidence: 99%

“…Detailed and comprehensive investigations are therefore required to establish the pathology of the disorder. 9,10,17 …”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Frequency-Specific Local Synchronization Changes in Paroxysmal Kinesigenic Dyskinesia

Liu

Miao

et al. 2016

Medicine

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An Electroencephalography Profile of Paroxysmal Kinesigenic Dyskinesia

Luo,

Huang,

et al. 2024

Advanced Science

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Paroxysmal kinesigenic dyskinesia (PKD) is associated with a disturbance of neural circuit and network activities, while its neurophysiological characteristics have not been fully elucidated. This study utilized the high‐density electroencephalogram (hd‐EEG) signals to detect abnormal brain activity of PKD and provide a neural biomarker for its clinical diagnosis and PKD progression monitoring. The resting hd‐EEGs are recorded from two independent datasets and then source‐localized for measuring the oscillatory activities and function connectivity (FC) patterns of cortical and subcortical regions. The abnormal elevation of theta oscillation in wildly brain regions represents the most remarkable physiological feature for PKD and these changes returned to healthy control level in remission patients. Another remarkable feature of PKD is the decreased high‐gamma FCs in non‐remission patients. Subtype analyses report that increased theta oscillations may be related to the emotional factors of PKD, while the decreased high‐gamma FCs are related to the motor symptoms. Finally, the authors established connectome‐based predictive modelling and successfully identified the remission state in PKD patients in dataset 1 and dataset 2. The findings establish a clinically relevant electroencephalography profile of PKD and indicate that hd‐EEG can provide robust neural biomarkers to evaluate the prognosis of PKD.

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The effect of chronic neuroglycopenia on resting state networks in GLUT1 syndrome across the lifespan

Vaudano

Olivotto

Ruggieri

et al. 2019

Human Brain Mapping

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Glucose transporter type I deficiency syndrome (GLUT1DS) is an encephalopathic disorder due to a chronic insufficient transport of glucose into the brain. PET studies in GLUT1DS documented a widespread cortico-thalamic hypometabolism and a signal increase in the basal ganglia, regardless of age and clinical phenotype. Herein, we captured the pattern of functional connectivity of distinct striatal, cortical, and cerebellar regions in GLUT1DS (10 children, eight adults) and in healthy controls (HC, 19 children, 17 adults) during rest. Additionally, we explored for regional connectivity differences in GLUT1 children versus adults and according to the clinical presentation. Compared to HC, GLUT1DS exhibited increase connectivity within the basal ganglia circuitries and between the striatal regions with the frontal cortex and cerebellum. The excessive connectivity was predominant in patients with movement disorders and in children compared to adults, suggesting a correlation with the clinical phenotype and age at fMRI study. Our findings highlight the primary role of the striatum in the GLUT1DS pathophysiology and confirm the dependency of symptoms to the patients' chronological age. Despite the reduced chronic glucose uptake, GLUT1DS exhibit increased connectivity changes in regions highly sensible to glycopenia. Our results may portrait the effect of neuroprotective brain strategy to overcome the chronic poor energy supply during vulnerable ages. K E Y W O R D S basal ganglia, cerebellum, children, functional connectivity, GLUT1DS, neuroglycopenia, striatum

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Increased interhemispheric resting-state functional connectivity in paroxysmal kinesigenic dyskinesia: A resting-state fMRI study

Cited by 22 publications

References 53 publications

Frequency-Specific Local Synchronization Changes in Paroxysmal Kinesigenic Dyskinesia

Frequency-Specific Local Synchronization Changes in Paroxysmal Kinesigenic Dyskinesia

An Electroencephalography Profile of Paroxysmal Kinesigenic Dyskinesia

The effect of chronic neuroglycopenia on resting state networks in GLUT1 syndrome across the lifespan

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