NeuroImage: Clinical

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ISSN / EISSN : 22131582 / 22131582
Current Publisher: Elsevier BV (10.1016)
Total articles ≅ 2,384
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Paul Reidler, Franziska Mueller, Lena Stueckelschweiger, Katharina Feil, Lars Kellert, Matthias P. Fabritius, Thomas Liebig, Steffen Tiedt, Daniel Puhr-Westerheide, W.G. Kunz
Published: 26 June 2020
NeuroImage: Clinical; doi:10.1016/j.nicl.2020.102329

Abstract:
Ipsilateral thalamic diaschisis (ITD) refers to the phenomenon of thalamic hypoperfusion or hypometabolism due to a distant cerebral injury. To further investigate the characteristics and spectrum of ITD, we analyzed quantitative measurements of thalamic hypoperfusion in acute anterior circulation stroke. We selected consecutive patients with large-vessel occlusion (LVO) anterior circulation stroke and available CT perfusion (CTP) examination on admission who underwent endovascular thrombectomy. Thalamic perfusion parameters on CTP were tested between ipsi- and contralesional thalamus and ischemic territory. Values were compared with thresholds from CTP analysis software. Associations of thalamic perfusion parameters with acute imaging and clinical data were determined in uni- and multivariate logistic regression analyses. Ninety-nine patients were included. All perfusion parameters indicated significant non-ischemic hypoperfusion of the thalamus, not reaching the levels of ischemia in the middle cerebral artery territory due to LVO (all p<0.002). Multiple perfusion parameters exhibited significant association with ischemic lesion extent (relative cerebral blood flow [CBF]: β =-0.23, p=0.022; Δtime to drain: β=0.33, p<0.001; ΔTmax: β=-0.36, p<0.001) and involvement of the Lentiform Nucleus (Δmean transit time: β=0.64, p=0.04; Δtime to drain: β=0.81, p=0.01; ΔTmax: β=-0.82, p=0.01). Symptom severity on admission exhibited minor significant association with reduction of thalamic CBF in uncorrected analysis (Odds ratio: 0.05, p=0.049), but short- and long-term outcomes were unaffected by perfusion status. ITD reached guideline-based software-threshold levels in only one patient. ITD in acute stroke is a non-binary phenomenon affected by lesion extent and involvement of the lentiform nucleus. We found uncorrected association of ITD with early clinical presentation, but no association with short- or long-term outcome was evident. Relevant misclassification of ITD by guideline-based CTP software was not indicated, which needs further dedicated testing.
Nadia Moreira Da Silva, Rob Forsyth, Andrew McEvoy, Anna Miserocchi, Jane De Tisi, Sjoerd B. Vos, Gavin P. Winston, John Duncan, Yujiang Wang, Peter N. Taylor
Published: 26 June 2020
NeuroImage: Clinical; doi:10.1016/j.nicl.2020.102320

Abstract:
To characterise temporal lobe epilepsy (TLE) surgery-induced changes in brain network properties, as measured using diffusion weighted MRI, and investigate their association with postoperative seizure-freedom. For 48 patients who underwent anterior temporal lobe resection, diffusion weighted MRI was acquired pre-operatively, 3-4 months post-operatively (N=48), and again 12 months post-operatively (N=13). Data for 17 controls were also acquired over the same period. After registering all subjects to a common space, we performed two complementary analyses of the subjects’ quantitative anisotropy (QA) maps. 1) A connectometry analysis which is sensitive to changes in subsections of fasciculi. 2) A graph theory approach which integrates connectivity information across the wider brain network. We found significant postoperative alterations in QA in patients relative to controls measured over the same period. Reductions were primarily located in the uncinate fasciculus and inferior fronto-occipital fasciculus ipsilaterally for all patients. Larger reductions were associated with postoperative seizure-freedom in left TLE. Increased QA was mainly located in corona radiata and corticopontine tracts. Graph theoretic analysis revealed widespread increases in nodal betweenness centrality, which were not associated with patient outcomes. Substantial alterations in QA occur in the months after epilepsy surgery, suggesting Wallerian degeneration and strengthening of specific white matter tracts. Greater reductions in QA were related to postoperative seizure freedom in left TLE.
Nadia Bounoua, Rickie Miglin, Jeffrey M. Spielberg, Naomi Sadeh
Published: 25 June 2020
NeuroImage: Clinical; doi:10.1016/j.nicl.2020.102321

Abstract:
Although the link between childhood maltreatment and violence perpetration in adulthood (i.e., the “cycle of violence”) is well-documented, the neural mechanisms driving these processes remain relatively unknown. The objectives of this study were to investigate whether cortical thickness in adulthood varies as a function of childhood assaultive trauma exposure and whether such neurobiological markers of early trauma relate to the perpetration of aggression across the lifespan. In a sample of 138 ethnically-diverse men and women, whole-brain analysis of the cortical mantle revealed that individuals with exposure to assaultive trauma before age 13 had less cortical thickness in two clusters that survived multiple comparison correction: a region that peaked in the left lateral orbitofrontal cortex (OFC) and a region peaking in the right pericalcarine cortex. Diminished cortical thickness in the left OFC cluster was, in turn, associated with greater physical aggression, and mediation analysis revealed that reductions in cortical thickness in this left prefrontal region partially accounted for the association between exposure to childhood assaultive trauma and lifetime perpetration of aggression in adulthood. Findings extend previous investigations into the morphological correlates of early assaultive trauma by implicating reductions in cortical thickness as a potential mechanism linking early violence exposure to violence perpetration that extends into adulthood.
Peter K. Moon, Jason Z. Qian, Emily McKenna, Kevin Xi, Nathan C. Rowe, Nathan N. Ng, Jimmy Zheng, Lydia T. Tam, Sarah J. MacEachern, Iram Ahmad, et al.
Published: 25 June 2020
NeuroImage: Clinical; doi:10.1016/j.nicl.2020.102328

Abstract:
Sensorineural hearing loss (SNHL) is the most prevalent congenital sensory deficit in children. Information regarding underlying brain microstructure could offer insight into neural development in deaf children and potentially guide therapies that optimize language development. We sought to quantitatively evaluate MRI-based cerebral volume and gray matter microstructure children with SNHL. We conducted a retrospective study of children with SNHL who obtained brain MRI at 3T. The study cohort comprised 63 children with congenital SNHL without known focal brain lesion or structural abnormality (33 males; mean age 5.3 years; age range 1 to 11.8 years) and 64 age-matched controls without neurological, developmental, or MRI-based brain macrostructure abnormality. An atlas-based analysis was used to extract quantitative volume and median diffusivity (ADC) in the following brain regions: cerebral cortex, thalamus, caudate, putamen, globus pallidus, hippocampus, amygdala, nucleus accumbens, brain stem, and cerebral white matter. SNHL patients were further stratified by severity scores and hearing loss etiology. Children with SNHL showed higher median ADC of the cortex (p=.019), thalamus (p<.001), caudate (p=.005), and brainstem (p=.003) and smaller brainstem volumes (p=.007) compared to controls. Patients with profound bilateral SNHL did not show any significant differences compared to patients with milder bilateral SNHL, but both cohorts independently had smaller brainstem volumes compared to controls. Children with unilateral SNHL showed greater amygdala volumes compared to controls (p=.021), but no differences were found comparing unilateral SNHL to bilateral SNHL. Based on etiology for SNHL, patients with Pendrin mutations showed higher ADC values in the brainstem (p=.029, respectively); patients with Connexin 26 showed higher ADC values in both the thalamus (p<.001) and brainstem (p<.001) compared to controls. SNHL patients showed significant differences in diffusion and volume in brain subregions, with region-specific findings for patients with Connexin 26 and Pendrin mutations. Future longitudinal studies could examine macro- and microstructure changes in children with SNHL over development and potential predictive role for MRI after interventions including cochlear implant outcome.
Marisa C. Ross, Josh M. Cisler
Published: 23 June 2020
NeuroImage: Clinical; doi:10.1016/j.nicl.2020.102319

Abstract:
Classical neural circuitry models of posttraumatic stress disorder (PTSD) are largely derived from univariate activation studies and implicate the fronto-limbic circuit as a main neural correlate of PTSD symptoms. Though well-supported by human neuroimaging literature, these models are limited in their ability to explain the widely distributed neural and behavioral deficits in PTSD. Emerging interest in the application of large-scale network methods to functional neuroimaging provides a new opportunity to overcome such limitations and conceptualize the neural circuitry of PTSD in the context of network patterns. This review aims to evaluate both the classical neural circuitry model and a new, network-based model of PTSD neural circuitry using a breadth of functional brain organization research in subjects with PTSD. Taken together, this literature suggests global patterns of reduced functional connectivity (FC) in PTSD groups as well as altered FC targets that reside disproportionately in canonical functional networks, especially the default mode network. This provides evidence for an integrative model that includes elements of both the classical models and network-based models to characterize the neural circuitry of PTSD.
Antonio Canosa, Fabrizio D'ovidio, Andrea Calvo, Cristina Moglia, Umberto Manera, Maria Claudia Torrieri, Rosario Vasta, Angelina Cistaro, Silvia Gallo, Barbara Iazzolino, et al.
Published: 12 June 2020
NeuroImage: Clinical; doi:10.1016/j.nicl.2020.102312

Abstract:
To evaluate the metabolic correlates of lifetime sport practice in ALS through brain 18F-FDG-PET. 131 patients completed a questionnaire about lifetime exposures, including physical activity related to sports, hobbies and occupations, and underwent brain 18F-FDG-PET. Exposure to sports was expressed as MET (Metabolic Equivalent of Task). We considered only regular practice (at least 2 hours/week, for at least three months). We compared brain metabolism between two groups: subjects who did not report regular sport practice during life (N-group) and patients who did (Y-group). The resulting significant clusters were used in each group as seed regions in a interregional correlation analysis (IRCA) to evaluate the impact of lifetime sport practice on brain networks typically involved by the neurodegenerative process of ALS. Each group was compared to healthy controls (HC, n=40). We found a significant, relative cerebellar hypermetabolism in the N-group compared to the Y-group. The metabolism of such cerebellar cluster resulted correlated to more significant and widespread metabolic changes in areas known to be affected by ALS (i.e. frontotemporal regions and corticospinal tracts) in the N-group as compared to the Y-group, despite the same level of disability as expressed by the ALS FRS-R. Such findings resulted independent of age, sex, site of onset (bulbar/spinal), presence/absence of C9ORF72 expansion, cognitive status and physical activity related to hobbies and occupations. When compared to HC, the N-group showed more widespread metabolic changes than the Y-group in cortical regions known to be relatively hypometabolic in ALS patients as compared to HC. We hypothesize that patients of the N-group might cope better with the neurodegenerative process, since they show more widespread metabolic changes as compared to the Y-group, despite the same level of disability. Nevertheless, further studies are necessary to corroborate this hypothesis.
Akila Weerasekera, Melissa Crabbé, Sandra Tomé, Willy Gsell, Diana Sima, Cindy Casteels, Tom Dresselaers, Christophe Deroose, Sabine Van Huffel, Dietmar Rudolf Thal, et al.
Published: 1 June 2020
NeuroImage: Clinical; doi:10.1016/j.nicl.2020.102327

Scott A. Jones, Angelica M. Morales, Amy L. Holley, Anna C. Wilson, Bonnie J. Nagel
Published: 1 June 2020
NeuroImage: Clinical; doi:10.1016/j.nicl.2020.102326

Brian N. Haagensen, Damian M. Herz, David Meder, Kristoffer H. Madsen, Annemette Løkkegaard, Hartwig R. Siebner
Published: 1 June 2020
NeuroImage: Clinical; doi:10.1016/j.nicl.2020.102330

Linda Orth, Jana Zweerings, Camellia N. Ibrahim, Irene Neuner, Pegah Sarkheil
Published: 1 June 2020
NeuroImage: Clinical; doi:10.1016/j.nicl.2020.102324

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