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At least 19 recordsLinked to original sources
PubMed2004

Longitudinal mapping of cortical thickness and brain growth in normal children.

Recent advances in magnetic resonance imaging (MRI) technology now allow the tracing of developmental changes in the brains of children. We applied computer-matching algorithms and new techniques for measuring cortical thickness (in millimeters) to the structural MRI images of 45 children scanned twice (2 yr apart) between the ages 5 and 11. Changes in brain size were also assessed, showing local brain growth progressing at a rate of approximately 0.4-1.5 mm per year, most prominently in frontal and occipital regions. Estimated cortical thickness ranged from 1.5 mm in occipital regions to 5.5 mm in dorsomedial frontal cortex. Gray matter thinning coupled with cortical expansion was highly significant in right frontal and bilateral parieto-occipital regions. Significant thickening was restricted to left inferior frontal (Broca's area) and bilateral posterior perisylvian (Wernicke's area on the left) regions. In the left hemisphere, gray matter thickness was correlated with changing cognitive abilities. For the first time, developmental changes in gray matter thickness, brain size, and structure-function relationships have been traced within the same individuals studied longitudinally during a time of rapid cognitive development.

Adult↗
PubMed1998

Ovulatory delay alters postnatal growth, behavior, and brain structure in rats.

To investigate the effect of a delay in ovulation on postnatal growth and development in resultant rat offspring, a 1-day ovulatory delay was induced by sodium pentobarbital, animals mated, and the offspring monitored. There were no differences between control and 1-day delayed offspring in the number of live or dead births, number of males or females, nor in the ratio of sexes. Delayed pups had a slightly lower birth weight, but then recovered to weigh more than controls by day 12. In the first two weeks post-parturition, delayed pups displayed an earlier ability to reorient themselves in a negative geotaxis test, but no differences by the righting reflex and reflex suspension tests. At postnatal day (pnd) 28, delayed pups exhibited decreased activity in a continuous corridor test, but no alterations in gait. At this time, the brains of delayed animals revealed thickening of cortical layers V plus VI. There were significant correlations between various developmental endpoints (body weight, negative geotaxis, continuous corridor activity, and gait) and the cortical layer thicknesses. The results indicate that ovulatory delay produces changes in brain cortical thickness, with correlative changes in growth and behavior. Although the mechanisms by which ovulatory delay alters postnatal development and brain structure are unknown, ovulatory delay may alter the uterine environment during early pregnancy.

Animals↗
PubMed2006

Measurement of cortical thickness in 3D brain MRI data: validation of the Laplacian method.

OBJECTIVES: We aimed to determine the precision of the Laplacian approach for cortical thickness measurement due to changes in computational and acquisition parameters. We compared these results to two other methods widely used in clinical research using brain MRI data. MATERIALS AND METHODS: Brain MRI scans were obtained in 10 healthy adults using three different sets of acquisition parameters. The first and the second acquisitions used different slice thickness but the same head position. The third scan was performed after head repositioning. We measured cerebral cortical thickness in all brain segmentations using three thickness methods: Laplacian, nearest distance, and the orthogonal projection. RESULTS: The Laplacian method demonstrated the least variability with regard to the effect of interchange of boundaries, slice thickness, and repositioning of the head, compared with the other two methods. CONCLUSION: The Laplacian method is the most precise and reliable tool for in vivo cortical thickness measurement using brain MRI data.

Adult↗
PubMed1997

Maternal protein restriction early in rat pregnancy alters brain development in the progeny.

We assessed the effects of a dietary protein restriction (5% vs. 20% casein in diet) initiated at conception and imposed during the first 2 weeks of rat gestation on postnatal brain development. At the end of the malnutrition period, protein-restricted animals exhibited significantly smaller fetal body weight and brain cortical thickness than controls. At birth and thereafter, body weight was normalized in the progeny. Similarly, brain weight and cytoarchitecture were normal in postnatal animals. In contrast, we observed, during the first 2 postnatal weeks, several abnormalities of brain development which affected all the studied areas for most of the studied parameters: (i) delayed astrocytogenesis as shown by a reduced GFAP staining; (ii) delayed production of hyaluronan in the extracellular matrix studied with binding of biotinylated hyaluronectin; (iii) abnormal neuronal differentiation as shown by reduced expression of MAP-5 and increased expression of MAP-1; (iv) abnormal synaptogenesis as shown by the increased expression of synaptophysin in the basal ganglia; (v) decreased programmed cell death. In adult prenatally protein-restricted animals, all the above parameters were normalized excepted MAP-1 labeling which remained high. In addition, we observed slight alterations of the ventilatory response to hypoxia in adult animals. The present study demonstrates that early protein malnutrition during embryonic development induces multiple, transient alterations of brain development. However, the almost complete normalization in adults of brain architecture and differentiation as well as our physiological data strongly suggest a remarkable plasticity of the developing brain following an early aggression.

Aging↗
PubMed2007

Small-world anatomical networks in the human brain revealed by cortical thickness from MRI.

An important issue in neuroscience is the characterization for the underlying architectures of complex brain networks. However, little is known about the network of anatomical connections in the human brain. Here, we investigated large-scale anatomical connection patterns of the human cerebral cortex using cortical thickness measurements from magnetic resonance images. Two areas were considered anatomically connected if they showed statistically significant correlations in cortical thickness and we constructed the network of such connections using 124 brains from the International Consortium for Brain Mapping database. Significant short- and long-range connections were found in both intra- and interhemispheric regions, many of which were consistent with known neuroanatomical pathways measured by human diffusion imaging. More importantly, we showed that the human brain anatomical network had robust small-world properties with cohesive neighborhoods and short mean distances between regions that were insensitive to the selection of correlation thresholds. Additionally, we also found that this network and the probability of finding a connection between 2 regions for a given anatomical distance had both exponentially truncated power-law distributions. Our results demonstrated the basic organizational principles for the anatomical network in the human brain compatible with previous functional networks studies, which provides important implications of how functional brain states originate from their structural underpinnings. To our knowledge, this study provides the first report of small-world properties and degree distribution of anatomical networks in the human brain using cortical thickness measurements.

Brain↗
PubMed2005

Developmental Vitamin D3 deficiency alters the adult rat brain.

There is growing evidence that Vitamin D(3) (1,25-dihydroxyvitamin D(3)) is involved in brain development. We have recently shown that the brains of newborn rats from Vitamin D(3) deficient dams were larger than controls, had increased cell proliferation, larger lateral ventricles, and reduced cortical thickness. Brains from these animals also had reduced expression of nerve growth factor (NGF) and glial cell line-derived neurotrophic factor. The aim of the current study was to examine if there were any permanent outcomes into adulthood when the offspring of Vitamin D(3) deficient dams were restored to a normal diet. The brains of adult rats were examined at 10 weeks of age after Vitamin D(3) deficiency until birth or weaning. Compared to controls animals that were exposed to transient early Vitamin D(3) deficiency had larger lateral ventricles, reduced NGF protein content, and reduced expression of a number genes involved in neuronal structure, i.e. neurofilament or MAP-2 or neurotransmission, i.e. GABA-A(alpha4). We conclude that transient early life hypovitaminosis D(3) not only disrupts brain development but leads to persistent changes in the adult brain. In light of the high incidence of hypovitaminosis D(3) in women of child-bearing age, the public health implications of these findings warrant attention.

Aging↗
PubMed1992

Cerebral anoxia tolerance in turtles: regulation of intracellular calcium and pH.

To investigate mechanisms of cerebral anoxia tolerance, cerebrocortical intracellular calcium ([Ca2+]i) and pH (pHi) regulation were compared in turtles (Trachemys scripta) and laboratory rats. [Ca2+]i and pHi in living 200 to 300-microns-thick cortical brain slices were measured with the fluorescent indicators fura-2/acetoxymethyl ester (AM) and 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein during exposure to anoxia. Within 5 min, [Ca2+]i increased to > 1,000 nM in rat brain slices exposed to anoxia but [Ca2+]i was normal even after 5 h of anoxia in turtles. ATP levels remained normal in anoxic turtle brain but fell rapidly in rats. During anoxia, pHi fell by 0.25 +/- 0.08 pH units in rats but only 0.10 +/- 0.04 in turtles (P < 0.05). Inhibition of glycolysis in anoxic turtle brain with iodoacetate resulted in large increases in [Ca2+]i but prior exposure of slices to anoxia resulted in greatly attenuated calcium entry. The reduction in calcium flux was greater with increasing exposure to anoxia, suggesting progressive arrest of calcium channel activity. Tolerance of cerebral anoxia in turtles may be related to anaerobic ATP production, arrest of calcium channels, and attenuation of changes in pHi.

Adenosine Triphosphate↗
PubMed1997

[Usefulness of rCBF SPECT in patients with encephalitis: comparison study with MRI].

Twenty-nine rCBF SPECT study was done in 17 patients with encephalitis. Five of 6 patients (83.3%) showed regional high uptake in acute phase within a week after onset and 16 of 23 studies (69.6%) showed regional low uptake in subacute and chronic phase. Six of 19 lesions (31.6%) with regional high uptake changed to low uptake and 11 lesions (57.9%) improved to normal uptake on follow up studies. Seventeen of 51 lesions with low uptake (33.3%) improved to normal uptake. On the comparative study with MRI, 8 of 18 (44.4%) high uptake area showed cortical thickness or high intensity on T2 weighted images. Thirty-six of 74 low uptake area (48.6%) showed cortical thickness, brain atrophy or high intensity on T2 weighted images. Forty-eight of 212 regions (22.6%) with normal MRI findings showed abnormal accumulation of cerebral tracer on rCBF SPECT studies. rCBF SPECT was useful tool for diagnosis and follow up management in patients with encephalitis.

Adolescent↗
PubMed1981

Neonatal Frontal Lesions in the rat: sparing of learned but not species-typical behavior in the presence of reduced brain weight and cortical thickness.

Rats with complete removal of the cortex anterior to bregma in adulthood (frontal cortex) were compared behaviorally and neuroanatomically with rats with similar removals at 7 or 25 days of age. Excision of the frontal cortex in adult rats produced transient aphagia, chronic motor abnormalities in feeding, a chronic drop in body weight, increased activity in running wheels, impaired performance at a spatial reversal learning task, and chronic abnormalities in a variety of species-typical behaviors, including swimming, food hoarding, and defensive burying. In contrast, similar lesions in infant rats failed to produce aphagia, a chronic drop in body weight, increased activity, or impaired learning of a spatial reversal task. Infant lesions did not allow sparing of complex species-typical behaviors, however, such as those involved in feeding, swimming, hoarding, or defensive burying. Furthermore, when the brains of neonatally operated rats were compared with those of control rats or rats operated on in adulthood, there were striking differences. The cerebral hemispheres of the neonatal operates were smaller both in surface dimensions and weight, the thalamus was smaller, and the cerebral cortex was thinner. These data imply that there may be substantially less sparing of function following frontal cortex lesions in infancy than previously believed and that neonatal frontal lesions in rats have significant effects on brain development in regions far removed from the actual site of surgical excision.

Aging↗
PubMed1987

Neocortical cell counts in normal human adult aging.

Fifty-one brains from clinically and neuropathologically normal individuals ranging in age from 24 to 100 years were studied to determine what changes occur in neocortical neuroectodermal cell populations as a function of normal aging. Twenty-mu-thick sections from the midfrontal, superior temporal, and inferior parietal areas were examined with an image-analysis apparatus with combined manual and automatic editing capacity. Neuroectodermal cells were counted, measured, and assigned to one of ten categories, which were later summarized in three: large neurons (greater than 90 mu 2), small neurons (41 to 90 mu 2), and glia (5 to 40 mu 2). Determinations were also made of brain weight, cortical thickness, neuronal density, neuron-glia ratio, and percentage of cell area. The results showed statistically significant age-related decrements in the following values: brain weight, cortical thickness in the midfrontal and superior temporal areas, large neurons in all three areas, and the neuron-glia ratio in the midfrontal and inferior parietal areas. The total number of neurons, neuronal density, and percentage of cell area were all unchanged. Increasing with age were the number of small neurons in the midfrontal cortex and glia in the midfrontal and superior temporal areas. The following conclusions were drawn: Aging affects the frontal and temporal lobes more than the parietal; the salient change is shrinkage of large neurons with consequently increasing numbers of small neurons; constant neuronal density coupled with diminished cortical volume (decreased brain weight and cortical thinning) indicate that there is some neuronal loss with age, but it is of much lesser magnitude than previously supposed; and the number of glia increases with age.

Adult↗
PubMed1988

Size and shape of the cerebral cortex in mammals. II. The cortical volume.

The geometry of the brain and cerebral cortex in mammals has been studied from an evolutionary perspective and is described in mathematical terms. The volume of the cerebral cortex, in contrast to the cortical surface area, scales to brain volume in a similar way, irrespective of the degree of cortical folding. Among mammals, Cetacea form a subgroup, in that their volumetric data fit an isometric model better than an allometric model. An index of corticalization is presented which contains information about both the mass of interconnective nerve fibers and the degree of intracortical processing. It is shown, furthermore, that a semilogarithmic equation appropriately describes the relationship between mean cortical thickness and brain volume. Finally, allometric equations between brain volume and cortical parameters, which can be used for predictive purposes, are presented.

Animals↗
PubMed2000

Three-dimensional mapping of cortical thickness using Laplace's equation.

We present a novel, computerized method of examining cerebral cortical thickness. The normal cortex varies in thickness from 2 to 4 mm, reflecting the morphology of neuronal sublayers. Cortical pathologies often manifest abnormal variations in thickness, with examples of Alzheimer's disease and cortical dysplasia as thin and thick cortex, respectively. Radiologically, images are 2-D slices through a highly convoluted 3-D object. Depending on the relative orientation of the slices with respect to the object, it is impossible to deduce abnormal cortical thickness without additional information from neighboring slices. We approach the problem by applying Laplace's Equation (V2psi = 0) from mathematical physics. The volume of the cortex is represented as the domain for the solution of the differential equation, with separate boundary conditions at the gray-white junction and the gray-CSF junction. Normalized gradients of psi form a vector field, representing tangent vectors along field lines connecting both boundaries. We define the cortical thickness at any point in the cortex to be the pathlength along such lines. Key advantages of this method are that it is fully three-dimensional, and the thickness is uniquely defined for any point in the cortex. We present graphical results that map cortical thickness everywhere in a normal brain. Results show global variations in cortical thickness consistent with known neuroanatomy. The application of this technique to visualization of cortical thickness in brains with known pathology has broad clinical implications.

Algorithms↗
PubMed2026

Cerebral Cortical Structural Variation and General Cognitive Ability: Evidence From Mendelian Randomization.

Understanding the cortical architecture underlying individual differences in general cognitive ability (GCA) remains a central question in cognitive neuroscience. Prior work has established associations between global brain size and GCA, yet the regional effects and directionality of these relationships remain debated. Using a genetically informed cortical parcellation in 11,289 UK Biobank participants, we examined associations between cortical surface area (SA), cortical thickness (CT), and GCA measured via verbal-numerical reasoning. Total SA showed a robust positive association with GCA. At the regional level, dorsolateral prefrontal and superior temporal SA exhibited the strongest positive associations, which persisted after adjustment for global SA. In contrast, CT showed comparatively modest associations. Using Mendelian randomization (MR) with genome-wide significant genetic instruments, we observed evidence consistent with a bidirectional relationship between total SA and GCA. At the regional level, dorsolateral prefrontal and temporal SA demonstrated evidence of MR-inferred directional effects on GCA, while GCA showed evidence of MR-inferred directional effects on total SA and perisylvian thickness. These findings support a polyregional SA architecture underlying GCA, with prominent contributions from prefrontal and temporal association cortices. Our results refine global brain-GCA models and highlight the value of genetically informed parcellation for identifying regional cortical contributions.

Humans↗
PubMed1983

Abnormalities in cortical and subcortical morphology after neonatal neocortical lesions in rats.

The brain weight, cortical thickness, cross-sectional areas of subcortical structures, and various retrograde changes were compared in rats with neonatal or adult ablation of all or part of the neocortex. Neonatal lesions produced a widespread reduction in brain size accompanied by a variety of major structural changes including modification of the thickness of the residual cortex, necrosis and calcification of subcortical structures, and gross distortion of the structure of the hippocampus. The modification of the cortical thickness, but not the other changes, depended on the site and extent of cortical removal: neonatal frontal cortex ablation reduced the thickness of the remaining neocortex, neonatal posterior cortex ablation had no significant effect upon the thickness of the remaining neocortex, and neonatal hemidecortication increased the thickness of the remaining neocortex.

Animals↗
PubMed1994

Regional difference in the neurotoxicity of ochratoxin A on the developing cerebral cortex in mice.

Pregnant mice were treated intraperitoneally with 3 mg/kg of ochratoxin A on day 10 of gestation. They were allowed to give birth and the offspring were killed at 6 weeks of age for observation. Prenatal exposure to ochratoxin A caused microcephaly in offspring. Their body weight, brain weight, cortical thickness and numerical densities of neurons and synapses in somatosensory and visual cortex were examined. The mice exposed in utero to ochratoxin A showed a significant deficit in brain weight compared to the age-matched control, but there was no significant difference in body weight between these two groups. The cortical thickness showed a significant decrease in both somatosensory and visual cortex. Normal control mice had about 66,000 neurons/mm3, while age-matched ochratoxin A-treated mice had about 91,000 neurons/mm3 in somatosensory cortex. There was a significant increase in OA-treated group. However, there was no significant difference in the numerical density of neurons in visual cortex. On the other hand, there was no significant difference in the numerical density of synapses in both somatosensory and visual cortex. The somatosensory cortex of control mice had about 13,000 synapses per neuron, whereas ochratoxin A-treated mice had about 9,400 synapses per neuron. In the visual cortex, no significant difference was seen in synapse-to-neuron ratios. The discrepancy in the numerical density of neurons and synapse-to-neuron ratios between the somatosensory and visual cortex might derive from a time difference in cortical neurogenesis.

Aging↗
PubMed1991

Developmental disturbance of rat cerebral cortex following prenatal low-dose gamma-irradiation: a quantitative study.

Pregnant rats were exposed to a single whole-body gamma-irradiation on Day 15 of gestation at a dose of 0.27, 0.48, 1.00, or 1.46 Gy. They were allowed to give birth and the offspring were killed at 6 or 12 weeks of age for microscopic and electron microscopic examinations of the cerebrum. Their body weight, brain weight, cortical thickness, and numerical densities of whole cells and synapses in somatosensory cortex were examined. Growth of the dendritic arborization of layer V pyramidal cells was also examined quantitatively with Golgi-Cox specimens. A significant dose-related reduction in brain weight was found in all irradiated groups. Neither gross malformation nor abnormality of cortical architecture was observed in the groups exposed to 0.27 Gy. A significant change was found in thickness of cortex in the groups exposed to 0.48 Gy or more. Cell packing density increased significantly in the group exposed to 1.00 Gy. Significant reduction in the number of intersections of dendrites with the zonal boundaries were found in the groups exposed to 0.27 Gy or more. There was no difference in the numerical density of synapses in layer I between the control and irradiated groups. These results suggested that doses as low as 0.27 Gy could cause a morphologically discernible change in the mammalian cerebrum.

Animals↗
PubMed2004

Mapping cortical thickness and gray matter concentration in first episode schizophrenia.

We mapped regional changes in cortical thickness and intensity-based cortical gray matter concentration in first episode schizophrenia. High-resolution magnetic resonance images were obtained from 72 (51 male, 21 female) first episode patients and 78 (37 male, 41 female) healthy subjects similar in age. Cortical pattern matching methods allowed comparisons of cortical thickness and gray matter concentration at thousands of homologous cortical locations between subjects in three dimensions. Principal components analyses reduced measures obtained across the cortex to identify global differences in cortical thickness/gray matter concentration. First principal component factor scores showed significant effects of diagnosis, sex and age for both cortical measures. Diagnosis and age effects remained significant after brain size correction. Cortical thickness and gray matter concentration values were highly correlated. Statistical maps showed significant regional gray matter thinning in frontal, temporal and parietal heteromodal association cortices bilaterally in first episode patients. Regional reductions in cortical gray matter concentration were similar but pronounced in the superior temporal lobe. Regional reductions in cortical thickness and gray matter concentration are present at disease onset in brain regions linked with functional disturbances in schizophrenia. Cortical thickness and gray matter concentration mapping produce similar results, although the concentration metric may be influenced by diagnostic differences in extra-cortical cerebrospinal fluid and surface curvature/complexity.

Adult↗
PubMed1994

Effects of isoflurane and hypothermia on glutamate receptor-mediated calcium influx in brain slices.

BACKGROUND: To understand how volatile anesthetics protect neurons during cerebral ischemia, we studied the effects of isoflurane on cerebral glutamate receptor-mediated calcium influx. Calcium influx via these key excitatory receptors may mediate pain transmission, memory, and the pathophysiologic sequelae of cerebral anoxia or ischemia. Because cerebral protection by hypothermia may involve a decrease in glutamate receptor activity, we also examined the interaction of temperature and isoflurane on glutamate receptor inhibition. METHODS: We measured glutamate receptor-mediated changes in cytosolic calcium in 300-microns-thick rat cortical brain slices. Temperature was varied to 28, 34, 37, or 39 degrees C and isoflurane partial pressure to 0.016-0.019 atm (equivalent to 1.16 minimum alveolar concentration [MAC], adjusted for temperature and age). Brain slices were loaded with fura-2 to permit measurement of cytosolic free calcium. Calcium changes due to the glutamate receptor agonist N-methyl-D-aspartate (NMDA) (50 microM), to ischemia levels of L-glutamate (1.0 mM) or to simulated ischemia (1.0 mM glutamate, 100 microM NaCN, and 3.5 mM iodoacetate) was then measured. Slice lactate dehydrogenase leakage and adenosine triphosphate were measured as indices of cellular integrity. RESULTS: Isoflurane reduced both L-glutamate and NMDA-mediated calcium fluxes by approximately 60%. Neither the activity of the NMDA receptor nor its inhibition by isoflurane was altered by temperature. The rate of calcium influx during ischemia was significantly reduced both by temperature and by isoflurane (P < 0.05). Adenosine triphosphate loss and lactate dehydrogenase leakage were reduced by isoflurane during simulated ischemia by 37% and 73% (P < 0.05), respectively. CONCLUSIONS: (1) At 1.16 MAC, isoflurane potently inhibits glutamate receptors and delays cellular injury induced by simulated ischemia, and (2) hypothermia does not reduce the intrinsic activity of cortical glutamate receptors but delays calcium accumulation during simulated ischemia. Isoflurane reduces the severity of key pathophysiologic events in an in vitro model of simulated cerebral ischemia.

Adenosine Triphosphate↗