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Epilepsia Open Jun 2021Recent neuroimaging studies have revealed differences in cortical and white matter brain structure in children with self-limiting rolandic epilepsy (RE). Despite this,...
OBJECTIVE
Recent neuroimaging studies have revealed differences in cortical and white matter brain structure in children with self-limiting rolandic epilepsy (RE). Despite this, reproducibility of the findings has been difficult, and there is no consensus about where and when structural differences are most apparent. We performed a systematic review of quantitative neuroimaging studies in children with RE to explore these questions.
METHODS
Using PRISMA guidelines, we used a multilayered search strategy to identify neuroimaging studies in RE. Publications were included if they were quantitative and derived from controlled group studies and passed a quality assessment. Findings of the studies were presented and stratified by duration of epilepsy and age of participants.
RESULTS
We identified six gray matter studies and five white matter studies. Consistent findings were found inside and outside the central sulcus, predominantly within the bilateral frontal and parietal lobes, striatal structures, such as the putamen and white matter, mainly involving the left superior longitudinal fasciculus and connections between the left pre- and postcentral gyrus. Stratification of the T1 studies by age found that cortical thickness differences varied between the under and over 10 year olds. Furthermore, the longer the duration of epilepsy, the less likely differences were detected. In white matter studies, there was a reduction in differences with increased age and duration of epilepsy.
SIGNIFICANCE
These findings would suggest that the development of regions of the cortex in children with RE is abnormal. These regions are more widespread than the suspected seizure onset zone. Moreover, the findings would suggest that these differences are evidence of neurodevelopmental delay rather than apparent "damage" from the epilepsy.
Topics: Child; Epilepsy, Rolandic; Gray Matter; Humans; Magnetic Resonance Imaging; Reproducibility of Results; White Matter
PubMed: 34033258
DOI: 10.1002/epi4.12468 -
Journal of Parkinson's Disease 2021The hallmark of Parkinson's disease is depletion of dopamine in the basal ganglia. Models of Parkinson's disease include dopamine as a contributor to disease... (Meta-Analysis)
Meta-Analysis
BACKGROUND
The hallmark of Parkinson's disease is depletion of dopamine in the basal ganglia. Models of Parkinson's disease include dopamine as a contributor to disease progression. However, intraneuronal levels of dopamine have not been reported.
OBJECTIVE
Meta-analytic methods were utilized to determine intracellular dopamine levels in Parkinson's disease.
METHODS
A systematic review of the literature and frequentist meta-analyses were performed. Dopamine levels were scaled for cell and axon numbers as well as VMAT2 protein levels.
RESULTS
Reduced tissue dopamine, dopaminergic cell bodies and VMAT2 protein were confirmed. The ratio of Parkinson's to normal brain intracellular dopamine scaled for either cell or axon number, each with VMAT2 level in the caudate ranged from 1.49 to 1.87 (p = 0.51 and p = 0.12, respectively) and in the putamen from 0.75 to 4.61 (p = 0.40 and 0.001, respectively).
CONCLUSION
Free, intracellular dopamine levels are not reduced in Parkinson's disease compared to normals to a similar degree as are total tissue concentrations, supporting the relevance of modulating VMAT2, neuromelanin and/or dopamine synthesis as rational neuroprotective strategies.
Topics: Basal Ganglia; Dopamine; Dopaminergic Neurons; Humans; Parkinson Disease; Putamen
PubMed: 34024786
DOI: 10.3233/JPD-212715 -
Neuropsychology Review Sep 2022Fatigue is one of the most debilitating symptoms for people with multiple sclerosis (PwMS). By consolidating a diverse and conflicting evidence-base, this systematic... (Meta-Analysis)
Meta-Analysis Review
Fatigue is one of the most debilitating symptoms for people with multiple sclerosis (PwMS). By consolidating a diverse and conflicting evidence-base, this systematic review and meta-analysis aimed to gain new insights into the neurobiology of MS fatigue. MEDLINE, ProQuest, CINAHL, Web of Science databases and grey literature were searched using Medical Subject Headings. Eligible studies compared neuroimaging and neurophysiological data between people experiencing high (MS-HF) versus low (MS-LF) levels of perceived MS fatigue, as defined by validated fatigue questionnaire cut-points. Data were available from 66 studies, with 46 used for meta-analyses. Neuroimaging studies revealed lower volumetric measures in MS-HF versus MS-LF for whole brain (-22.74 ml; 95% CI: -37.72 to -7.76 ml; p = 0.003), grey matter (-18.81 ml; 95% CI: -29.60 to -8.03 ml; p < 0.001), putamen (-0.40 ml; 95% CI: -0.69 to -0.10 ml; p = 0.008) and acumbens (-0.09 ml; 95% CI: -0.15 to -0.03 ml; p = 0.003) and a higher volume of T1-weighted hypointense lesions (1.10 ml; 95% CI: 0.47 to 1.73 ml; p < 0.001). Neurophysiological data showed reduced lower-limb maximum voluntary force production (-19.23 N; 95% CI: -35.93 to -2.53 N; p = 0.02) and an attenuation of upper-limb (-5.77%; 95% CI:-8.61 to -2.93%; p < 0.0001) and lower-limb (-2.16%; 95% CI:-4.24 to -0.07%; p = 0.04) skeletal muscle voluntary activation, accompanied by more pronounced upper-limb fatigability (-5.61%; 95% CI: -9.57 to -1.65%; p = 0.006) in MS-HF versus MS-LF. Results suggest that MS fatigue is characterised by greater cortico-subcortical grey matter atrophy and neural lesions, accompanied by neurophysiological decrements, which include reduced strength and voluntary activation. Prospero registration Prospero registration number: CRD42016017934.
Topics: Brain; Cross-Sectional Studies; Fatigue; Humans; Multiple Sclerosis; Organ Size
PubMed: 33961198
DOI: 10.1007/s11065-021-09508-1 -
AJNR. American Journal of Neuroradiology Jul 2021Neurologic events have been reported in patients with coronavirus disease 2019 (COVID-19). However, a model-based evaluation of the spatial distribution of these events...
BACKGROUND
Neurologic events have been reported in patients with coronavirus disease 2019 (COVID-19). However, a model-based evaluation of the spatial distribution of these events is lacking.
PURPOSE
Our aim was to quantitatively evaluate whether a network diffusion model can explain the spread of small neurologic events.
DATA SOURCES
The MEDLINE, EMBASE, Scopus, and LitCovid data bases were searched from January 1, 2020, to July 19, 2020.
STUDY SELECTION
Thirty-five case series and case studies reported 317 small neurologic events in 123 unique patients with COVID-19.
DATA ANALYSIS
Neurologic events were localized to gray or white matter regions of the Illinois Institute of Technology (gray-matter and white matter) Human Brain Atlas using radiologic images and descriptions. The total proportion of events was calculated for each region. A network diffusion model was implemented, and any brain regions showing a significant association (< .05, family-wise error-corrected) between predicted and measured events were considered epicenters.
DATA SYNTHESIS
Within gray matter, neurologic events were widely distributed, with the largest number of events (∼10%) observed in the bilateral superior temporal, precentral, and lateral occipital cortices, respectively. Network diffusion modeling showed a significant association between predicted and measured gray matter events when the spread of pathology was seeded from the bilateral cerebellum (=0.51, < .001, corrected) and putamen (=0.4, = .02, corrected). In white matter, most events (∼26%) were observed within the bilateral corticospinal tracts.
LIMITATIONS
The risk of bias was not considered because all studies were either case series or case studies.
CONCLUSIONS
Transconnectome diffusion of pathology via the structural network of the brain may contribute to the spread of neurologic events in patients with COVID-19.
Topics: Brain; COVID-19; Cerebral Cortex; Gray Matter; Humans; Magnetic Resonance Imaging; White Matter
PubMed: 33888458
DOI: 10.3174/ajnr.A7113 -
Translational Psychiatry Jan 2021Substance use disorders (SUDs) are characterized by a compulsion to seek and consume one or more substances of abuse, with a perceived loss of control and a negative... (Meta-Analysis)
Meta-Analysis
Substance use disorders (SUDs) are characterized by a compulsion to seek and consume one or more substances of abuse, with a perceived loss of control and a negative emotional state. Prolonged substance use seems to be associated with morphological changes of multiple neural circuits, in particular the frontal-striatal and limbic pathways. Such neuroadaptations are evident across several substance disorders, but may vary depending on the type of substance, consumption severity and/or other unknown factors. We therefore identified studies investigating the effects of SUDs using volumetric whole-brain voxel-based morphometry (VBM) in gray (GM) and white matter (WM). We performed a systematic review and meta-analysis of VBM studies using the anatomic likelihood estimation (ALE) method implemented in GingerALE (PROSPERO pre-registration CRD42017071222 ). Sixty studies met inclusion criteria and were included in the final quantitative meta-analysis, with a total of 614 foci, 94 experiments and 4938 participants. We found convergence and divergence in brain regions and volume effects (higher vs. lower volume) in GM and WM depending on the severity of the consumption pattern and type of substance used. Convergent pathology was evident across substances in GM of the insula, anterior cingulate cortex, putamen, and thalamus, and in WM of the thalamic radiation and internal capsule bundle. Divergent pathology between occasional use (cortical pathology) and addiction (cortical-subcortical pathology) provides evidence of a possible top-down neuroadaptation. Our findings indicate particular brain morphometry alterations in SUDs, which may inform our understanding of disease progression and ultimately therapeutic approaches.
Topics: Brain; Gray Matter; Humans; Magnetic Resonance Imaging; Neuroimaging; Substance-Related Disorders; White Matter
PubMed: 33431833
DOI: 10.1038/s41398-020-01128-2 -
Frontiers in Neuroscience 2020Brand love is a critical concept for building a relationship between brands and consumers because falling in love with a brand can lead to strong brand loyalty. Despite...
Brand love is a critical concept for building a relationship between brands and consumers because falling in love with a brand can lead to strong brand loyalty. Despite the importance of marketing strategies, however, the underlying neural mechanisms of brand love remain unclear. The present study used an activation likelihood estimation meta-analysis method to investigate the neural correlates of brand love and compared it with those of maternal and romantic love. In total, 47 experiments investigating brand, maternal, and romantic love were examined, and the neural systems involved for the three loves were compared and contrasted. Results revealed that the putamen and insula were commonly activated in the three loves. Moreover, activated brain regions in brand love were detected in the dorsal striatum. Activated regions for maternal love were detected in the cortical area and globus pallidus and were associated with pair bonds, empathy, and altruism. Finally, those for romantic love were detected in the hedonic, strong passionate, and intimate-related regions, such as the nucleus accumbens and ventral tegmental area. Thus, the common regions of brain activation between brand and romantic love were in the dorsal striatum. Meanwhile, no common activated regions were observed between brand and maternal love except for the regions shared among the three love types. Although brand love shared little with the two interpersonal (maternal and romantic) loves and relatively resembled aspects of romantic rather than maternal love, our results demonstrated that brand love may have intrinsically different dispositions from the two interpersonal loves.
PubMed: 33100955
DOI: 10.3389/fnins.2020.534671 -
PloS One 2020Iron is involved in many processes in the brain including, myelin generation, mitochondrial function, synthesis of ATP and DNA and the cycling of neurotransmitters....
Iron is involved in many processes in the brain including, myelin generation, mitochondrial function, synthesis of ATP and DNA and the cycling of neurotransmitters. Disruption of normal iron homeostasis can result in iron accumulation in the brain, which in turn can partake in interactions which amplify oxidative damage. The development of MRI techniques for quantifying brain iron has allowed for the characterisation of the impact that brain iron has on cognition and neurodegeneration. This review uses a systematic approach to collate and evaluate the current literature which explores the relationship between brain iron and cognition. The following databases were searched in keeping with a predetermined inclusion criterion: Embase Ovid, PubMed and PsychInfo (from inception to 31st March 2020). The included studies were assessed for study characteristics and quality and their results were extracted and summarised. This review identified 41 human studies of varying design, which statistically assessed the relationship between brain iron and cognition. The most consistently reported interactions were in the Caudate nuclei, where increasing iron correlated poorer memory and general cognitive performance in adulthood. There were also consistent reports of a correlation between increased Hippocampal and Thalamic iron and poorer memory performance, as well as, between iron in the Putamen and Globus Pallidus and general cognition. We conclude that there is consistent evidence that brain iron is detrimental to cognitive health, however, more longitudinal studies will be required to fully understand this relationship and to determine whether iron occurs as a primary cause or secondary effect of cognitive decline.
Topics: Adult; Aged; Aged, 80 and over; Brain; Child; Cognition; Female; Humans; Iron; Male; Middle Aged
PubMed: 33057378
DOI: 10.1371/journal.pone.0240697 -
Psychiatry Research. Neuroimaging Jan 2021Differentiating bipolar disorder from unipolar depression is one of the most difficult clinical questions posed in pediatric psychiatric practices, as misdiagnosis can...
Differentiating bipolar disorder from unipolar depression is one of the most difficult clinical questions posed in pediatric psychiatric practices, as misdiagnosis can lead to severe repercussions for the affected child. This study aimed to examine the existing literature that investigates brain differences between bipolar and unipolar mood disorders in children directly, across all neuroimaging modalities. We performed a systematic literature search through PubMed, PsycINFO, Embase, and Medline databases with defined inclusion and exclusion criteria. Nine research studies were included in the systematic qualitative review, including three structural MRI studies, five functional MRI studies, and one MR spectroscopy study. Relevant variables were extracted and brain differences between bipolar and unipolar mood disorders in children as well as healthy controls were qualitatively analyzed. Across the nine studies, our review included 228 subjects diagnosed with bipolar disorder, 268 diagnosed with major depressive disorder, and 299 healthy controls. Six of the reviewed studies differentiated between bipolar and unipolar mood disorders. Differentiation was most commonly found in the anterior cingulate cortex (ACC), insula, and dorsal striatum (putamen and caudate) brain areas. Despite its importance, the current neuroimaging literature on this topic is scarce and presents minimal generalizability.
Topics: Adolescent; Bipolar Disorder; Child; Depressive Disorder, Major; Gyrus Cinguli; Humans; Magnetic Resonance Imaging; Neuroimaging
PubMed: 33046342
DOI: 10.1016/j.pscychresns.2020.111201 -
Frontiers in Psychiatry 2020The use of modern neuroimaging approaches has demonstrated resting-state regional cerebral blood flow (rCBF) to be tightly coupled to resting cerebral glucose metabolism...
The use of modern neuroimaging approaches has demonstrated resting-state regional cerebral blood flow (rCBF) to be tightly coupled to resting cerebral glucose metabolism (rCMRglu) in healthy brains. In schizophrenia, several lines of evidence point toward aberrant neurovascular coupling, especially in the prefrontal regions. To investigate this, we used Signed Differential Mapping to undertake a voxel-based bimodal meta-analysis examining the relationship between rCBF and rCMRglu in schizophrenia, as measured by arterial spin labeling (ASL) and Flurodeoxyglucose positron emission tomography (FDG-PET) respectively. We used 19 studies comprised of data from 557 patients and 584 controls. Our results suggest that several key regions implicated in the pathophysiology of schizophrenia such as the frontoinsular cortex, dorsal ACC, putamen, and temporal pole show conjoint metabolic and perfusion abnormalities in patients. In contrast, discordance between metabolism and perfusion were seen in superior frontal gyrus and cerebellum, indicating that factors contributing to neurovascular uncoupling (e.g. inflammation, mitochondrial dysfunction, oxidative stress) are likely operates at these loci. Studies enrolling patients on high doses of antipsychotics had showed larger rCBF/rCMRglu effects in patients in the left dorsal striatum. Hybrid ASL-PET studies focusing on these regions could confirm our proposition regarding neurovascular uncoupling at superior frontal gyrus in schizophrenia.
PubMed: 32848931
DOI: 10.3389/fpsyt.2020.00754 -
Frontiers in Human Neuroscience 2020Many studies have revealed the structural or functional brain changes induced by occupational factors. However, it remains largely unknown how occupation-related...
Many studies have revealed the structural or functional brain changes induced by occupational factors. However, it remains largely unknown how occupation-related connectivity shapes the brain. In this paper, we denote occupational neuroplasticity as the neuroplasticity that takes place to satisfy the occupational requirements by extensively professional training and to accommodate the long-term, professional work of daily life, and a critical review of occupational neuroplasticity related to the changes in brain structure and functional networks has been primarily presented. Furthermore, meta-analysis revealed a neurophysiological mechanism of occupational neuroplasticity caused by professional experience. This meta-analysis of functional neuroimaging studies showed that experts displayed stronger activation in the left precentral gyrus [Brodmann area (BA)6], left middle frontal gyrus (BA6), and right inferior frontal gyrus (BA9) than novices, while meta-analysis of structural studies suggested that experts had a greater gray matter volume in the bilateral superior temporal gyrus (BA22) and right putamen than novices. Together, these findings not only expand the current understanding of the common neurophysiological basis of occupational neuroplasticity across different occupations and highlight some possible targets for neural modulation of occupational neuroplasticity but also provide a new perspective for occupational science research.
PubMed: 32760257
DOI: 10.3389/fnhum.2020.00215