Abstract
Infantile spasms (IS) syndrome is an age-dependent epileptic encephalopathy, which occurs in children characterized by spasms, impaired consciousness, and hypsarrhythmia. Abnormalities in default mode network (DMN) might contribute to the loss of consciousness during seizures and cognitive deficits in children with IS. The purpose of the present study was to investigate the changes in DMN with functional connectivity (FC) and amplitude of low-frequency fluctuation (ALFF), the two methods to discover the potential neuronal underpinnings of IS. The consistency of the two calculate methods of DMN abnormalities in IS patients was also our main focus. To avoid the disturbance of interictal epileptic discharge, our testing was performed within the interictal durations without epileptic discharges. Resting-state fMRI data were collected from 13 patients with IS and 35 sex- and age-matched healthy controls. FC analysis with seed in posterior cingulate cortex (PCC) was used to compare the differences between two groups. We chose PCC as the seed region because PCC is the only node in the DMN that directly interacts with virtually all other nodes according to previous studies. Furthermore, the ALFF values within the DMN were also calculated and compared between the two groups. The FC results showed that IS patients exhibited markedly reduced connectivity between posterior seed region and other areas within DMN. In addition, part of the brain areas within the DMN showing significant difference of FC had significantly lower ALFF signal in the patient group than that in the healthy controls. The observed disruption in DMN through the two methods showed that the coherence of brain signal fluctuation in DMN during rest was broken in IS children. Neuronal functional impairment or altered integration in DMN would be one neuroimaging characteristic, which might help us to understand the underlying neural mechanism of IS. Further studies are needed to determine whether the disturbed FC and ALFF observed in the DMN are related to cognitive performance in IS patients.
Highlights
Infantile spasms (IS) syndrome, or West syndrome, one kind of intractable epileptic encephalopathy, is characterized by early-onset flexion–extension motor spasms, mental retardation or regression, developmental delay, and a pathognomonic electroencephalography (EEG) pattern of hypsarrhythmia, which consists of a chaotic and disorganized activity with asynchronous largeDecreased Neuronal Activity in default mode network (DMN) amplitude slow waves mixed with single, multifocal spikes and sharp waves followed by attenuation [1,2,3]
The between-group differences in DMN, which was defined by the functional connectivity (FC) with seed in the posterior cingulate cortex (PCC), were achieved through two-sample t-test
The between-group differences in DMN, which was defined by the increased amplitude of low-frequency fluctuation (ALFF) in healthy controls, were obtained through two-sample t-test
Summary
Infantile spasms (IS) syndrome, or West syndrome, one kind of intractable epileptic encephalopathy, is characterized by early-onset flexion–extension motor spasms, mental retardation or regression, developmental delay, and a pathognomonic electroencephalography (EEG) pattern of hypsarrhythmia, which consists of a chaotic and disorganized activity with asynchronous largeDecreased Neuronal Activity in DMN amplitude slow waves mixed with single, multifocal spikes and sharp waves followed by attenuation [1,2,3]. Because epileptic seizure itself causes and aggravates behavioral and developmental performances, neurocognitive outcome of IS is poor [4, 5]. The potential neuronal underpinnings of impaired cognition and functional brain reorganization are not fully elucidated. The functional brain networks that are involved in cognitive processing can be identified through fMRI. Brain regions with negative blood oxygen level-dependent (BOLD) activity during cognitive processing are defined as default mode network (DMN) in which the regions are functionally connected with each other during rest when spontaneous fluctuations of the BOLD time course occur [7]. We intended to measure the functional changes in DMN to interpret the neuronal underpinnings with resting-state fMRI
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