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[PMID]: 29524847
[Au] Autor:Creed M
[Ad] Address:University of Maryland School of Medicine, Department of Pharmacology, 655 West Baltimore Street, Bressler Research Building, 4-021, Baltimore, MD 21201, USA. Electronic address: mcreed@som.umaryland.edu.
[Ti] Title:Current and emerging neuromodulation therapies for addiction: insight from pre-clinical studies.
[So] Source:Curr Opin Neurobiol;49:168-174, 2018 Mar 07.
[Is] ISSN:1873-6882
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Neuromodulation therapies such as deep brain stimulation or transcranial magnetic stimulation have shown promise in reducing symptoms of addiction when applied to the prefontal cortex, nucleus accumbens or subthalamic nucleus. Pre-clinical investigations implicate modulation of the cortico-basal ganglia network in these therapeutic effects, and this mechanistic understanding is necessary to optimize stimulation paradigms. Recently, the principle that neuromodulation can reverse drug-evoked synaptic plasticity and reduce behavioral symptoms of addiction has inspired novel stimulation paradigms that have long-term effects in animal models. Pre-clinical studies have also raised the possibility that tailoring neuromodulation protocols can modulate distinct symptoms of addiction. Combining mechanistic knowledge of circuit dysfunction with emerging technologies for non-invasive neuromodulation holds promise for developing therapies for addiction and related disorders.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

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[PMID]: 29524643
[Au] Autor:Onishi O; Ikoma K; Oda R; Yamazaki T; Fujiwara H; Yamada S; Tanaka M; Kubo T
[Ad] Address:Department of Orthopaedics, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, 602-8566 465, Kajiicho, Kamigyo-ku Kyoto-shi, Kyoto, Japan. Electronic address: pni_oki@yahoo.co.jp.
[Ti] Title:Sequential Variation in Brain Functional Magnetic Resonance Imaging After Peripheral Nerve Injury: A Rat Study.
[So] Source:Neurosci Lett;, 2018 Mar 07.
[Is] ISSN:1872-7972
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:Although treatment protocols are available, patients experience both acute neuropathic pain and chronic neuropathic pain, hyperalgesia, and allodynia after peripheral nerve injury. The purpose of this study was to identify the brain regions activated after peripheral nerve injury using functional magnetic resonance imaging (fMRI) sequentially and assess the relevance of the imaging results using histological findings. To model peripheral nerve injury in male Sprague-Dawley rats, the right sciatic nerve was crushed using an aneurysm clip, under general anesthesia. We used a 7.04T MRI system. T weighted image, coronal slice, repetition time, 7 ms; echo time, 3.3 ms; field of view, 30 mm  30 mm; pixel matrix, 64  64 by zero-filling; slice thickness, 2 mm; numbers of slices, 9; numbers of average, 2; and flip angle, 8 degrees. fMR images were acquired during electrical stimulation to the rat's foot sole; after 90 min, c-Fos immunohistochemical staining of the brain was performed in rats with induced peripheral nerve injury for 3, 6, and 9 weeks. Data were pre-processed by realignment in the Statistical Parametric Mapping 8 software. A General Linear Model first level analysis was used to obtain T-values. One week after the injury, significant changes were detected in the cingulate cortex, insular cortex, amygdala, and basal ganglia; at 6 weeks, the brain regions with significant changes in signal density were contracted; at 9 weeks, the amygdala and hippocampus showed activation. Histological findings of the rat brain supported the fMRI findings. We detected sequential activation in the rat brain using fMRI after sciatic nerve injury. Many brain regions were activated during the acute stage of peripheral nerve injury. Conversely, during the chronic stage, activation of the amygdala and hippocampus may be related to chronic-stage hyperalgesia, allodynia, and chronic neuropathic pain.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  3 / 34795 MEDLINE  
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[PMID]: 29524600
[Au] Autor:Vitale F; Capozzo A; Mazzone P; Scarnati E
[Ad] Address:Department of Biotechnological and Applied Clinical Sciences (DISCAB), University of L'Aquila, Via Vetoio 2, 67100 L'Aquila, Italy.
[Ti] Title:Neurophysiology of the pedunculopontine tegmental nucleus.
[So] Source:Neurobiol Dis;, 2018 Mar 07.
[Is] ISSN:1095-953X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The interest in the pedunculopontine tegmental nucleus (PPTg), a structure located in the brainstem at the level of the pontomesencephalic junction, has greatly increased in recent years because it is involved in the regulation of physiological functions that fail in Parkinson's disease and because it is a promising target for deep brain stimulation in movement disorders. The PPTg is highly interconnected with the main basal ganglia nuclei and relays basal ganglia activity to thalamic and brainstem nuclei and to spinal effectors. In this review, we address the functional role of the main PPTg outputs directed to the basal ganglia, thalamus, cerebellum and spinal cord. Together, the data that we discuss show that the PPTg may influence thalamocortical activity and spinal motoneuron excitability through its ascending and descending output fibers, respectively. Cerebellar nuclei may also relay signals from the PPTg to thalamic and brainstem nuclei. In addition to participating in motor functions, the PPTg participates in arousal, attention, action selection and reward mechanisms. Finally, we discuss the possibility that the PPTg may be involved in excitotoxic degeneration of the dopaminergic neurons of the substantia nigra through the glutamatergic monosynaptic input that it provides to these neurons.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

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[PMID]: 29506576
[Au] Autor:Sbbeler FJ; Carrera I; Pasloske K; Ranasinghe MG; Kircher P; Kstner SBR
[Ad] Address:Small Animal Clinic (Sbbeler, Kstner), University of Veterinary Medicine Hanover Foundation, Bnteweg 9, 30559, Hannover, Germany. franz.josef.soebbeler@tiho-hannover.de.
[Ti] Title:Effects of isoflurane, sevoflurane, propofol and alfaxalone on brain metabolism in dogs assessed by proton magnetic resonance spectroscopy ( H MRS).
[So] Source:BMC Vet Res;14(1):69, 2018 Mar 05.
[Is] ISSN:1746-6148
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: The purpose of this study was to determine the effects of isoflurane, sevoflurane, propofol and alfaxalone on the canine brain metabolite bioprofile, measured with single voxel short echo time proton magnetic resonance spectroscopy at 3 Tesla. Ten adult healthy Beagle dogs were assigned to receive isoflurane, sevoflurane, propofol and alfaxalone at 3 different dose rates each in a randomized cross-over study design. Doses for isoflurane, sevoflurane, propofol and alfaxalone were F 'Iso 1.7vol%, 2.1vol%, 2.8vol%, F 'Sevo 2.8vol%, 3.5vol% and 4.7vol%, 30, 45 and 60mgkgh and 10, 15 and 20mgkgh respectively. A single voxel Point Resolved Spectroscopy Sequence was performed on a 3T MRI scanner in three brain regions (basal ganglia, parietal and occipital lobes). Spectral data were analyzed with LCModel. Concentration of total N-acetylaspartate (tNAA), choline, creatine, inositol and glutamine and glutamate complex (Glx) relative to water content was obtained. Plasma concentration of lactate, glucose, triglycerides, propofol and alfaxalone were determined. Statistics were performed using repeated measures ANOVA or Wilcoxon Sign Rank test with alpha = 5%. RESULTS: Plasma glucose increased with isoflurane, sevoflurane and alfaxalone but decreased with propofol. Plasma lactate increased with all anesthetics (isoflurane > sevoflurane > propofol > alfaxalone). Cerebral lactate could not be detected. Only minor changes in cerebral metabolite concentrations of tNAA, choline, inositol, creatine and Glx occurred with anesthetic dose changes. CONCLUSION: The metabolomic profile detected with proton magnetic resonance spectroscopy at 3 Tesla of canine brain showed only minor differences between doses and anesthetics related to tNAA, choline, creatine, inositol and Glx.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process
[do] DOI:10.1186/s12917-018-1396-1

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[PMID]: 29482716
[Au] Autor:Zhang S; Mano H; Lee M; Yoshida W; Kawato M; Robbins TW; Seymour B
[Ad] Address:Computational and Biological Learning Laboratory, Department of Engineering, University of Cambridge, Cambridge, United Kingdom.
[Ti] Title:The control of tonic pain by active relief learning.
[So] Source:Elife;7, 2018 Feb 27.
[Is] ISSN:2050-084X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Tonic pain after injury characterises a behavioural state that prioritises recovery. Although generally suppressing cognition and attention, tonic pain needs to allow effective relief learning to reduce the cause of the pain. Here, we describe a central learning circuit that supports learning of relief and concurrently suppresses the level of ongoing pain. We used computational modelling of behavioural, physiological and neuroimaging data in two experiments in which subjects learned to terminate tonic pain in static and dynamic escape-learning paradigms. In both studies, we show that active relief-seeking involves a reinforcement learning process manifest by error signals observed in the dorsal putamen. Critically, this system uses an uncertainty ('associability') signal detected in pregenual anterior cingulate cortex that both controls the relief learning rate, and endogenously and parametrically modulates the level of tonic pain. The results define a self-organising learning circuit that reduces ongoing pain when learning about potential relief.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review

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[PMID]: 29481966
[Au] Autor:Fiore VG; Nolte T; Rigoli F; Smittenaar P; Gu X; Dolan RJ
[Ad] Address:School of Behavioral and Brain Sciences, University of Texas at Dallas, 2200 West Mockingbird Lane, Dallas, TX 75235, USA; Wellcome Trust Centre for Neuroimaging, University College London, 12 Queen Square, London WC1N 3BG, UK. Electronic address: vincenzo.fiore@utdallas.edu.
[Ti] Title:Value encoding in the globus pallidus: fMRI reveals an interaction effect between reward and dopamine drive.
[So] Source:Neuroimage;173:249-257, 2018 Feb 24.
[Is] ISSN:1095-9572
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The external part of the globus pallidus (GPe) is a core nucleus of the basal ganglia (BG) whose activity is disrupted under conditions of low dopamine release, as in Parkinson's disease. Current models assume decreased dopamine release in the dorsal striatum results in deactivation of dorsal GPe, which in turn affects motor expression via a regulatory effect on other nuclei of the BG. However, recent studies in healthy and pathological animal models have reported neural dynamics that do not match with this view of the GPe as a relay in the BG circuit. Thus, the computational role of the GPe in the BG is still to be determined. We previously proposed a neural model that revisits the functions of the nuclei of the BG, and this model predicts that GPe encodes values which are amplified under a condition of low striatal dopaminergic drive. To test this prediction, we used an fMRI paradigm involving a within-subject placebo-controlled design, using the dopamine antagonist risperidone, wherein healthy volunteers performed a motor selection and maintenance task under low and high reward conditions. ROI-based fMRI analysis revealed an interaction between reward and dopamine drive manipulations, with increased BOLD activity in GPe in a high compared to low reward condition, and under risperidone compared to placebo. These results confirm the core prediction of our computational model, and provide a new perspective on neural dynamics in the BG and their effects on motor selection and cognitive disorders.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

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[PMID]: 29228180
[Au] Autor:Tetzloff KA; Duffy JR; Clark HM; Strand EA; Machulda MM; Schwarz CG; Senjem ML; Reid RI; Spychalla AJ; Tosakulwong N; Lowe VJ; Jack CR; Josephs KA; Whitwell JL
[Ad] Address:Department of Radiology, Mayo Clinic, Rochester, MN, USA.
[Ti] Title:Longitudinal structural and molecular neuroimaging in agrammatic primary progressive aphasia.
[So] Source:Brain;141(1):302-317, 2018 Jan 01.
[Is] ISSN:1460-2156
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:The agrammatic variant of primary progressive aphasia affects normal grammatical language production, often occurs with apraxia of speech, and is associated with left frontal abnormalities on cross-sectional neuroimaging studies. We aimed to perform a detailed assessment of longitudinal change on structural and molecular neuroimaging to provide a complete picture of neurodegeneration in these patients, and to determine how patterns of progression compare to patients with isolated apraxia of speech (primary progressive apraxia of speech). We assessed longitudinal structural MRI, diffusion tensor imaging and 18F-fluorodeoxyglucose PET in 11 agrammatic aphasia subjects, 20 primary progressive apraxia of speech subjects, and 62 age and gender-matched controls with two serial assessments. Rates of change in grey matter volume and hypometabolism, and white matter fractional anisotropy, mean diffusivity, radial diffusivity and axial diffusivity were assessed at the voxel-level and for numerous regions of interest. The greatest rates of grey matter atrophy in agrammatic aphasia were observed in inferior, middle, and superior frontal gyri, premotor and motor cortices, as well as medial temporal lobe, insula, basal ganglia, and brainstem compared to controls. Longitudinal decline in metabolism was observed in the same regions, with additional findings in medial and lateral parietal lobe. Diffusion tensor imaging changes were prominent bilaterally in inferior and middle frontal white matter and superior longitudinal fasciculus, as well as right inferior fronto-occipital fasciculus, superior frontal and precentral white matter. More focal patterns of degeneration of motor and premotor cortex were observed in primary progressive apraxia of speech. Agrammatic aphasia showed greater rates of grey matter atrophy, decline in metabolism, and white matter degeneration compared to primary progressive apraxia of speech in the left frontal lobe, predominantly inferior and middle frontal grey and white matter. Correlations were also assessed between rates of change on neuroimaging and rates of clinical decline. Progression of aphasia correlated with rates of degeneration in frontal and temporal regions within the language network, while progression of parkinsonism and limb apraxia correlated with degeneration of motor cortex and brainstem. These findings demonstrate that disease progression in agrammatic aphasia is associated with widespread neurodegeneration throughout regions of the language network, as well as connecting white matter tracts, but also with progression to regions outside of the language network that are responsible for the development of motor symptoms. The fact that patterns of progression differed from primary progressive apraxia of speech supports the clinical distinction of these syndromes.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1093/brain/awx293

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[PMID]: 29496635
[Au] Autor:Kelm-Nelson CA; Trevino MA; Ciucci MR
[Ad] Address:Department of Surgery, Division of Otolaryngology, University of Wisconsin-Madison, Madison, WI, USA. Electronic address: CAKelm@wisc.edu.
[Ti] Title:Quantitative Analysis of Catecholamines in the Pink1 -/- Rat Model of Early-onset Parkinson's Disease.
[So] Source:Neuroscience;, 2018 Feb 27.
[Is] ISSN:1873-7544
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Parkinson's disease (PD) related to homozygous mutations in the Pink1 gene is associated with nigrostriatal dopamine depletion and a wide range of sensorimotor deficits. In humans and animal models of PD, not all sensorimotor deficits are levodopa-responsive. We hypothesized that the underlying mechanisms of locomotion, limb control, and vocal communication behavior include other pathologies. Here, Pink1 -/- rats were treated with an oral dose of levodopa and limb motor and vocal communication behaviors were measured. Levodopa significantly improved some aspects of locomotion but did not improve ultrasonic vocalization intensity or frequency. Catecholamine concentrations in the striatum (SR), substantia nigra (SN), and locus coeruleus (LC) were analyzed to test the hypothesis that behavioral deficits would correlate to altered protein levels. There were no differences in dopamine concentrations in the SR and SN of Pink1 -/- animals compared to wild-type controls. There was a significant increase in norepinephrine concentration in the SN of Pink1 -/- animals. Moreover, an observed decrease in norepinephrine concentrations in the LC is consistent with the hypothesis that early-stage PD includes noradrenergic loss in the brainstem, and is congruent with a significant increase in catechol-O-methyltransferase expression in the LC of Pink1 -/- animals. Pearson's correlations showed that increases in time to traverse a tapered balance beam are significantly associated with reductions in striatal dopamine. Ultrasonic vocalization complexity was positively correlated with LC norepinephrine concentrations. These data support the evolving hypothesis that differences in neural substrates and early-onset noradrenergic mechanisms in the brainstem may contribute to pathogenesis in the Pink1 -/- rat.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

  9 / 34795 MEDLINE  
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[PMID]: 29451896
[Au] Autor:Ji H; Li D; Wu Y; Zhang Q; Gu Q; Xie H; Ji T; Wang H; Zhao L; Zhao H; Yang Y; Feng H; Xiong H; Ji J; Yang Z; Kou L; Li M; Bao X; Chang X; Zhang Y; Li L; Li H; Niu Z; Wu X; Xiao J; Jiang Y; Wang J
[Ad] Address:Department of Pediatrics, Peking University First Hospital, Beijing, China.
[Ti] Title:Hypomyelinating disorders in China: The clinical and genetic heterogeneity in 119 patients.
[So] Source:PLoS One;13(2):e0188869, 2018.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:OBJECTIVE: Hypomyelinating disorders are a group of clinically and genetically heterogeneous diseases characterized by neurological deterioration with hypomyelination visible on brain MRI scans. This study was aimed to clarify the clinical and genetic features of HMDs in Chinese population. METHODS: 119 patients with hypomyelinating disorders in Chinese population were enrolled and evaluated based on their history, clinical manifestation, laboratory examinations, series of brain MRI with follow-up, genetic etiological tests including chromosomal analysis, multiplex ligation probe amplification, Sanger sequencing, targeted enrichment-based next-generation sequencing and whole exome sequencing. RESULTS: Clinical and genetic features of hypomyelinating disorders were revealed. Nine different hypomyelinating disorders were identified in 119 patients: Pelizaeus-Merzbacher disease (94, 79%), Pelizaeus-Merzbacher-like disease (10, 8%), hypomyelination with atrophy of the basal ganglia and cerebellum (3, 3%), GM1 gangliosidosis (5, 4%), GM2 gangliosidosis (3, 3%), trichothiodystrophy (1, 1%), Pol III-related leukodystrophy (1, 1%), hypomyelinating leukodystrophy type 9 (1, 1%), and chromosome 18q deletion syndrome (1, 1%). Of the sample, 94% (112/119) of the patients were genetically diagnosed, including 111 with mutations distributing across 9 genes including PLP1, GJC2, TUBB4A, GLB1, HEXA, HEXB, ERCC2, POLR3A, and RARS and 1 with mosaic chromosomal change of 46, XX,del(18)(q21.3)/46,XX,r(18)(p11.32q21.3)/45,XX,-18. Eighteen novel mutations were discovered. Mutations in POLR3A and RARS were first identified in Chinese patients with Pol III-related leukodystrophy and hypomyelinating leukodystrophy, respectively. SIGNIFICANCE: This is the first report on clinical and genetic features of hypomyelinating disorders with a large sample of patients in Chinese population, identifying 18 novel mutations especially mutations in POLR3A and RARS in Chinese patients, expanding clinical and genetic spectrums of hypomyelinating disorders.
[Mh] MeSH terms primary: Genetic Heterogeneity
Hereditary Central Nervous System Demyelinating Diseases/epidemiology
[Mh] MeSH terms secundary: China/epidemiology
Chromosome Banding
Female
Hereditary Central Nervous System Demyelinating Diseases/diagnostic imaging
Hereditary Central Nervous System Demyelinating Diseases/genetics
Hereditary Central Nervous System Demyelinating Diseases/pathology
Humans
Infant
Infant, Newborn
Karyotyping
Magnetic Resonance Imaging
Male
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:180217
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188869

  10 / 34795 MEDLINE  
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[PMID]: 29410079
[Au] Autor:Vogelbacher C; Mbius TWD; Sommer J; Schuster V; Dannlowski U; Kircher T; Dempfle A; Jansen A; Bopp MHA
[Ad] Address:Department of Psychiatry and Psychotherapy, University Marburg, Marburg, Germany; Marburg Center for Mind, Brain and Behavior (MCMBB), Marburg, Germany.
[Ti] Title:The Marburg-Mnster Affective Disorders Cohort Study (MACS): A quality assurance protocol for MR neuroimaging data.
[So] Source:Neuroimage;172:450-460, 2018 Feb 01.
[Is] ISSN:1095-9572
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Large, longitudinal, multi-center MR neuroimaging studies require comprehensive quality assurance (QA) protocols for assessing the general quality of the compiled data, indicating potential malfunctions in the scanning equipment, and evaluating inter-site differences that need to be accounted for in subsequent analyses. We describe the implementation of a QA protocol for functional magnet resonance imaging (fMRI) data based on the regular measurement of an MRI phantom and an extensive variety of currently published QA statistics. The protocol is implemented in the MACS (Marburg-Mnster Affective Disorders Cohort Study, http://for2107.de/), a two-center research consortium studying the neurobiological foundations of affective disorders. Between February 2015 and October 2016, 1214 phantom measurements have been acquired using a standard fMRI protocol. Using 444 healthy control subjects which have been measured between 2014 and 2016 in the cohort, we investigate the extent of between-site differences in contrast to the dependence on subject-specific covariates (age and sex) for structural MRI, fMRI, and diffusion tensor imaging (DTI) data. We show that most of the presented QA statistics differ severely not only between the two scanners used for the cohort but also between experimental settings (e.g. hardware and software changes), demonstrate that some of these statistics depend on external variables (e.g. time of day, temperature), highlight their strong dependence on proper handling of the MRI phantom, and show how the use of a phantom holder may balance this dependence. Site effects, however, do not only exist for the phantom data, but also for human MRI data. Using T1-weighted structural images, we show that total intracranial (TIV), grey matter (GMV), and white matter (WMV) volumes significantly differ between the MR scanners, showing large effect sizes. Voxel-based morphometry (VBM) analyses show that these structural differences observed between scanners are most pronounced in the bilateral basal ganglia, thalamus, and posterior regions. Using DTI data, we also show that fractional anisotropy (FA) differs between sites in almost all regions assessed. When pooling data from multiple centers, our data show that it is a necessity to account not only for inter-site differences but also for hardware and software changes of the scanning equipment. Also, the strong dependence of the QA statistics on the reliable placement of the MRI phantom shows that the use of a phantom holder is recommended to reduce the variance of the QA statistics and thus to increase the probability of detecting potential scanner malfunctions.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher


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