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Contralateral Hemisphere (contralateral + hemisphere)
Selected AbstractsVictor Horsley's Contribution to Jacksonian EpileptologyEPILEPSIA, Issue 11 2005Mervyn J. Eadie Summary:,Purpose: To describe Victor Horsley's contribution to John Hughlings Jackson's understanding of the mechanisms involved in the generalization of convulsive epileptic seizures. Methods: I reviewed Horsley's writings and other relevant late 19th century medical literature. Results: Horsley's combination of strategically sited surgical lesions and cerebral cortex stimulation studies in experimental animals showed that, contrary to Hughlings Jackson's earlier belief, epileptic activity arising in one cerebral hemisphere had to spread to the contralateral hemisphere before bilateral convulsing could occur. Conclusions: On the basis of well-designed experiments, Horsley made a major contribution to the understanding of epileptic seizure propagation mechanisms. [source] Contralateral EEG Slowing and Amobarbital Distribution in Wada Test: An Intracarotid SPECT StudyEPILEPSIA, Issue 2 2000Seung Bong Hong Summary: Purpose: To relate the occurrence of contralateral electroencephalogram slowing (CES) to amobarbital distribution, we performed electroencephalogram (EEG) monitoring and intracarotid single photon emission computed tomography (SPECT) during an intracarotid amobarbital procedure (IAP). Methods: IAP was performed on 22 patients with temporal lobe epilepsy. CES was defined as the occurrence of significant EEG slowing on the contralateral hemisphere (>50% of the ipsilateral hemisphere slowing) after amobarbital injection. To map the distribution of the amobarbital, we injected a mixture of amobarbital and 99m technetium-ethylcysteinate dimer (99m Tc-ECD) into the internal carotid artery and performed a brain SPECT 2 h later. In the SPECT images, regions of interest were determined by ipsilateral and contralateral anterior cerebral artery territories (iACA, cACA), ipsilateral and contralateral middle cerebral artery territories (iMCA, cMCA), and ipsilateral and contralateral posterior cerebral artery territories (iPCA, cPCA), as well as ipsilateral and contralateral anterior and posterior mesial temporal regions (iAMT, cAMT, iPMT, cPMT). The perfusion of amobarbital was interpreted visually in each region. Results: Amobarbital was distributed in the iMCA in all the patients; in the iACA in 20 (90.9%) patients; in the iAMT in 14 (63.5%); and in the iPCA and iPMT in only two (9.1%). CES was observed in 13 (59.1%) patients. Cross-perfusion of amobarbital in limited areas of the cACA were observed in only four of 13 patients. Wada retention memory scores (WRMS) showed no significant difference between the CES- (n = 9) and CES+ (n = 13) groups. Conclusions: Amobarbital rarely perfused the iPCA territory and the iPMT region and was rarely delivered to the contralat-eral hemisphere. The occurrence of CES was not related to the cross-perfusion of amobarbital. CES appears to be produced by a transient functional disconnection from the ipsilateral hemisphere. [source] Cerebral bloodflow and oxygen metabolism in borderzone and territorial infarcts due to symptomatic carotid artery occlusionEUROPEAN JOURNAL OF NEUROLOGY, Issue 4 2004J. De Reuck It remains controversial whether borderzone infarcts are due to compromised cerebral perfusion and whether territorial infarcts are caused by artery-to-artery emboli in case of occlusion of the internal carotid artery. The present positron emission tomography study compares with normal controls, the average regional cerebral bloodflow (rCBF), regional oxygen extraction fraction (rOEF) and regional cerebral metabolic rate for oxygen (rCMRO2) in the infarct area, the peri-infarct zone, the remaining homolateral hemisphere and in the contralateral hemisphere of 10 patients with borderzone and 17 patients with territorial infarcts, due to internal carotid artery occlusion by atherosclerosis and by cervical dissection. The steady-state technique with oxygen-15 was used. A nearly significant increase of rOEF with lowered rCBF and rCMRO2 was observed in the peri-infarct zone of patients with territorial infarcts. In patients with borderzone infarcts rCMRO2 was decreased in the peri-infarct zone, in the remaining homolateral hemisphere and in the contralateral hemisphere without changes in rCBF and rOEF. The present study finds no arguments that impaired cerebral perfusion is a more frequent cause of borderzone than of territorial infarcts. [source] Callosal contribution to ocular dominance in rat primary visual cortexEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 7 2010Chiara Cerri Abstract Ocular dominance (OD) plasticity triggered by monocular eyelid suture is a classic paradigm for studying experience-dependent changes in neural connectivity. Recently, rodents have become the most popular model for studies of OD plasticity. It is therefore important to determine how OD is determined in the rodent primary visual cortex. In particular, cortical cells receive considerable inputs from the contralateral hemisphere via callosal axons, but the role of these connections in controlling eye preference remains controversial. Here we have examined the role of callosal connections in binocularity of the visual cortex in naïve young rats. We recorded cortical responses evoked by stimulation of each eye before and after acute silencing, via stereotaxic tetrodotoxin (TTX) injection, of the lateral geniculate nucleus ipsilateral to the recording site. This protocol allowed us to isolate visual responses transmitted via the corpus callosum. Cortical binocularity was assessed by visual evoked potential (VEP) and single-unit recordings. We found that acute silencing of afferent geniculocortical input produced a very significant reduction in the contralateral-to-ipsilateral (C/I) VEP ratio, and a marked shift towards the ipsilateral eye in the OD distribution of cortical cells. Analysis of absolute strength of each eye indicated a dramatic decrease in contralateral eye responses following TTX, while those of the ipsilateral eye were reduced but maintained a more evident input. We conclude that callosal connections contribute to normal OD mainly by carrying visual input from the ipsilateral eye. These data have important implications for the interpretation of OD plasticity following alterations of visual experience. [source] Visualization of corticofugal projections during early cortical development in a ,-GFP-transgenic mouseEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 1 2007Erin C. Jacobs Abstract The first postmitotic neurons in the developing neocortex establish the preplate layer. These early-born neurons have a significant influence on the circuitry of the developing cortex. However, the exact timing and trajectory of their projections, between cortical hemispheres and intra- and extra-cortical regions, remain unresolved. Here, we describe the creation of a transgenic mouse using a 1.3 kb golli promoter element of the myelin basic protein gene to target expression of a ,,green fluorescent protein (GFP) fusion protein in the cell bodies and processes of pioneer cortical neurons. During embryonic and early neonatal development, the timing and patterning of process extension from these neurons was examined. Analysis of ,-GFP fluorescent fibers revealed that progression of early labeled projections was interrupted unexpectedly by transient pauses at the corticostriatal and telencephalic,diencephalic boundaries before invading the thalamus just prior to birth. After birth the pioneering projections differentially invaded the thalamus, excluding some nuclei, e.g. medial and lateral geniculate, until postnatal days 10,14. Early labeled projections were also found to cross to the contralateral hemisphere as well as to the superior colliculus. These results indicate that early corticothalamic projections appear to pause before invading specific subcortical regions during development, that there is developmental regulation of innervation of individual thalamic nuclei, and that these early-generated neurons also establish early projections to commissural and subcortical targets. [source] Early midline interactions are important in mouse optic chiasm formation but are not critical in man: a significant distinction between man and mouseEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 11 2006Magella M. Neveu Abstract The optic chiasm is one of the most popular models for studying axon guidance. Here axons make a key binary decision either to cross the midline to innervate the contralateral hemisphere or to remain uncrossed. In rodents, midline interactions between axons from the two eyes are critical for normal development, as early removal of one eye systematically disrupts hemispheric projections from the remaining eye, increasing the crossed projection at the expense of the uncrossed. This is similar to the abnormal decussation pattern seen in albinos. This pattern is markedly different in marsupials where early eye removal has no impact on projections from the remaining eye. These differences are related to the location of the uncrossed projection through the chiasm. In rodents these axons approach the midline whereas in marsupials they remain segregated laterally. We provide anatomical evidence in man suggesting that, unlike in rodents, uncrossed axons are confined laterally and do not mix in each hemi-chiasm, which is a pattern similar to that found in marsupials. Further, we demonstrate electrophysiologically, using visual cortical evoked potentials, that the failure of one eye to develop in man has no impact on the hemispheric projections from the remaining eye. These data demonstrate that the mechanisms regulating chiasmal development in man differ from those in rodents but may be similar to those in marsupials. We suggest that mouse models of the organization and development of the optic chiasm are not common to placental mammals in general. [source] Age-related changes in the dynamics of human albino visual pathwaysEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 7 2003Magella M. Neveu Abstract A deficiency of melanin in the retinal pigment epithelium, which regulates the development of neural retina, leads to chiasmal misrouting such that the uncrossed pathway (to the ipsilateral hemisphere) is reduced relative to the crossed pathway (to the contralateral hemisphere). This study examines age-related changes in the flash and pattern appearance visual evoked potentials (VEP) of human albinos. Scalp recorded cortical VEPs to flash (FVEP) and pattern appearance stimulation were recorded in 58 albino (8 months to 60 years) and 34 normal subjects (4,55 years). VEPs were analysed by amplitude and latency. The contralateral hemisphere FVEP amplitude decreased with age in albino subjects, as in both hemispheres in normals. However, the ipsilateral hemisphere FVEP amplitude was significantly lower in young albino subjects, initially giving a marked interhemispheric asymmetry, but this normalized with age. Significant interhemispheric FVEP latency asymmetries were not observed. The contralateral pattern appearance VEP latency in albino subjects decreased with age, as in both hemispheres in normals; the ipsilateral latency increased significantly with age. Significant interhemispheric pattern appearance VEP amplitude asymmetries were not observed. These novel and unexpected observations indicate significant age-related changes in the retinocortical pathways of the human albino. These changes have implications for our understanding of development and plasticity of the central visual pathways. [source] Monocular visual activation patterns in albinism as revealed by functional magnetic resonance imagingHUMAN BRAIN MAPPING, Issue 1 2004Bernd Schmitz Abstract Human albinism is characterized by a disturbance of the chiasmatic projection system leading to predominant representation of just one eye in the contralateral hemisphere. Patients show congenital nystagmus without perceiving oscillopsia. The purpose of the present study was to demonstrate the consequences of atypical chiasmatic crossing with monocular visual stimulation using functional magnetic resonance imaging (fMRI). Sixteen patients with albinism and fifteen normally pigmented controls were stimulated with a monocular visual activation paradigm using flickering checkerboards. In patients, we observed contralaterally dominated activation of visual cortices correlating to clinical albinism parameters. This confirms albinism as a continuous range of hypopigmentation disorders. Additionally, albinos showed activation of the superior colliculus and of visual motion areas although the stimulus was stationary. Activation of visual motion areas is due probably to congenital nystagmus without a conscious correlate like oscillopsia. Hum. Brain Mapping 23:40,52, 2004. © 2004 Wiley-Liss, Inc. [source] Proton magnetic resonance spectroscopic imaging to differentiate between nonneoplastic lesions and brain tumors in children,JOURNAL OF MAGNETIC RESONANCE IMAGING, Issue 2 2006Roula Hourani MD Abstract Purpose To investigate whether in vivo proton magnetic resonance spectroscopic imaging (MRSI) can differentiate between 1) tumors and nonneoplastic brain lesions, and 2) high- and low-grade tumors in children. Materials and Methods Thirty-two children (20 males and 12 females, mean age = 10 ± 5 years) with primary brain lesions were evaluated retrospectively. Nineteen patients had a neuropathologically confirmed brain tumor, and 13 patients had a benign lesion. Multislice proton MRSI was performed at TE = 280 msec. Ratios of N-acetyl aspartate/choline (NAA/Cho), NAA/creatine (Cr), and Cho/Cr were evaluated in the lesion and the contralateral hemisphere. Normalized lesion peak areas (Chonorm, Crnorm, and NAAnorm) expressed relative to the contralateral hemisphere were also calculated. Discriminant function analysis was used for statistical evaluation. Results Considering all possible combinations of metabolite ratios, the best discriminant function to differentiate between nonneoplastic lesions and brain tumors was found to include only the ratio of Cho/Cr (Wilks' lambda, P = 0.012; 78.1% of original grouped cases correctly classified). The best discriminant function to differentiate between high- and low-grade tumors included the ratios of NAA/Cr and Chonorm (Wilks' lambda, P = 0.001; 89.5% of original grouped cases correctly classified). Cr levels in low-grade tumors were slightly lower than or comparable to control regions and ranged from 53% to 165% of the control values in high-grade tumors. Conclusion Proton MRSI may have a promising role in differentiating pediatric brain lesions, and an important diagnostic value, particularly for inoperable or inaccessible lesions. J. Magn. Reson. Imaging 2006. Published 2005 Wiley-Liss, Inc. [source] Nuclear factor I gene expression in the developing forebrainTHE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 3 2008Céline Plachez Abstract Three members of the Nuclear Factor I (Nfi) gene family of transcription factors; Nfia, Nfib, and Nfix are highly expressed in the developing mouse brain. Nfia and Nfib knockout mice display profound defects in the development of midline glial populations and the development of forebrain commissures (das Neves et al. [1999] Proc Natl Acad Sci U S A 96:11946,11951; Shu et al. [2003] J Neurosci 23:203,212; Steele-Perkins et al. [2005] Mol Cell Biol 25:685,698). These findings suggest that Nfi genes may regulate the substrate over which the commissural axons grow to reach targets in the contralateral hemisphere. However, these genes are also expressed in the cerebral cortex and, thus, it is important to assess whether this expression correlates with a cell-autonomous role in cortical development. Here we detail the protein expression of NFIA and NFIB during embryonic and postnatal mouse forebrain development. We find that both NFIA and NFIB are expressed in the deep cortical layers and subplate prenatally and display dynamic expression patterns postnatally. Both genes are also highly expressed in the developing hippocampus and in the diencephalon. We also find that principally neither NFIA nor NFIB are expressed in callosally projecting neurons postnatally, emphasizing the role for midline glial cell populations in commissure formation. However, a large proportion of laterally projecting neurons express both NFIA and NFIB, indicating a possible cell-autonomous role for these transcription factors in corticospinal neuron development. Collectively, these data suggest that, in addition to regulating the formation of axon guidance substrates, these genes also have cell-autonomous roles in cortical development. J. Comp. Neurol. 508:385,401, 2008. © 2008 Wiley-Liss, Inc. [source] Brain engraftment and therapeutic potential of stem/progenitor cells derived from mouse skinTHE JOURNAL OF GENE MEDICINE, Issue 4 2006Patrizia Tunici Abstract Skin stem/progenitor cells (SKPs) derive from the dermis and in culture can generate mesodermal and neural progenies. To investigate their potential for the treatment of brain diseases, we first injected SKPs into the brain of syngeneic mice. Brain histology indicated that most SKPs remained undifferentiated and clustered at the injection site, while, in vitro, 17% of SKPs expressed neural markers, as assessed by flow cytometry. After labeling with magnetodendrimers, murine and human SKPs were detected by magnetic resonance imaging even 5 months after brain injection. To evaluate their therapeutic potential on malignant gliomas, IL-4 SKPs (i.e. SKPs transduced by a lentiviral vector carrying the cDNA of the anti-glioma cytokine interleukin-4) were injected into GL261 experimental gliomas. IL-4-SKPs prolonged significantly the survival of tumor-bearing mice: furthermore, GL261 gliomas attracted SKPs originally injected into the contralateral hemisphere. Thus, prolonged survival, capacity for transgene expression, and lack of uncontrolled proliferation suggest that SKPs warrant further consideration as therapeutic tools for brain tumors and, possibly, other neurological disorders. Copyright © 2006 John Wiley & Sons, Ltd. [source] T2*-weighted magnetic resonance imaging with hyperoxia in acute ischemic strokeANNALS OF NEUROLOGY, Issue 1 2010Krishna A. Dani MBChB Objective We describe the first clinical application of transient hyperoxia ("oxygen challenge") during T2*-weighted magnetic resonance imaging (MRI), to detect differences in vascular deoxyhemoglobin between tissue compartments following stroke. Methods Subjects with acute ischemic stroke were scanned with T2*-weighted MRI and oxygen challenge. For regions defined as infarct core (diffusion-weighted imaging lesion) and presumed penumbra (perfusion-diffusion mismatch [threshold = Tmax ,4 seconds], or regions exhibiting diffusion lesion expansion at day 3), T2*-weighted signal intensity,time curves corresponding to the duration of oxygen challenge were generated. From these, the area under the curve, gradient of incline of the signal increase, time to maximum signal, and percentage signal change after oxygen challenge were measured. Results We identified 25 subjects with stroke lesions >1ml. Eighteen subjects with good quality T2*-weighted signal intensity,time curves in the contralateral hemisphere were analyzed. Curves from the diffusion lesion had a smaller area under the curve, percentage signal change, and gradient of incline, and longer time to maximum signal (p < 0.05, n = 17) compared to normal tissue, which consistently showed signal increase during oxygen challenge. Curves in the presumed penumbral regions (n = 8) showed varied morphology, but at hyperacute time points (<8 hours) showed a tendency to greater percentage signal change. Interpretation Differences in T2*-weighted signal intensity,time curves during oxygen challenge in brain regions with different pathophysiological states after stroke are likely to reflect differences in deoxyhemoglobin concentration, and therefore differences in metabolic activity. Despite its underlying complexities, this technique offers a possible novel mode of metabolic imaging in acute stroke. ANN NEUROL 2010;68:37,47 [source] Magnetic resonance cerebral metabolic rate of oxygen utilization in hyperacute stroke patientsANNALS OF NEUROLOGY, Issue 2 2003Jin-Moo Lee MD The purpose of this study was to explore the feasibility of obtaining magnetic resonance,measured cerebral metabolic rate of oxygen utilization (MR-CMRO2) in acute ischemic stroke patients. Seven stroke patients were serially imaged: 4.5 ± 0.9 hours (tp1), 3 to 5 days (tp2), and 1 to 3 months (tp3) after symptom onset. Diffusion-weighted, perfusion-weighted, and multiecho gradient-echo/spin-echo images were acquired; cerebral blood flow and oxygen extraction fraction maps were obtained from which CMRO2 was calculated as the product of cerebral blood flow and oxygen extraction fraction. The final infarct lesions obtained from tp3 T2-weighted images and the "penumbra" obtained from the tp1 perfusion-weighted image,defined lesion were coregistered onto tp1 CMRO2 maps. CMRO2 values in the region of brain that eventually infarcted were reduced to 0.40 ± 0.24 of the respective region on the contralateral hemisphere. The "salvaged penumbra" defined by the area of mismatch between the final infarct and the tp1 perfusion-weighted lesion demonstrated an average CMRO2 value of 0.55 ± 0.11 of the contralateral hemisphere. Although our results are preliminary and require further evaluation, the ability to obtain in vivo measurements of MR-CMRO2 noninvasively potentially can provide information for determining brain tissue viability in acute ischemic stroke patients. [source] Selective Neuronal Vulnerability Following Mild Focal Brain Ischemia in the MouseBRAIN PATHOLOGY, Issue 4 2003Juri Katchanov The evolution of cellular damage over time and the selective vulnerability of different neuronal subtypes was characterized in the striatum following 30-minute middle cerebral artery occlusion and reperfusion in the mouse. Using autoradiography we found an increase in the density of [3H]PK11195 binding sites,likely reflecting microglial activation,in the lesion border at 3 days and in the whole striatum from 10 days to 6 weeks. This was accompanied by a distinct loss of [3H]flumazenil and [3H]CGP39653 binding sites from 10 days up to 6 weeks reflecting neuronal loss. Brain ischemia resulted in a substantial loss of medium spiny projection neurons as seen at three days by Nissl staining, TUNEL and immunocytochemistry using antibodies against microtubule-associated protein (MAP2), NeuN, (,-opioid receptors, substance P, Lenkephalin, neurokinin B, choline acetyltransferase, parvalbumin, calretinin and somatostatin. Both patch and matrix compartments were involved in ischemic damage. In contrast, the numbers of cholinergic, GABAergic, and somatostatin-containing interneurons in the ischemic striatum were not different from those in the contralateral hemisphere at 3 and 14 days. A low density of glutamate receptors, the ability to sequester calcium by calcium-binding proteins and other hitherto unidentified factors may explain this relative resistance of interneurons to acute ischemia. [source] Hemifacial spasm or somatoform disorder , postexcitatory inhibition after transcranial magnetic cortical stimulation asa diagnostic toolACTA NEUROLOGICA SCANDINAVICA, Issue 5 2000S. Kotterba Hemifacial spasm (HFS) presents a frequent movement disorder. It is thought to have an organic origin. It therefore has to be distinguished from other facial involuntary movements, especially psychogenic tics, because the therapeutic approach differs. The present study opted to evaluate the diagnostic value of the postexcitatory inhibition (pI) after transcranial magnetic stimulation (TMS). After stimulating the contralateral hemisphere with the conventional flat coil and recording from the mentalis muscle, in 10 healthy controls and 10 patients postexcitatory inhibition was determined. PI showed no side to side difference in healthy controls (96.9±12.7 ms right, 87.9±10.8 ms left side, interhemispheric difference 6.4±3.8 ms). In 8 patients with hemifacial spasm, the duration of pI on the non-affected side did not differ from the healthy controls (87.9±43.5 ms). During spasm, pI on the affected side shortened increasingly until no inhibition could be induced. Afterwards the spasm pI was prolonged significantly (up to 140 ms longer than opposite side) before returning to normal values. Two patients presented no side differences of pI during the "spasm". An emotional conflict situation could be evaluated, supporting the diagnosis of somatoform disorder. As postexcitatory inhibition is mainly due to cerebral mechanisms, the electrophysiological results of the study pointed to a cortical influence on the hemifacial spasm. TMS seems to be an electrophysiological tool which allows a differentiation between organic and psychogenic spasm and enables a different therapeutic approach. [source] Glial aromatization increases the expression of bone morphogenetic protein-2 in the injured zebra finch brainJOURNAL OF NEUROCHEMISTRY, Issue 1 2008Bradley J. Walters Abstract In songbirds, brain injury upregulates glial aromatase. The resulting local estrogen synthesis mitigates apoptosis and enhances cytogenesis by poorly understood mechanisms. Bone morphogenetic proteins (BMPs), long studied for their role in neural development, are also neuroprotective and cytogenic in the adult brain. BMPs remain uncharacterized in songbirds, as do the mechanisms regulating their post-injury expression. We first established the expression of BMPs 2, 4, 6, and 7 in the adult zebra finch brain using RT-PCR. Next, we determined the effect of neural insult on BMP expression, by comparing BMP transcripts between injured and uninjured telencephalic hemispheres using semi-quantitative PCR. The expression of BMPs 2 and 4, but not 6 and 7, increased 24 h post-injury. To determine the influence of aromatase on BMP expression, we compared BMP expression following delivery of the aromatase inhibitor Fadrozole or vehicle into contralateral hemispheres. Fadrozole decreased BMP2, but not BMP4, expression, suggesting that aromatization may induce BMP2 expression following injury. Since BMPs are gliogenic and neurotrophic, future studies will test if the neuroprotective and cytogenic effects of aromatase upregulation are mediated by BMP2. Songbirds may be excellent models towards understanding the role of local estrogen synthesis and its downstream mechanisms on neuroprotection and repair. [source] | |||||||||||||