Proton Chemical Shift Imaging of the Brain in Pediatric and Adult Developmental Stuttering

O’Neill, Joseph; Dong, Zhengchao; Bansal, Ravi; Ivanov, Iliyan; Hao, Xuejun; Desai, Jay; Pozzi, Elena; Peterson, Bradley S.

doi:10.1001/jamapsychiatry.2016.3199

Cited by 9 publications

(8 citation statements)

References 58 publications

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“…These findings are consistent with previous anatomical studies reporting reduced gray matter volumes and reduced fractional anisotropy in the left or bilateral IFG [ 17 – 19 ], as well as with previous fMRI studies reporting lower intrinsic functional connectivity in the left IFG [ 39 ] and deficient left hemisphere connectivity between inferior frontal and premotor cortices under auditory and visual stimulation [ 63 ]. Our finding of reduced intrinsic functional connectivity of the IFG is also consistent with our prior findings of reduced perfusion and reduced spectroscopic indices of neural density in Broca’s region in the same sample of participants as included in the present study [ 5 , 10 ].…”

Section: Discussionsupporting

confidence: 93%

“…Other DTI studies have also shown that adults who stutter have reduced fractional anisotropy (FA) in the left sensorimotor cortex [ 21 – 22 ]. Our recent spectroscopy study in the same participants of the present study reported reduced levels of N-acetyl aspartate (NAA), an index of neural density, in inferior and superior frontal cortices (including Broca’s region) and caudate nucleus, and increased NAA in the posterior cingulate, lateral parietal, and parahippocampal cortices, as well as the hippocampus and amygdala [ 5 ].…”

Section: Introductionmentioning

confidence: 92%

“…Prior neuroimaging studies have revealed structural and functional differences in people who stutter (PWS) compared with fluent speakers. The preponderance of evidence currently suggests that the pathogenesis of stuttering involves neural systems involved in the production and control of speech, those within Broca’s region of the inferior frontal gyrus and associated portions of the arcuate fasciculus, as well as their interconnections with cortico-striato-thalamo-cortical (CSTC) loops [ 5 – 11 ]. Voxel-based morphometry studies using anatomical Magnetic Resonance Imaging (MRI) have reported atypical leftward asymmetry [ 8 , 12 – 13 ] and increased white matter volumes in the superior temporal gyrus (STG), middle temporal gyrus (MTG), inferior frontal gyrus (IFG), middle frontal gyrus (MFG) and corpus callosum [ 14 – 16 ] of adults who stutter compared with controls.…”

Section: Introductionmentioning

confidence: 99%

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Functional neural circuits that underlie developmental stuttering

et al. 2017

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The aim of this study was to identify differences in functional and effective brain connectivity between persons who stutter (PWS) and typically developing (TD) fluent speakers, and to assess whether those differences can serve as biomarkers to distinguish PWS from TD controls. We acquired resting-state functional magnetic resonance imaging data in 44 PWS and 50 TD controls. We then used Independent Component Analysis (ICA) together with Hierarchical Partner Matching (HPM) to identify networks of robust, functionally connected brain regions that were highly reproducible across participants, and we assessed whether connectivity differed significantly across diagnostic groups. We then used Granger Causality (GC) to study the causal interactions (effective connectivity) between the regions that ICA and HPM identified. Finally, we used a kernel support vector machine to assess how well these measures of functional connectivity and granger causality discriminate PWS from TD controls. Functional connectivity was stronger in PWS compared with TD controls in the supplementary motor area (SMA) and primary motor cortices, but weaker in inferior frontal cortex (IFG, Broca’s area), caudate, putamen, and thalamus. Additionally, causal influences were significantly weaker in PWS from the IFG to SMA, and from the basal ganglia to IFG through the thalamus, compared to TD controls. ICA and GC indices together yielded an accuracy of 92.7% in classifying PWS from TD controls. Our findings suggest the presence of dysfunctional circuits that support speech planning and timing cues for the initiation and execution of motor sequences in PWS. Our high accuracy of classification further suggests that these aberrant brain features may serve as robust biomarkers for PWS.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 92%

Section: Introductionmentioning

confidence: 99%

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Functional neural circuits that underlie developmental stuttering

et al. 2017

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“…The pathophysiology of stuttering is still unclear. There is, however, increasing evidence of subtle structural and functional differences in the brains of adults and children who stutter relative to their fluent peers [Beal et al, 2013;Chang et al, 2015Chang et al, , 2017Chang and Zhu, 2013;Connally et al, 2014;Cykowski et al, 2010;Desai et al, 2017;O'Neill et al, 2017;Watkins et al, 2008]. One line of research investigated the property of white matter microstructure by measuring fractional anisotropy (FA), which reflects white matter coherence or integrity, through diffusion tensor imaging (DTI).…”

Section: Introductionmentioning

confidence: 99%

White matter developmental trajectories associated with persistence and recovery of childhood stuttering

Chow

Chang

2017

Human Brain Mapping

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Stuttering affects the fundamental human ability of fluent speech production, and can have a significant negative impact on an individual’s psychosocial development. While the disorder affects about 5% of all preschool children, approximately 80% of them recover naturally within a few years of stuttering onset. The pathophysiology and neuroanatomical development trajectories associated with persistence and recovery of stuttering are still largely unknown. Here, we report the first mixed longitudinal diffusion tensor imaging (DTI) study of childhood stuttering. A total of 195 high quality DTI scans from 35 children who stutter (CWS) and 43 controls between 3-12 years of age were acquired, with an average of three scans per child, each collected approximately a year apart. Fractional anisotropy (FA), a measure reflecting white matter structural coherence, was analyzed voxel-wise to examine group and age-related differences using a linear mixed-effects (LME) model. Results showed that CWS exhibited decreased FA relative to controls in the left arcuate fasciculus, underlying the inferior parietal and posterior temporal areas, and the mid body of corpus callosum. Further, white matter developmental trajectories reflecting growth rate of these tract regions differentiated children with persistent stuttering from those who recovered from stuttering. Specifically, we found a reduction in FA growth rate (i.e., slower FA growth with age) in persistent children relative to fluent controls in the left arcuate fasciculus and corpus callosum, which was not evident in recovered children. These findings provide first glimpses into the possible neural mechanisms of onset, persistence, and recovery of childhood stuttering.

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“…The spatial normalization faithfully preserved the MRS data into the high-resolution anatomical MRI space, as our previously published study demonstrated that the region-of-interest based findings matched the voxelwise findings. [38] We normalized the low-resolution MRS data into the high-resolution anatomical space for the following two reasons. (1) We wanted to generate within-individual metabolites maps that were adjusted for the partial volume of various brain tissues as an MRS voxel at a 1000 mm 3 resolution contains varying amounts of gray matter (GM), white matter (WM), and cerebrospinal fluid (CSF).…”

Section: Methodsmentioning

confidence: 99%

Effects of the antidepressant medication duloxetine on brain metabolites in persistent depressive disorder: A randomized, controlled trial

et al. 2019

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Background To assess whether patients with Persistent Depressive Disorder ( PDD ) have abnormal levels of N -acetyl-aspartate ( NAA ) and whether those levels normalize following treatment with the antidepressant medication duloxetine. Furthermore, we conducted post hoc analyses of other important brain metabolites to understand better the cellular and physiological determinants for changes in NAA levels. Methods We acquired proton (1H) magnetic resonance spectroscopic imaging ( MRSI ) data on a 3 Tesla (3T), GE Magnetic Resonance Imaging ( MRI ) scanner in 41 patients (39.9±10.4 years, 22 males) with PDD at two time points: before the start and at the end of a 10-week, placebo-controlled, double-blind, randomized controlled trial ( RCT ) of the antidepressant medication duloxetine. Patients were randomized such that 21 patients received the active medication and 20 patients received placebo during the 10 week period of the trial. In addition, we acquire 1H MRSI data once in 29 healthy controls (37.7±11.2 years, 17 males). Findings Patients had significantly higher baseline concentrations of NAA across white matter ( WM ) pathways and subcortical gray matter, and in direct proportion to the severity of depressive symptoms. NAA concentrations declined in duloxetine-treated patients over the duration of the trial in the direction toward healthy values, whereas concentrations increased in placebo-treated patients, deviating even further away from healthy values. Changes in NAA concentration did not mediate medication effects on reducing symptom severity, however; instead, changes in symptom severity partially mediated the effects of medication on NAA concentration, especially in the caudate and putamen. Interpretation These findings, taken together, suggest that PDD is not a direct consequence of elevated NAA concentrations, but that a more fundamental pathophysiological process likely causes PDD and determines the severity of its symptoms. The findings also suggest that although duloxetine normalized NAA concentrations in patients, it did so by modulating the severity of depressive symptoms. Medication presumably reduced depressive symptoms through other, as yet unidentified, brain processes. Trial registration ClinicalTrials.gov NCT00360724 .

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Proton Chemical Shift Imaging of the Brain in Pediatric and Adult Developmental Stuttering

Cited by 9 publications

References 58 publications

Functional neural circuits that underlie developmental stuttering

Functional neural circuits that underlie developmental stuttering

White matter developmental trajectories associated with persistence and recovery of childhood stuttering

Effects of the antidepressant medication duloxetine on brain metabolites in persistent depressive disorder: A randomized, controlled trial

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