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In JoVE (1)
- Yerel Gyrification Endeksi hesapla Adım Adım Öğretici: MR Görüntüleri Kortikal Katlama nasıl ölçülür
Other Publications (18)
- Biological Psychiatry
- Psychiatry Research
- Neuropsychologia
- Child and Adolescent Psychiatric Clinics of North America
- Schizophrenia Research
- IEEE Transactions on Medical Imaging
- Neuropsychologia
- Journal of Rehabilitation Research and Development
- Developmental Disabilities Research Reviews
- Developmental Medicine and Child Neurology
- Developmental Neuroscience
- Journal of the International Neuropsychological Society : JINS
- Schizophrenia Research
- Archives of General Psychiatry
- Journal of Neurodevelopmental Disorders
- Biological Psychiatry
- Neuroscience and Biobehavioral Reviews
- Journal of Sleep Research
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Articles by Marie Schaer in JoVE
JoVE Clinical and Translational Medicine
Yerel Gyrification Endeksi hesapla Adım Adım Öğretici: MR Görüntüleri Kortikal Katlama nasıl ölçülür
1Department of Psychiatry, University of Geneva School of Medicine, 2Signal Processing Laboratory, École Polytechnique Fédérale de Lausanne, 3Department of Radiology, University Hospital Center and University of Lausanne, 4Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital
Ölçüm gyrification (kortikal katlama) herhangi bir yaşta, erken beyin gelişiminde bir pencere temsil eder. Bu nedenle, daha önce yarımkürede üzerinde puan binlerce yerel gyrification ölçmek için bir algoritma geliştirdi
Other articles by Marie Schaer on PubMed
Decreased Anterior Cingulate Volume in Combat-related PTSD
Neuroanatomical data point to functional relationships between the anterior cingulate cortex (ACC) and subcortical centers regulating fear, in particular, the amygdala. Functional brain imaging has disclosed divergent patterns of ACC activation in persons with posttraumatic stress disorder (PTSD). In addition, two preliminary structural imaging studies have found evidence of smaller ACC volume in PTSD. We explored associations between PTSD and ACC volume in a relatively large sample of adult combat veterans in which PTSD, lifetime alcohol abuse/dependence, and Vietnam versus Gulf War service were crossed.
Abnormal Patterns of Cortical Gyrification in Velo-cardio-facial Syndrome (deletion 22q11.2): an MRI Study
Velo-cardio-facial syndrome (VCFS), also known as 22q11.2 deletion syndrome, is a common genetic condition associated with increased risk for developing schizophrenia. Given that cortical malformations play an integral role in the pattern of neuroanatomical alterations associated with VCFS, the aim of the present study was to quantify and localize gyral abnormalities. Magnetic resonance images were obtained on a 1.5 T scanner. The gyrification index (GI), a measure of the degree of cortical complexity, was differentially calculated for each lobe using a semi-automated protocol. The GI was calculated for 37 patients affected by VCFS as well as for 36 comparison individuals group-matched for age, handedness, and gender. The subjects affected by VCFS showed a significant decrease in the GI in the frontal and parietal lobes compared with the control group. The pattern of decreased gyrification in the frontal and parietal lobes further defines the structural changes associated with the syndrome and suggests underlying abnormalities in neural connectivity. Aberrant connectivity may be partially responsible for the cognitive and behavioral impairments in the syndrome, as well as the high incidence of schizophrenia among affected individuals.
Hippocampal Volume Reduction in 22q11.2 Deletion Syndrome
Hippocampal volume reduction and decreased memory skills form a characteristic neurofunctional alteration observed in schizophrenia. Individuals affected with 22q11.2 deletion syndrome (22q11DS), while exhibiting memory deficits throughout development, are also at high risk for developing schizophrenia. The present study sought to investigate hippocampal volume reduction as separate of global grey matter reduction in a large, independent sample of individuals with 22q11DS. Volumetric data from structural magnetic resonance imaging was obtained for 43 individuals affected with 22q11DS, aged 6-39 years of age, as well as for 40 healthy individuals matched for age and gender. Drawing of the amygdala was included to enhance the delineation of the hippocampus, and circumscription of both the amygdala and the hippocampus were executed using an increased resolution matrix. After controlling for total grey volume reductions observed in affected individuals, a significant decrease in hippocampus volume was observed in the 22q11DS group, driven by significant bilateral volumetric reduction of the body of the hippocampus. These results are discussed in reference to memory and cerebral alterations already reported in 22q11DS. Further, the specific implications of hippocampus body volume reduction are outlined in light of its anatomical relationships and its function in memory. Finally, reduction of hippocampal volume in 22q11DS is examined in the context of psychiatric risk status associated to the deletion.
From Genes to Brain: Understanding Brain Development in Neurogenetic Disorders Using Neuroimaging Techniques
For almost two decades, a considerable amount of work has been devoted to the accurate delineation of normal and abnormal brain development using cerebral MRI. In the broad field of neuroimaging research, specific genetic conditions associated with impaired cognitive performances or with psychiatric symptoms have received increased attention because of their potential for revealing insight on the biologic correlates of behavior. First delineated by volumetric measurements of cerebral lobes or regions of interest, new image processing techniques are currently defining cerebral phenotypes associated with neurogenetic disorders with increasing precision. In this article the authors review the contribution of structural brain imaging in advancing our understanding of the pathogenic processes underlying altered brain development in Down, fragile X, and velocardiofacial (22q11DS) syndromes.
Structural Changes to the Fusiform Gyrus: a Cerebral Marker for Social Impairments in 22q11.2 Deletion Syndrome?
Identifying the neural underpinnings of socio-emotional deficits in 22q11.2 deletion syndrome (22q11DS) may elucidate recurrent psychosis in affected individuals. In the current study, we investigate volumetric changes in 22q11DS to the fusiform gyrus (FG), a region associated with hypoactivity during fMRI, by manually tracing the FG in 42 individuals with 22q11DS and 54 healthy controls. Larger anterior FG volumes and smaller posterior volumes bilaterally are observed in 22q11DS after controlling for total brain volume. The results demonstrate structural changes to the FG in 22q11DS, providing evidence for neural vulnerability in regions related to social cognition.
A Surface-based Approach to Quantify Local Cortical Gyrification
The high complexity of cortical convolutions in humans is very challenging both for engineers to measure and compare it, and for biologists and physicians to understand it. In this paper, we propose a surface-based method for the quantification of cortical gyrification. Our method uses accurate 3-D cortical reconstruction and computes local measurements of gyrification at thousands of points over the whole cortical surface. The potential of our method to identify and localize precisely gyral abnormalities is illustrated by a clinical study on a group of children affected by 22q11 Deletion Syndrome, compared to control individuals.
Cingulate Gyral Reductions Are Related to Low Executive Functioning and Psychotic Symptoms in 22q 11.2 Deletion Syndrome
A similar pattern of deficits in executive function and neuroanatomical abnormalities is shared between 22q 11.2 deletion syndrome (22q 11DS) and schizophrenia, suggesting that common cerebral alterations may lead to cognitive dysfunction and promote the appearance of psychotic symptoms in 22q 11DS individuals. Specifically, there is increasing evidence for involvement of the cingulate gyrus (CG) in executive dysfunction and the expression of positive symptoms in schizophrenia. The aim of our study is to examine CG morphology in a 22q 11DS population and its potential role as a cerebral marker of executive dysfunction and the manifestation of psychotic symptoms. Using region of interest (ROI)-based analysis, we compared CG volumes from 58 children and adults affected by 22q 11DS with 64 healthy age- and gender-matched controls. After covarying for total cranium grey matter and age, a bilateral reduced CG grey matter volume, driven by a decrease in anterior CG cortex, was observed among 22q 11DS patients. Further post hoc analyses suggest correlations between right CG cortical reductions, low-executive functioning and the occurrence of psychotic symptoms. The CG structural abnormalities observed in 22q 11DS are consistent with previous reports in schizophrenic patients and are associated with pre-morbid cognitive impairments. The mechanisms by which these changes may modulate executive functioning and the expression of psychosis are discussed.
Right Anterior Cingulate Cortical Volume Covaries with Respiratory Sinus Arrhythmia Magnitude in Combat Veterans
Existing data suggest anterior cingulate cortex (ACC) plays a role in autonomic regulation. In persons with posttraumatic stress disorder (PTSD), autonomic regulation appears impaired and smaller mean ACC volume has been reported. This study examined relationships between ACC volume and the magnitude of respiratory sinus arrhythmia (RSA) in 77 U.S. combat veterans at rest, 40 of whom met criteria for PTSD. RSA magnitude did not differ in combat survivors with and without PTSD, which contradicts studies comparing civilians with PTSD to nontraumatized controls. RSA magnitude was positively correlated with right but not left hemisphere ACC volume. This finding was statistically independent of the presence or absence of PTSD.
Genes, Brain Development and Psychiatric Phenotypes in Velo-cardio-facial Syndrome
Velo-cardio-facial syndrome (VCFS) has been in the focus of intensive research over the last 15 years. The syndrome represents a homogeneous model for studying the effect of a decreased dosage of genes on the development of brain structure and function and, consequently, on the emergence of schizophrenia-like psychotic disorder. In this review, we describe the psychiatric phenotype of children, adolescents, and young adults with VCFS. We redefine the concept of "behavioral phenotype" and suggest that psychosis fulfills the criteria of a behavioral phenotype of the syndrome. Identifying the risk factors for the emergence of psychosis in VCFS is a major goal of several large-scale longitudinal studies that are currently underway. We review the knowledge gained so far about risk factors for psychosis in VCFS, including early neuropsychiatric symptoms, development of brain structure and function, and the effect of a reduced dosage of genes from the 22q11 deletion region. Although the brain structure in subjects with VCFS is not drastically different from typically developing controls, newer imaging modalities that measure white matter tracts, cortical thickness, and cortical gyrification are likely to identify more subtle and specific neuroanatomical substrates of the syndrome. Among the 24 genes within the deletion region, the role of catechol-O-methyltransferase (COMT) on the VCFS phenotype has been investigated in depth. The findings suggest that because of haploinsufficiency of the COMT gene individuals with VCFS are exposed to a high level of prefrontal dopamine, and this interferes with their prefrontal cognitive functioning and may contribute to their high rate of psychosis and other psychiatric disorders. The other genes and environmental factors that shape the unique neuropsychiatric phenotype of VCFS are yet to be discovered.
Congenital Heart Disease Affects Local Gyrification in 22q11.2 Deletion Syndrome
22q11.2 deletion syndrome (22q11.2DS) is a common genetic condition associated with cognitive and learning impairments. In this study, we applied a three-dimensional method for quantifying gyrification at thousands of points over the cortical surface to imaging data from 44 children, adolescents, and young adults with 22q11.2DS (17 males, 27 females; mean age 17y 2mo [SD 9y 1mo], range 6-37y), and 53 healthy participants (21 males, 32 females; mean age 15y 4mo [SD 8y 6mo]; range 6-40y). Several clusters of reduced gyrification were observed, further substantiating the pattern of cerebral alterations presented by children with the syndrome. Comparisons within 22q11.2DS demonstrated an effect of congenital heart disease (CHD) on cortical gyrification, with reduced gyrification at the parieto-temporo-occipital junction in patients with CHD, as compared with patients without CHD. Reductions in gyrification can resemble mild polymicrogyria, suggesting early abnormal neuronal proliferation or migration and providing support for an effect of hemodynamic factors on brain development in 22q11.2DS. The results also shed light on the pathophysiology of acquired brain injury in other populations with CHD.
Prefrontal Plasticity and Stress Inoculation-induced Resilience
Coping with mild early life stress tends to make subsequent coping efforts more effective and therefore more likely to be used as a means of arousal regulation and resilience. Here we show that this developmental learning-like process of stress inoculation increases ventromedial prefrontal cortical volumes in peripubertal monkeys. Larger volumes do not reflect increased cortical thickness but instead represent surface area expansion of ventromedial prefrontal cortex. Expansion of ventromedial prefrontal cortex coincides with increased white matter myelination inferred from diffusion tensor magnetic resonance imaging. These findings suggest that the process of coping with early life stress increases prefrontal myelination and expands a region of cortex that broadly controls arousal regulation and resilience.
Hippocampal Volume and Declarative Memory Function in Combat-related PTSD
The proposition that declarative memory deficits are systematically related to smaller hippocampal volume was tested in a relatively large sample (n = 95) of U.S. military veterans with and without combat-related posttraumatic stress disorder. This correlative analysis was extended by including multiple measures of verbal and visual declarative memory and multiple memory-relevant regional brain volumes that had been shown to exhibit main effects of PTSD in prior work. Small-to-moderate effects were observed on verbal declarative memory in line with a recent meta-analysis; nevertheless, little or no evidence of systematic linear covariation between memory measures and brain volumes was observed.
Deviant Trajectories of Cortical Maturation in 22q11.2 Deletion Syndrome (22q11DS): a Cross-sectional and Longitudinal Study
22q11.2 deletion syndrome (22q11DS) is associated with an increased susceptibility to develop schizophrenia. Despite a large body of literature documenting abnormal brain structure in 22q11DS, cerebral changes associated with brain maturation in 22q11DS remained largely unexplored. To map cortical maturation from childhood to adulthood in 22q11.2 deletion syndrome, we used cerebral MRI from 59 patients with 22q11DS, aged 6 to 40, and 80 typically developing controls; three year follow-up assessments were also available for 32 patients and 31 matched controls. Cross-sectional cortical thickness trajectories during childhood and adolescence were approximated in age bins. Repeated-measures were also conducted with the longitudinal data. Within the group of patients with 22q11DS, exploratory measures of cortical thickness differences related to COMT polymorphism, IQ, and schizophrenia were also conducted. We observed deviant trajectories of cortical thickness changes with age in patients with 22q11DS. In affected preadolescents, larger prefrontal thickness was observed compared to age-matched controls. Afterward, we observed greater cortical loss in 22q11DS with a convergence of cortical thickness values by the end of adolescence. No compelling evidence for an effect of COMT polymorphism on cortical maturation was observed. Within 22q11DS, significant differences in cortical thickness were related to cognitive level in children and adolescents, and to schizophrenia in adults. Deviant trajectories of cortical thickness from childhood to adulthood provide strong in vivo cues for a defect in the programmed synaptic elimination, which in turn may explain the susceptibility of patients with 22q11DS to develop psychosis.
Smaller Global and Regional Cortical Volume in Combat-related Posttraumatic Stress Disorder
Two sets of findings predict smaller cerebral cortical gray matter volume in adult posttraumatic stress disorder (PTSD). Measures of intracranial tissue volume and cerebral tissue volume have been observed to be smaller in adolescents with maltreatment-related PTSD. Second, lower intelligence, a risk factor for PTSD, is associated with smaller cerebral tissue volumes. Nevertheless, to our knowledge, only 1 study has observed globally smaller cerebral tissue volume in adults with PTSD.
Regional Cortical Volumes and Congenital Heart Disease: a MRI Study in 22q11.2 Deletion Syndrome
Children with congenital heart disease (CHD) who survive surgery often present impaired neurodevelopment and qualitative brain anomalies. However, the impact of CHD on total or regional brain volumes only received little attention. We address this question in a sample of patients with 22q11.2 deletion syndrome (22q11DS), a neurogenetic condition frequently associated with CHD. Sixty-one children, adolescents, and young adults with confirmed 22q11.2 deletion were included, as well as 80 healthy participants matched for age and gender. Subsequent subdivision of the patients group according to CHD yielded a subgroup of 27 patients with normal cardiac status and a subgroup of 26 patients who underwent cardiac surgery during their first years of life (eight patients with unclear status were excluded). Regional cortical volumes were extracted using an automated method and the association between regional cortical volumes, and CHD was examined within a three-condition fixed factor. Robust protection against type I error used Bonferroni correction. Smaller total cerebral volumes were observed in patients with CHD compared to both patients without CHD and controls. The pattern of bilateral regional reductions associated with CHD encompassed the superior parietal region, the precuneus, the fusiform gyrus, and the anterior cingulate cortex. Within patients, a significant reduction in the left parahippocampal, the right middle temporal, and the left superior frontal gyri was associated with CHD. The present results of global and regional volumetric reductions suggest a role for disturbed hemodynamic in the pathophysiology of brain alterations in patients with neurodevelopmental disease and cardiac malformations.
Catechol-O-methyltransferase Val158Met Polymorphism Moderates Anterior Cingulate Volume in Posttraumatic Stress Disorder
Posttraumatic stress disorder (PTSD) is associated with structural and functional compromise of the anterior cingulate cortex (ACC), which may in turn be associated with impairment of its ability to regulate the amygdala. The Val158Met polymorphism in the catechol-O-methyltransferase gene, which substantially influences dopamine inactivation in the frontal lobe in general and in ACC in particular, may moderate ACC integrity in PTSD.
Degrees of Separation: A Quantitative Neuroimaging Meta-analysis Investigating Self-specificity and Shared Neural Activation Between Self- and Other-reflection
In functional neuroimaging studies, self-specificity has been investigated by contrasting other-relevant processing against the self. Our meta-analysis investigates self-specificity with respect to degrees of self-relatedness (SR) of the other (i.e. close and public other). Literature suggests a dorsal-ventral component of self- and other-reflection within the MPFC, which has yet to be analyzed according to varying SR, nor has it been quantified statistically. In the present meta-analysis, we pursued three main objectives. First, we conducted whole-brain ALE meta-analyses using contemporary literature analyzing self>close other and self>public other contrasts to determine self-specific regions sensitive to SR. Next, we conducted ALE and conjunction analyses of studies employing self>control, close other>control, or public other>control contrasts to determine shared regions of activation. Third, we conducted post hoc analyses to quantify any observed dorsal-ventral distinction, employing novel methodology using a surface-based coordinates system. We observed significant activation in the dACC and vACC for self>close other and self>public other, whereas anterior insula was observed only for self>public other. An MPFC dorsal-ventral distinction was observed and quantified whereby public other>control was significantly more dorsal than self>control and close other>control. Our results are discussed with regards to SR. Prospective avenues of research exploiting our methodology are proposed.
Cortical Morphometry in Narcolepsy with Cataplexy
The sleep-wake disorder narcolepsy with cataplexy is associated with the loss of hypocretin-(orexin-) producing neurons in the lateral hypothalamus. Several studies have reported abnormal cerebral activation in patients with narcolepsy with cataplexy. It remains unclear, however, whether these functional changes are related to structural alterations, particularly at the cortical level. To quantify structural brain changes associated with narcolepsy with cataplexy, we used high-resolution T1-weighted magnetic resonance imaging (MRI) in 12 patients compared with 12 healthy participants matched for age and gender. Subcortical and regional cortical volumes were measured using a method unbiased by non-linear registration. Further whole-brain analyses were conducted, measuring cortical characteristics, such as cortical thickness and gyrification, at thousands of points across each hemisphere using validated algorithms. Statistical analyses accounted for an effect of age and gender. We observed decreased cortical volume in the left paracentral lobule and increased cortical volume in the left caudal part of the middle frontal gyrus in narcoleptic patients compared with controls. Cortical thickness in prefrontal areas was inversely correlated with the severity of narcolepsy. Further, we observed several clusters of cortical thinning in patients with childhood or adolescent onset of narcolepsy compared with patients with adult onset of the disease. Our results suggest that specific anatomical changes may differentiate subgroups of narcolepsy patients with different clinical profiles (such as varying symptom severity or different age at onset). Future studies with larger groups of sleepy patients are required to assess whether distinct patterns of anatomical changes may distinguish narcolepsy from non-hypocretin-deficient hypersomnia disorders.
