Xinyu Hu1, Wenyu Liu2, Dong Zhou2, Qiyong Gong1, and Xiaoqi Huang1
1Huaxi MR Research Center (HMRRC), West China Hospital of Sichuan University, Chengdu, China, 2Department of Neurology, West China Hospital of Sichuan University, Chengdu, China
Synopsis
We
performed the first resting-state fMRI study integrating both whole-brain
functional connectivity (FC) and seed-based FC analyses to explore the
network-level neural function alterations in patients with periventricular
nodular heterotopia (PNH). Our findings (i) identified lower functional
connectivity strength (FCS, an index of whole-brain connectivity) in bilateral
insula, higher FC in the precuneus and lower FC in the anterior cingulate
cortex/medial prefrontal cortex and cerebellum networks in PNH patients and
(ii) demonstrated that the significant insular hypoactivation represented the
cortical hub of the whole-brain networks in PNH, which might be of clinical
significance in predicting disability progression of PNH.
Introduction
Periventricular nodular heterotopia (PNH) is a common
structural malformation of cortical development in which nodules of neurons are
ectopically retained along the lateral ventricles [1]. The clinical manifestations of PNH is characterized by seizure disorder
ranging from mild to intractable, mental retardation, hypotonia and reading
dysfluency [2]. Previous researches using
diffusion MRI or structural MRI have revealed white matter disruption of the
corpus callosum in PNH patients compared with controls [3, 4] and demonstrated that the strength of abnormal structural connectivity
is higher among PNH patients with the longest duration of epilepsy [5]. However, the involvement of functional connectivity
(FC) alterations in the pathogenesis of PNH remained elusive. Therefore, the
aim of the current study was to explore the resting-state network-level neural
function alterations in patients with PNH by integrating both whole-brain FC
and seed-based FC analytical approaches [6].
Specifically, we firstly evaluated abnormalities in whole-brain FC, as measured
by functional connectivity
strength (FCS) [7], in PNH patients compared with controls. Additionally,
regions with significant FCS alterations were selected as seeds in subsequent
seed-based FC analyses [8]. Finally, we
investigated the associations between these functional neural substrates and
clinical features in PNH patients.Methods
38 patients diagnosed with PNH related epilepsy were recruited from
the epilepsy center of the West China Hospital while 38 healthy controls (HCS) matched
for age and gender were enrolled through posters. This investigation was
approved by the local ethical committee and all subjects had provided informed
consent. Assessment of mental state was performed by Mini-mental State
Examination (MMSE). The 14-item Hamilton Anxiety Scale (HAMA) and 17-item
Hamilton Depression Scale (HAMD) were used to rate anxiety and depressive
symptoms, respectively. Resting-state
fMRI data of all the
participants were acquired via a 3-Tesla Siemens MRI system with an 8 channel
phase array head coil (TR/TE=2000/30msec,
flip angle=90°, slice thickness=5mm with no gap, 30 axial slices, 200 volumes
in each run).
The preprocessing of functional
images was
performed using DPABI software [9]. The calculation of
FCS maps was performed using REST toolbox [10].
Afterwards, we chose the regions with FCS alterations in PNH compared with HCS
as seeds to conduct additional seed-based interregional correlation analyses in
order to explore more specific abnormalities of FC patterns related to the
identified hubs. The statistical analyses of FCS and seed-based FC maps between
PNH patients and HCS were conducted using the voxel-based two-sample t-test in SPM8
(http://www.fil.ion.ucl.ac.uk/spm). The voxel level statistical threshold was
set at P < 0.001 with a minimum cluster extent of 100 voxels without
correction. Meanwhile, the statistical threshold of cluster level was set at P
< 0.05 with family-wise error (FWE) correction. Areas with significant FCS
or FC alterations between groups were extracted as regions of interest for
Pearson correlation analyses with clinical variables including MMSE scores, HAMA
scores, HAMD scores, seizure frequency and duration of epilepsy.
Results
In comparison with controls, FCS reduction of bilateral insula was
identified in PNH patients (P < 0.05, FWE correction) (Figure 1). Meanwhile,
PNH patients showed higher FC in the precuneus and lower FC in the left
cerebellum and anterior cingulate cortex (ACC) extending to medial PFC with
seed placed in the left insula where higher FCS was detected (P<0.05, FWE correction).
These findings of FC alterations remained reproducible when the seed was placed
in the right insula (P<0.05, FWE correction) (Figure 2). Pearson correlation
analyses revealed that the epilepsy duration was negatively correlated with FCS
value in the left insula (r = -0.39, P = 0.015) and right insula (r = -0.36, P
= 0.028), separately.Discussion
In the current study, we found FCS reductions in the
bilateral insular areas and higher FC in the precuneus in patients with PNH
relative to controls. The insula is the core structure of the salience network
(SN) which plays a key role in regulating the dynamic changes of external
stimuli and internal events [11]. while
the precuneus is the main component of the default mode network (DMN), which is
involved in the monitoring of internal processes including autobiographical and
self-monitoring [12]. The hypoactivation
of the insula and the hyperactivation of precuneus suggested the disequilibrium
between the DMN and the SN might be associated with the pathophysiology of PNH.Conclusion
Using the resting-state FCS analytical approach, we
identified significant insular hypoactivation in PNH patients, which suggests
that the insula might represent the cortical hub of the whole-brain networks in
this condition. Meanwhile, Pearson correlation findings indicated the insular
FCS might be of clinical significance in predicting disability progression in PNH
patients. Additionally, the disruption of resting-state FC in the DMN and the
fronto-limbic-cerebellar circuits pointed to a connectivity-based
neuropathological process in PNH. Acknowledgements
This study was supported by National Nature Science Foundation (Grant NO. 81671669), Science and Technology Project of Sichuan Province (Grant NO. 2017JQ0001)References
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