Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “brain structure”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 505 records · Page 28Linked to original sources
PubMed2004

[Changes in brain structure caused by neuroleptic medication].

A couple of studies showed that neuroleptic treatment affects brain morphology. This paper reviews findings of volumetric longitudinal studies on treated schizophrenics, longitudinal studies considering the effect of different neuroleptic treatments on brain morphology, and studies on neuroleptic-naive patients with schizophrenia. The latter studies show enlargement of ventricles, diminished volume of the thalamus and reduced gray matter in different cortical regions. Findings on the nucleus caudatus, hippocampus, and amygdala are inconsistent. The volumes of the putamen and globus pallidus are unchanged. Medication with typical antipsychotics leads to increased volume of the nucleus caudatus while atypical antipsychotics do not change the volume of the nucleus caudatus.

Antipsychotic Agents↗
PubMed1999

A fuzzy logic approach to identifying brain structures in MRI using expert anatomic knowledge.

We report a novel computer method for automatic labeling of structures in 3D MRI data sets using expert anatomical knowledge that is coded in fuzzy sets and fuzzy rules. The method first identifies major structures and then uses spatial relationships to these landmarks to recognize other structures. This labeling process simulates the iterative process that we ourselves use to locate structures in images. We demonstrate its application in three data sets, labeling brain MRI by locating the longitudinal and lateral fissures and the central sulci and then determining boundaries for the frontal lobes. Our method is adaptable to the identification of other anatomical structures.

Brain↗
PubMed2003

A simulation model for analysing brain structure deformations.

Recent developments of medical software applications--from the simulation to the planning of surgical operations--have revealed the need for modelling human tissues and organs, not only from a geometric point of view but also from a physical one, i.e. soft tissues, rigid body, viscoelasticity, etc. This has given rise to the term 'deformable objects', which refers to objects with a morphology, a physical and a mechanical behaviour of their own and that reflects their natural properties. In this paper, we propose a model, based upon physical laws, suitable for the realistic manipulation of geometric reconstructions of volumetric data taken from MR and CT scans. In particular, a physically based model of the brain is presented that is able to simulate the evolution of different nature pathological intra-cranial phenomena such as haemorrhages, neoplasm, haematoma, etc and to describe the consequences that are caused by their volume expansions and the influences they have on the anatomical and neuro-functional structures of the brain.

Brain↗
PubMed1981

[Interaction of brain structures regulating the vocal and respiratory systems].

Unit activity data revealed an obvious interrelationship between the brain vocal and respiratory systems. Modification of evoked reaction of the vocal system depends on stimulated central nuclei and parameters of stimulating electric current. The threshold of evoked vocal reaction is higher than the threshold sufficient for modification of respiration and neuronal activity. The data obtained suggest that not all the structures related to the respiratory regulation bear control over the generation of species specific cries.

Animals↗
PubMedDate not supplied

In utero alcohol exposure: functional and structural brain damage.

Pregnant rats were intubated with alcohol throughout gestation. Control animals received vehicle and were pair-fed. At birth, all offspring were surrogate-fostered to nontreated dams. At 11 weeks of age, alcohol-exposed animals did not perform as well in a two-way shock avoidance task. The brains of these animals also exhibited significant deficits in dendritic structure in the area of the hippocampus. These behavioral observations may be a counterpart to the learning deficits associated with fetal alcohol effects, e.g., fetal alcohol syndrome in humans and animals, and the neuroanatomical observations suggest a structural basis for these learning deficits.

Animals↗
PubMed2004

A voxel-based investigation of brain structure in male adolescents with autistic spectrum disorder.

Autistic spectrum disorder (ASD) has been associated with abnormal neuroanatomy in many imaging and neuropathological studies. Both global brain volume differences and differences in the size of specific neural structures have been reported. Here, we report a voxel-based morphometric whole brain analysis, using a group specific template, on 16 individuals of normal intelligence with autistic spectrum disorder (ASD), and a group of 16 age-, sex- and IQ-matched controls. Total grey matter volume was increased in the ASD group relative to the control group, with local volume increases in the right fusiform gyrus, the right temporo-occipital region and the left frontal pole extending to the medial frontal cortex. A local decrease in grey matter volume was found in the right thalamus. A decrease in global white matter volume in the ASD group did not reach significance. We found the increase in grey matter volume in ASD subjects was greatest in those areas recognised for their role in social cognition, particularly face recognition (right fusiform gyrus), mental state attribution: 'theory of mind' (anterior cingulate and superior temporal sulcus) and perception of eye gaze (superior temporal gyrus). The picture as a whole may reflect an abnormally functioning social cognitive neural network. We suggest that increased grey matter volume may play a pivotal role in the aetiology of the autistic syndrome.

Adolescent↗
PubMed2003

Different brain structures mediate drinking and sleep suppression elicited by the somatostatin analog, octreotide, in rats.

When injected into the cerebral ventricles, the somatostatin analog, octreotide (OCT) elicits prompt drinking, vasopressin secretion and increases in blood pressure that are attributed to the activation of the intracerebral angiotensinergic system. In addition, OCT induces sleep responses that might be mediated by an inhibition of hypothalamic neurons producing growth hormone-releasing hormone (GHRH). OCT (0.02 microg in 0.2 microl) was microinjected into various brain sites to determine the structures inducing drinking and/or sleep suppression in response to OCT in rats. Drinking (>1 ml water in 10 min) was elicited in 17 rats out of 86 tested. The positive drinking sites resided in or around the subfornical organ (SFO) and the paraventricular nucleus. Both structures are part of the reported angiotensinergic dipsogenic circuit of the brain. These microinjections failed to elicit consistent sleep effects. Sleep suppression (>10% recording time in hour 1) was observed after injection of OCT either into the arcuate nucleus (n=7), where the majority of GHRHergic neurons reside, or into the medial preoptic area/anterior hypothalamus (n=8), where GHRH acts to promote sleep. Administration of OCT into far lateral sites of the lateral preoptic area and lateral hypothalamus stimulated sleep in hour 1 (n=10), perhaps via inhibiting cholinergic neurons previously implicated in arousal. The results are consistent with the hypothesis that somatostatin is involved in the regulation of both water intake and sleep, and suggest that different structures, and therefore different somatostatinergic neuronal pools, mediate these actions.

Animals↗
PubMed1996

Glucose metabolism in the cortical and subcortical brain structures in multiple system atrophy and Parkinson's disease: a positron emission tomographic study.

The brain glucose metabolism was studied by PET with 18F-FDG in 11 patients with multiple system atrophy (MSA) and 12 patients with idiopathic Parkinson's disease (PD). Seven of the 11 MSA patients were diagnosed as having olivopontocerebellar atrophy, two had striatonigral degeneration, while two demonstrated Shy-Drager syndrome. The glucose metabolic rates for each region in the PD patients showed no difference from the normal controls. The frontal, temporal and parietal cortical glucose metabolic rates and the caudate, the putaminal, the cerebellar and the brainstem glucose metabolic rates in the MSA patients decreased significantly from the controls. The atrophy of the cerebellum and the brainstem in the MSA patients were scored by MRI. The cerebellar and brainstem glucose metabolism in the MSA patients decreased as the atrophy score in such regions advanced in each group; however, some patients with no atrophy showed a decreased glucose metabolism. Although the cerebellar and the brainstem glucose metabolism decreased in all MSA patients, such a decrease was not observed in the SND patients. The decrease in the glucose metabolism for the non-cortical regions in the MSA patients seems to be due to a diffuse depletion of the neurons not restricted to the nigrostriatal neurons. Deafferentation to the cerebral cortices seems to result in a decreased cortical metabolism. The differences in the glucose metabolism between MSA and PD as assessed by PET may be caused by the pathophysiological differences between MSA and PD, and such differences therefore appear to be useful when making a differential diagnosis between MSA and PD. The relative sparing of the brainstem and cerebellar glucose metabolism is considered to be a feature of patients with SND.

Adult↗
PubMed2002

ELF a beta-spectrin is a neuronal precursor cell marker in developing mammalian brain; structure and organization of the elf/beta-G spectrin gene.

Spectrins play a pivotal role in axonal transport, neurite extension, the organization of synaptic vesicles, as well as for protein sorting in the Golgi apparatus and cell membrane. Among spectrins there is great variability in sequence composition, tissue distribution, and function, with two known genes encoding the alpha-chain, and at least five encoding the beta-chain. It remains unclear as to whether novel beta-spectrins such as elf1-4 are distinct genes or beta-G-spectrin isoforms. The role for ELF in the developing nervous system has not been identified to date. In this study we demonstrate the genomic structure of elf-3, as well as the expression of ELF in the developing mouse brain using a peptide specific antibody against its distinctive amino-terminal end. Full genomic structural analyses reveal that elf-3 is composed of 31 exons spanning approximately 67 kb, and confirm that elf and mouse brain beta-G-spectrin share multiple exons, with a complex form of exon/intron usage. In embryonic stages, E9-12, anti-ELF localized to the primary brain vesicular cells that also labeled strongly with anti-nestin but not anti-vimentin. At E12-14, anti-ELF localized to axonal sprouts in the developing neuroblasts of cortex and purkinje cell layer of the cerebellum, as well as in cell bodies in the diencephalon and metencephalon. Double labeling identified significant co-localization of anti-ELF, nestin and dystrophin in sub ventricular zone cells and in stellate-like cells of the developing forebrain. These studies define clearly the expression of ELF, a new isoform of beta-G-spectrin in the developing brain. Based on its expression pattern, ELF may have a role in neural stem cell development and is a marker of axonal sprouting in mid stages of embryonic development.

Alternative Splicing↗
PubMed2002

Twin-singleton differences in brain structure using structural equation modelling.

Twin studies are important to investigate genetic influences on variation in human brain morphology in health and disease. However, the twin method has been criticized for its alleged non-generalizability due to differences in the intrauterine and family environment of twins, compared with singletons. To test whether twin-singleton differences complicate interpretation of genetic contributions on variation in brain volume, brains from 112 pairs of twins and 34 of their siblings with a mean (standard deviation) age of 30.7 (9.6) years were scanned using MRI. The influence of birth order, zygosity and twin-sibling differences on brain volume measures was analysed using maximum-likelihood model fitting. Variances were homogeneous across birth order, zygosity and twin-singleton status. Irrespective of zygosity, intracranial volume was smaller in second-born twins compared with first-born twins and compared with siblings. Grey matter volume was smaller in second-born twins compared with first-born twins. White matter was smaller in twins compared with siblings. Differences in grey and white matter between these groups were no longer significant after correction for intracranial volume. Total brain, and lateral and third ventricle volumes were comparable in twins and singletons. In conclusion, second-born twins have a smaller intracranial volume than their first-born co-twins and siblings. This suggests aberrant early brain development in second-born twins, which is consistent with the suboptimal pre- and perinatal environment related to birth order in twins. Since other brain volume measures were comparable between the groups, twin studies can provide reliable estimates of heritabilities in brain volume measures and these can be generalized to the singleton population.

Adult↗
PubMed1992

Magnetic resonance imaging of the brain structures in the posterior fossa in retarded autistic children.

Midsagittal magnetic resonance images of the brains of retarded autistic children were compared to those of non-autistic mental retardation patients and controls. We found that the whole brain stem and particularly two of its components (the midbrain and medulla oblongata) were significantly smaller in retarded autistic children and mental retardation cases than in control children. The pons area was significantly smaller in mental retardation cases as compared to control children but did not differ between autistic and control children. Moreover, there was no difference in the brain stem between retarded autistic children and mental retardation cases. We also noted no difference in the cerebellar vermis area among retarded autistic children, mental retardation cases and control children. The ratio of the midbrain to posterior fossa area was significantly smaller only in autistic patients. Although the significance of these results is unknown, further examination of autistic children with a normal IQ is necessary.

Autistic Disorder↗