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PubMed2004

[Neuroanatomical study of the internal structures of the brain based on brain fiber dissection].

From the beginning of the 17th Century, anatomists started to elucidate numerous tracts and fasciculi of the brain using fiber dissection techniques. Due to the complexities associated with tissue preparation and the time-consuming nature of traditional techniques the popularity of this method has gradually declined with the advent of modern neuroimaging techniques such as MRI. Many novel approaches to deep brain lesions have recently been devised following the development of skull base surgery. In comparison, the study of functional neuroanatomy has been relatively neglected. Understanding how neuronal fibers in the brain interconnect and communicate neuronal functions is critical when performing surgery for malignant glioma and epilepsy, as brain parenchyma has to be resected and neuronal fibers are interrupted. In the preoperative planning process we have applied anatomical studies using brain fiber dissection techniques. Brain fiber dissection offers the advantage of exposing association, commissural and projection fibers of cerebral white matter in three dimensions. Brain fiber dissection appears useful for assisting neurosurgeons to acquire neurosurgical skills and become familiar with neuroanatomical features. The techniques and significance of brain fiber dissection are described herein.

Brain↗
PubMed2004

[Study on mesenchymal stem cells entering the brain through the blood-brain barrier].

OBJECTIVE: Neonatal hypoxic-ischemic encephalopathy (HIE) harms the lives and health of newborn infants and children severely. The prognosis is not satisfied, especially of the severe HIE. Mesenchymal stem cells (MSCs) can secrete a series of growth factors and neurotrophic factors. As well they have the potential ability to differentiate to the neural cells in vitro and in vivo. Therefore MSCs transplantation has been employed as a source of progenitor cells for cell therapy in patients with HIE in order to promote recovery of brain function and reduce the sequelae. Studies have shown that MSCs could enter the cerebral parenchyma and differentiate to neural cells through systemic infusion, but most of the researches applied adult stroke animal models. This study used neonatal HIE models to test the hypothesis that MSCs could enter the brain of newborn Wistar rats through the blood-brain barrier (BBB) by intraperitoneal infusion followed by observing the characteristics of the distribution and differentiation of MSCs in brain tissues, and exploring the effects of hypoxic-ischemic brain damage to the penetration and differentiation of MSCs. METHODS: Isolation and purification of MSCs were established from the whole bone marrow of juvenile Wistar rats by removing the nonadherent cells in primary and passage cultures. For cellular identification, MSCs of three to five passages were continuously pre-labeled with 5-bromo-2-deoxyuridine (BrdU) for 72 hours before transplantation. Animal models of HIE were built in 7-day-postnatal Wistar rats according to the method described by Rice. Two hours after hypoxia-ischemia, rats in HIE group (n = 8) were intraperitoneally infused with MSCs (4 x 10(6), 0.5 ml). In control group (n = 8), 7-day-postnatal normal Wistar rats were intraperitoneally infused with the same amount of MSCs. All rats were sacrificed and their cerebra were sectioned by cryomicrotome 14 days after transplantation. Immunohistochemical staining with chromogen diaminobenzidine (DAB) was used to detect and measure the cells derived from MSCs, and study the characteristics of distribution. To determine the differentiation of the BrdU positive cells entering the brains, immunofluorescence double labeling for BrdU and neural cells specific antigens was performed. RESULTS: MSCs were distributed throughout the cerebra in both groups at the 14th day after transplantation. The number of MSCs detected was 2415 +/- 226 in the control group, and 3626 +/- 461 in HIE group, respectively (t = 6.68, P < 0.05). More BrdU reactive cells were observed in the right ischemic hemisphere (1904 +/- 267) than in the contralateral hemisphere (1723 +/- 204), (t = 4.47, P < 0.05). No significant difference was found while comparing both cerebral hemispheres of the control group (t = 0.31, P > 0.05). In the HIE group, MSCs distributed more extensively, and some focal aggregations of MSCs were noticed. A few MSCs expressed Nestin-protein marker of neural progenitor cells, and almost none of the MSCs which expressed proteins characteristic of neuron (e.g. NSE) and astrocyte (e.g. GFAP) was detected at the 14th day after transplantation. CONCLUSION: 1. MSCs could enter the cerebral parenchyma through BBB and migrate throughout the brain by intraperitoneal infusion. 2. More MSCs injected intraperitoneally were localized and directed to the sites of hypoxic-ischemic brain damage. 3. Transplanted MSCs could not differentiate to neuron and astrocyte without other interventions during 14 days after transplantation.

Animals↗
PubMed2006

[Aquaporin water channels in the brain and molecular mechanisms of brain edema].

Aquaporins(AQPs) are a family of water selective channel. Transcripts of AQP1, AQP3, AQP4, AQP5, AQP8, and AQP9 are detected in the brain. Especially in astrocytes, AQP4 is abundantly expressed in end feet at the blood-brain barrier. Brain AQPs play important roles in the regulation of water homeostasis and the cerebro spinal fluid formation. Recently, AQP4 and AQP9 have been reported to involve in the brain water accumulation in the brain edema. Studies of transgenic mouse and brain injury models reveal that AQP4 may play a role not in the edema formation, but in the fluid elimination. Further study of AQPs functions in the brain may provide new insights into the brain edema and allow the design of novel anti edema medications.

Animals↗
PubMed1988

Delivery of melanoma-associated immunoglobulin monoclonal antibody and Fab fragments to normal brain utilizing osmotic blood-brain barrier disruption.

Iodinated monoclonal antibodies (IgG 96.5 and two monomeric Fab fragments 96.5 and 48.7) to melanoma-associated antigens were administered after osmotic blood-brain barrier (BBB) opening in normal rats. Osmotic BBB disruption significantly (P less than 0.0001) increased monoclonal antibody delivery to the brain. Following BBB opening and intracarotid administration, there was no difference in the disrupted brain concentration integral area under the curve between Fab and IgG over the 72-h experimental period. However, Fab concentration in the disrupted brain was initially higher than IgG, and the clearance was more rapid (P less than 0.0001), decreasing 50% by approximately 4.5 h compared to 25.5 h for IgG. Plasma clearance was also more rapid for the Fab than IgG. The levels decreased 50% by 1.5 h for Fab and 15 h for IgG. The route and timing of antibody infusion had a significant effect on delivery to the disrupted brain with the Fab fragments but not with the intact IgG. Antibody recovered from disrupted brain retained its immunological reactivity as measured by a cell binding assay for at least 24 h. IgG and Fab delivery to the ipsilateral brain after BBB disruption increased (P less than 0.001) with increasing dose over a more than 3-log dose range. These data provide information applicable to the therapeutic use of monoclonal antibodies in brain tumor treatment.

Animals↗
PubMed1993

[Relationship between cerebral circulatory arrest and loss of brain functions--analysis of patients in a state of impending brain death].

To clarify the temporal discrepancies between cerebral circulatory arrest and loss of brain functions in relation to neuroradiological differences of brain damage, we analyzed 100 cases of impending brain death evaluated by neurological findings and continuous, simultaneous neuromonitoring of somatosensory and brainstem auditory evoked potentials (SEP, BAEP), compressed spectral arrays (CSA), and transcranial Doppler sonography (TCD). A) Cases of supratentorial lesions: 1) Loss of brain functions after supratentorial circulatory arrest (TCD) were advanced rostrocaudally -(SEP N20 > CSA) > (BAEP III-V > SEP P13/14). 2) All patients demonstrated supratentorial circulatory arrest (TCD) after both neurological and cerebral (CSA) functions had been lost for more than 6 hours or after loss of neurological, cerebral (CSA), and brainstem (BAEP, SEP) functions. B) Cases of diffuse or infratentorial lesions: Supratentorial circulation persisted in a few cases after loss of all brain functions. C) The interval from supratentorial circulatory arrest to brainstem function loss was longer than that to cerebral function loss. Both intervals were less than 24 hours in almost all cases. In applying ancillary studies to the diagnosis of brain death, consideration should be given to the time lag between cerebral circulatory arrest and loss of brain functions caused by pathophysiological differences in brain damage.

Adolescent↗
PubMed1997

MR-based brain and cerebrospinal fluid measurement after traumatic brain injury: correlation with neuropsychological outcome.

PURPOSE: To determine the magnitude and time course of changes in the volume of brain and intracranial cerebrospinal fluid (CSF) spaces in patients who have sustained traumatic brain injury and to assess the relationship between these findings and long-term cognitive traumatic outcome. METHODS: Axial intermediate and T2-weighted MR images of 123 patients with traumatic brain injury were quantified using a multispectral segmentation algorithm. Measurements were corrected for differences in age, sex, and head size using a previously reported normative database. Brain morphology was compared across groups formed on the basis of chronicity of injury. Cognitive functioning and severity of injury were statistically correlated with brain measurements. RESULTS: Time-dependent expansion of CSF spaces and decreases in brain volume were observed. Increases in ventricular CSF volume, particularly in the temporal horns and third ventricle, preceded subsequent changes in total brain and subarachnoid CSF. High and moderate correlation was observed between volume measures and cognitive outcome and injury severity. Particularly strong was the relation between the volume of the left temporal horn and verbal IQ scores. CONCLUSION: Predictable time-dependent atrophic changes occurring after traumatic brain injury can be quantified using MR volumetric studies. Our results suggest significant contributions by both diffuse and focal mechanisms of injury. In the postacute period (more than 70 days after injury), MR volumetric studies may be predictive of eventual cognitive outcome.

Adolescent↗
PubMed2004

Human fetal brain imaging by magnetoencephalography: verification of fetal brain signals by comparison with fetal brain models.

Fetal magnetoencephalogram (fMEG) is measured in the presence of a large interference from maternal and fetal magnetocardiograms (mMCG and fMCG). This cardiac interference can be successfully removed by orthogonal projection of the corresponding spatial vectors. However, orthogonal projection redistributes the fMEG signal among channels. Such redistribution can be readily accounted for in the forward solution, and the signal topography can also be corrected. To assure that the correction has been done properly, and also to verify that the measured signal originates from within the fetal head, we have modeled the observed fMEG by two extreme models where the fetal head is assumed to be either electrically transparent or isolated from the abdominal tissue. Based on the measured spontaneous, sharp wave, and flash-evoked fMEG signals, we have concluded that the model of the electrically isolated fetal head is more appropriate for fMEG analysis. We show with the help of this model that the redistribution due to projection was properly corrected, and also, that the measured fMEG is consistent with the known position of the fetal head. The modeling provides additional confidence that the measured signals indeed originate from within the fetal head.

Algorithms↗