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This review outlines the current use of magnetic resonance (MR) techniques to study digestion and highlights their potential for providing markers of digestive processes such as texture changes and nutrient breakdown. In vivo digestion research can be challenging due to practical constraints and biological complexity. Therefore, digestion is primarily studied using in vitro models. These would benefit from further in vivo validation. NMR is widely used to characterise food systems. MRI is a related technique that can be used to study both in vitro model systems and in vivo gastro-intestinal processes. MRI allows visualisation and quantification of gastric processes such as gastric emptying and coagulation. Both MRI and NMR scan sequences can be configured to be sensitive to different aspects of gastric or intestinal contents. For example, magnetisation transfer and chemical exchange saturation transfer can detect proton (1H) exchange between water and proteins. MRI techniques have the potential to provide molecular-level and quantitative information on in vivo gastric (protein) digestion. This requires careful validation in order to understand what these MR markers of digestion mean in a specific digestion context. Combined with other measures they can be used to validate and inform in vitro digestion models. This may bridge the gap between in vitro and in vivo digestion research and can aid the optimisation of food properties for different applications in health and disease.
Advanced imaging techniques are enhancing research capacity focussed on the developmental origins of adult health and disease (DOHaD) hypothesis, and consequently increasing awareness of future health risks across various subareas of DOHaD research themes. Understanding how these advanced imaging techniques in animal models and human population studies can be both additively and synergistically used alongside traditional techniques in DOHaD-focussed laboratories is therefore of great interest. Global experts in advanced imaging techniques congregated at the advanced imaging workshop at the 2019 DOHaD World Congress in Melbourne, Australia. This review summarizes the presentations of new imaging modalities and novel applications to DOHaD research and discussions had by DOHaD researchers that are currently utilizing advanced imaging techniques including MRI, hyperpolarized MRI, ultrasound, and synchrotron-based techniques to aid their DOHaD research focus.
Embolic ischemic strokes cause significant mortality and morbidity worldwide. It has been proposed that some of these strokes are due to unstable carotid plaques with intraplaque hemorrhage (IPH) but a low overall degree of stenosis. Our aim was to test a fat-saturated T1-weighted (T1WI) black-blood sequence on MRI for the detection of IPH in symptomatic individuals and to quantify the relation between IPH, severity of stenoses, and ischemic brain lesions.
Materials and Methods:
Sixty-two patients were examined by 3T MRI. Sequences included brain diffusion-weighted imaging (DWI) as well as 3D turbo spin echo (TSE) fat-saturated black-blood T1 of the carotid bifurcations, to detect IPH as a focal intraplaque hyperintensity. Both carotid arteries were analyzed in each patient. The North American Symptomatic Carotid Endarterectomy Trial scale was used for quantification of stenosis degree.
Thirty-six out of 62 patients (mean age, 74) showed brain ischemia on DWI. Fifteen of these 36 patients (42%) had associated ipsilateral IPH at the carotid bifurcation or the proximal internal carotid artery. Mean degree of stenosis in this group was 50%. In 21 patients with ischemia without IPH, the mean degree of stenosis was 44%.
MRI with 3D TSE fat-saturated black-blood T1 technique is a safe, reliable, and noninvasive tool for the detection of IPH. A high percentage (42%) of ischemic events in patients with low- to moderate-degree stenosis were associated with IPH, an easily detectable imaging biomarker of plaque vulnerability. The ability to confirm IPH by MRI may help stratify patients into different risk and treatment groups in the future.
Sex difference in the brain is of great interest, because it is believed to reveal the “real” or biologically predetermined basis for differences between men's and women’s behavior. However, current neuroscience research does not support this conception. First, most male/female brain differences are attributable to body size; thus, all brain structures are 10% larger in males, but after accounting for individuals’ total brain volume, sex/gender explains only ~1% of the variance in structural volumes at both the cortical and subcortical level. Other differences, such as higher ratio of gray:white matter and density of interhemispheric connections in women, are also found to be due to brain size rather than sex per se. Second, functional measures of brain activity (fMRI) have not revealed reliable differences in the neural circuits that process verbal, spatial, and emotional information, even though men and women as groups perform differently on such tasks. Finally, it is important to appreciate that brain structure and function are both influenced by experience, or neuroplasticity, so even when small differences are identified, it is not possible to determine whether they were induced by “Nature” (sexually differentiated genes and hormone levels) or “Nurture” (gender enculturation). Overall, measures of brain structure and function exhibit far more overlap than difference between males and females. In spite of much hype, current brain findings do not explain any of the well-described male/female differences in behavior, interests, or mental health.
Optimal placental function is critical for fetal development, and therefore a crucial consideration for understanding the developmental origins of health and disease (DOHaD). The structure of the fetal side of the placental vasculature is an important determinant of fetal growth and cardiovascular development. There are several imaging modalities for assessing feto-placental structure including stereology, electron microscopy, confocal microscopy, micro-computed tomography, light-sheet microscopy, ultrasonography and magnetic resonance imaging. In this review, we present current methodologies for imaging feto-placental vasculature morphology ex vivo and in vivo in human and experimental models, their advantages and limitations and how these provide insight into placental function and fetal outcomes. These imaging approaches add important perspective to our understanding of placental biology and have potential to be new tools to elucidate a deeper understanding of DOHaD.
Perinatal stroke occurs around the time of birth and leads to lifelong neurological disabilities including hemiparetic cerebral palsy. Magnetic resonance imaging (MRI) has revolutionized our understanding of developmental neuroplasticity following early injury, quantifying volumetric, structural, functional, and metabolic compensatory changes after perinatal stroke. Such techniques can also be used to investigate how the brain responds to treatment (interventional neuroplasticity). Here, we review the current state of knowledge of how established and emerging neuroimaging modalities are informing neuroplasticity models in children with perinatal stroke. Specifically, we review structural imaging characterizing lesion characteristics and volumetrics, diffusion tensor imaging investigating white matter tracts and networks, task-based functional MRI for localizing function, resting state functional imaging for characterizing functional connectomes, and spectroscopy examining neurometabolic changes. Key challenges and exciting avenues for future investigations are also considered.
A previously healthy 48-year-old female presented to the emergency department with a 2-week history of low back pain, progressive lower extremities weakness, and right leg numbness. There were no bowel or bladder dysfunction symptoms. Spine magnetic resonance imaging (MRI) showed an intradural cystic lesion dorsal to the spinal cord at the level of L1 measuring 1.6 × 2.1 × 4.1 cm, which was T1 hypointense and T2 hyperintense, with a small soft tissue component and no gadolinium enhancement (Figure 1). A small lipomatous component was also noted. There were no associated vertebral anomalies. The patient underwent a T12-L2 laminectomy and cyst resection, which was subtotal due to the cyst adherence to the conus medullaris. Histopathology showed characteristic features of a neurenteric cyst, with respiratory-type epithelium in the cyst wall (Figure 2). Eight months later, follow-up MRI showed no evidence of recurrence. The patient reported improved sensation in the lower extremities; however, there was some residual weakness predominantly in the proximal hip flexors bilaterally.
Being overweight is associated with reduced functional capacity in Fontan patients. Increased adiposity leads to accumulation of epicardial and intra-abdominal visceral fat, which produce proinflammatory cytokines and may affect endothelial function. This retrospective study to evaluate the association between visceral fat and Fontan haemodynamics included 23 Fontan patients >18 years old with MRI and catheterization data available. Epicardial fat volume indexed to body surface area was measured by cardiac MRI, and intra-abdominal visceral fat thickness and subcutaneous fat thickness were derived from abdominal MRI. Stepwise regression models were used to determine univariable and multivariable associations between fat measures and haemodynamics. Mean age was 28.2 ± 9.5 years and body mass index was 26 ± 4 kg/m2. Mean central venous pressure was 13 ± 3 mmHg and pulmonary vascular resistance index was 1.23WU·m2 (interquartile range: 0.95–1.56). Epicardial fat volume was associated with age (r2 = 0.37, p = 0.002), weight (r2 = 0.26, p = 0.013), body mass index (r2 = 0.27, p = 0.011), and intra-abdominal visceral fat (r2 = 0.30, p = 0.018). Subcutaneous fat thickness did not relate to these measures. There was modest correlation between epicardial fat volume and pulmonary vascular resistance (r2 = 0.27, p = 0.02) and a trend towards significant correlation between intra-abdominal fat thickness and pulmonary vascular resistance (r2 = 0.21, p = 0.06). Subcutaneous fat thickness was not associated with Fontan haemodynamics. In multivariable analysis, including age and visceral fat measures, epicardial fat was independently correlated with pulmonary vascular resistance (point estimate 0.13 ± 0.05 per 10 ml/m2 increase, p = 0.03). In conclusion, in adults with Fontan circulation, increased visceral fat is associated with higher pulmonary vascular resistance. Excess visceral fat may represent a therapeutic target to improve Fontan haemodynamics.
Contrast-enhanced magnetic resonance imaging (CEMRI) of the head is frequently employed in investigations of sensorineural hearing loss (SNHL). The yield of these studies is perceptibly low and seemingly at odds with the aims of wise resource allocation and risk reduction within the Canadian healthcare system. The purpose of our study was to audit the use and diagnostic yield of CEMRI for the clinical indication of SNHL in our institution and to identify characteristics that may be leveraged to improve yield and optimize resource utilization.
Materials and methods:
The charts of 500 consecutive patients who underwent CEMRI of internal auditory canal for SNHL were categorized as cases with relevant positive findings on CEMRI and those without relevant findings. Demographics, presenting symptoms, interventions and responses, ordering physicians, and investigations performed prior to CEMRI testing were recorded. Chi-squared test and t-test were used to compare proportions and means, respectively.
CEMRI studies revealed relevant findings in 20 (6.2%) of 324 subjects meeting the inclusion criteria. Pre-CEMRI testing beyond audiometry was conducted in 35% of those with relevant positive findings compared to 7.3% of those without (p < 0.001). Auditory brainstem response/vestibular-evoked myogenic potentials were abnormal in 35% of those with relevant CEMRI findings compared to 6.3% of those without (p < 0.001).
CEMRI is a valuable tool for assessing potential causes of SNHL, but small diagnostic yield at present needs justification for contrast injection for this indication. Our findings suggest preferred referral from otolaryngologists exclusively, and implementation of a non-contrast MRI for SNHL may be a better diagnostic tool.
This study examined the relationship between patient performance on multiple memory measures and regional brain volumes using an FDA-cleared quantitative volumetric analysis program – Neuroreader™.
Ninety-two patients diagnosed with mild cognitive impairment (MCI) by a clinical neuropsychologist completed cognitive evaluations and underwent MR Neuroreader™ within 1 year of testing. Select brain regions were correlated with three widely used memory tests. Regression analyses were conducted to determine if using more than one memory measures would better predict hippocampal z-scores and to explore the added value of recognition memory to prediction models.
Memory performances were most strongly correlated with hippocampal volumes than other brain regions. After controlling for encoding/Immediate Recall standard scores, statistically significant correlations emerged between Delayed Recall and hippocampal volumes (rs ranging from .348 to .490). Regression analysis revealed that evaluating memory performance across multiple memory measures is a better predictor of hippocampal volume than individual memory performances. Recognition memory did not add further predictive utility to regression analyses.
This study provides support for use of MR Neuroreader™ hippocampal volumes as a clinically informative biomarker associated with memory performance, which is a critical diagnostic feature of MCI phenotype.
Amnestic mild cognitive impairment (aMCI) is characterized by delayed P300 latency and reduced grey matter (GM) volume, respectively. The relationship between the features in aMCI is unclear. This study was to investigate the relationship between the altered P300 latency and the GM volume in aMCI.
Thirty-four aMCI and 34 well-matched normal controls (NC) were studied using electroencephalogram during a visual oddball task and scanned with MRI. Both tests were finished in the same day.
As compared with the NC group, the aMCI group exhibited delayed P300 latency in parietal cortex and reduced GM volumes in bilateral temporal pole and left hippocampus/parahippocampal gyrus. A remarkable negative correlation was found between delayed P300 latency and reduced left hippocampal volume only in the aMCI group. Interestingly, the mediating analysis found P300 latency significantly mediated the association between right supramarginal gyrus volume and information processing speed indicated by Stroop Color and Word Test A scores.
The association between delayed P300 latency and reduced left hippocampal volume in aMCI subjects suggests that reduced left hippocampal volume may be the potential structural basis of delayed P300 latency.
In Early Onset Schizophrenia (EOS; onset before the 18th birthday) late brain maturational changes may interact with disease mechanisms leading to a wave of back to front structural changes during adolescence. To further explore this effect we examined the relationship between age of onset and duration of illness on brain morphology in adolescents with EOS.
Subjects and methods
Structural brain magnetic resonance imaging scans were obtained from 40 adolescents with EOS. We used Voxel Based Morphometry and multiple regressions analyses, implemented in SPM, to examine the relationship between gray matter volume with age of onset and illness duration.
Age of onset showed a positive correlation with regional gray matter volume in the right superior parietal lobule (Brodmann Area 7). Duration of illness was inversely related to regional gray matter volume in the left inferior frontal gyrus (BA 11/47).
Parietal gray matter loss may contribute to the onset of schizophrenia while orbitofrontal gray matter loss is associated with illness duration.
Several studies have independently suggested that patients with schizophrenia are more likely to have an enlarged cavum septum pellucidum (CSP) and an absent adhesio interthalamica (AI), respectively. However, neither finding has been consistently replicated and it is unclear whether there is an association between these two midline brain abnormalities. Thus, we compared the prevalence of absent AI and the prevalence, size and volume of CSP in 38 patients with schizophrenia and 38 healthy controls using magnetic resonance imaging (MRI). There were no between group differences in the presence or volume of CSP; however, an enlarged CSP was commoner among patients than controls. There was also a positive correlation between CSP ratings and volumes. No differences in the presence or absence of the AI were found between patients and controls; however, an absent AI was commoner in male patients with schizophrenia than females. There was absolutely no overlap between the presence of a large CSP and an absence of AI. In conclusion, our findings are in line with several case series and other MRI investigations that have shown a higher incidence of putatively developmental brain abnormalities in patients with schizophrenia, particularly in males, and support the neurodevelopmental model of this disorder.
The goal of this study was to detect abnormalities in white matter integrity connecting the mediodorsal nucleus of the thalamus and the prefrontal cortex using fiber-tracking technique. Diffusion tensor imaging was acquired in 20 patients with schizophrenia and 20 normal comparison subjects. Fiber tracking was performed on the anterior thalamic peduncle, and the tractography was used to determine the cross-sectional area, mean fractional anisotropy, and standard deviation of fractional anisotropy for every step separately in the right and left hemispheres. Compared with normal subjects, patients showed a significant reduction in the cross-sectional area of the left anterior thalamic peduncle. There were no significant differences for the mean fractional anisotropy bilaterally between the two groups, but significant differences for the standard deviation of fractional anisotropy in both hemispheres. Reduction in the cross-sectional area of the left anterior thalamic peduncle suggests the presence of the failure of left-hemisphere lateralization. In schizophrenic patients a significant increase of the standard deviation of fractional anisotropy raise the possibility that the inhomogeneity of white matter integrity, which is densely or sparsely distributed by site. These findings might provide further evidence for disruption of white matter integrity between the thalamus and the prefrontal cortex in schizophrenia.
Structural brain abnormalities have been described in autism but studies are often small and contradictory. We aimed to identify which brain regions can reliably be regarded as different in autism compared to healthy controls.
A systematic search was conducted for magnetic resonance imaging studies of regional brain size in autism. Data were extracted and combined using random effects meta-analysis. The modifying effects of age and IQ were investigated using meta-regression.
The total brain, cerebral hemispheres, cerebellum and caudate nucleus were increased in volume, whereas the corpus callosum area was reduced. There was evidence for a modifying effect of age and IQ on the cerebellar vermal lobules VI–VII and for age on the amygdala.
Autism may result from abnormalities in specific brain regions and a global lack of integration due to brain enlargement. Inconsistencies in the literature partly relate to differences in the age and IQ of study populations. Some regions may show abnormal growth trajectories.
The concept of deficit schizophrenia is regarded as one of the most promising attempts to reduce heterogeneity within schizophrenia. This paper summarizes the clinical, neurocognitive, brain imaging and electrophysiological correlates of this subtype of schizophrenia. Attempts to identify genetic and non-genetic risk factors are reviewed. Methodological limitations of studies supporting the efficacy of atypical antipsychotics in the treatment of the syndrome are highlighted. Two decades of research on deficit schizophrenia have failed to prove that it represents the extreme end of a severity continuum in schizophrenia, while some findings support the claim that it may be a separate disease entity.
Prepulse inhibition (PPI) of the startle response provides an operational index of sensorimotor gating that is reliably demonstrable in both human and animal subjects. Patients with schizophrenia, first-degree relatives of patients with schizophrenia, patients with schizotypal personality disorder and healthy individuals scoring high on psychometric measures of psychosis-proneness display reduced PPI. This study examined associations between individual differences in “psychosis-proneness” and brain activity during a tactile prepulse inhibition paradigm previously found to reveal activation in controls and deficient activation in schizophrenia patients in the striatum, thalamus, insula, hippocampal, temporal, inferior frontal, and inferior parietal regions.
Fourteen right-handed healthy men underwent psychophysiological testing and functional magnetic resonance imaging (fMRI) during a 15-min tactile PPI paradigm involving the use of tactile stimuli as both the pulse (a 40-ms presentation of 30 psi air-puff) and the prepulse (a 20-ms presentation of 6 psi air-puff presented 30-ms or 120-ms before the pulse). Individual differences in “psychosis-proneness” were assessed with Psychoticism scale of the Eysenck Personality Questionnaire-Revised (EPQ-R).
High psychosis-proneness was associated with lower PPI and reduced activity in the inferior frontal gyrus, insula extending to putamen and thalamus, parahippocampal gyrus, and inferior parietal and middle temporal regions. No regional activity correlated positively with psychosis-proneness.
The present observations extend the findings observed previously in people with schizophrenia to people with high psychosis-proneness, providing support to continuum theories of psychosis with implications for understanding trait-related neural deficits in schizophrenia.
Posttraumatic stress disorder (PTSD) is reliably associated with reduced brain volume relative to healthy controls, in areas similar to those found in depression. We investigated whether in a PTSD sample brain volumes in these areas were related to reporting specific symptoms of PTSD or to overall symptom severity.
Structural MRI scans were obtained from 28 participants diagnosed with PTSD according to DSM-IV-TR. Participants reported the extent of individual PTSD symptoms using the Posttraumatic Diagnostic Scale. Voxel-based morphometry applying the Dartel algorithm implemented within SPM5 was used to identify volumetric changes, related to PTSD total, symptom cluster, and individual symptom scores.
Brain volume was unrelated to overall PTSD severity, but greater reexperiencing scores predicted reduced volumes in the middle temporal and inferior occipital cortices. Increased reports of flashbacks predicted reduced volume in the insula/parietal operculum and in the inferior temporal gyrus.
The data illustrate the value of analyses at the symptom level within a patient population to supplement group comparisons of patients and healthy controls. Areas identified were consistent with a neurobiological account of flashbacks implicating specific abnormalities in the ventral visual stream.
Several preclinical studies have demonstrated neuronal effects of glucocorticoids on the hippocampus (HC), a limbic structure with anterior–posterior anatomical and functional segmentation. We propose a volumetric magnetic resonance imaging analysis of hippocampus head (HH), body (HB) and tail (HT) using Cushing's disease (CD) as model, to investigate whether there is a differential sensitivity to glucocorticoid neuronal damage in these segments. We found a significant difference in the HH bilaterally after 12 months from trans-sphenoidal surgical selective resection of the adrenocorticotropic hormone (ACTH)-secreting pituitary micro-adenomas. This pre–post surgery difference could contribute to better understand the pathopysiology of CD as an in vivo model for stress-related hypercortisolemic neuropsychiatric disorders.