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PubMed1995

NG-nitro-L-arginine delays the development of brain injury during focal ischemia in rats.

BACKGROUND AND PURPOSE: The present study was designed to determine the effect of nitro-L-arginine, the inhibitor of nitric oxide synthesis, on the evolution of cytotoxic brain edema during focal cerebral ischemia. METHOD: Diffusion-weighted and contrast-enhanced, perfusion-sensitive magnetic resonance imaging was performed in anesthetized, mechanically ventilated rats at 30 minutes and 1, 2, and 3 hours after occlusion of the middle cerebral artery combined with coagulation of the basilar artery. At the onset of ischemia, the animals were infused intravenously with 0.5 mL of either 0.9% NaCl or nitro-L-arginine (30 mg/kg). The severity of cytotoxic edema was evaluated based on changes in the water apparent diffusion coefficient (ADC) derived from diffusion-weighted images. The size of the area affected by ischemia was evaluated 3 hours after occlusion using 2,3,5-triphenyltetrazolium chloride (TTC) staining. RESULTS: The percentage decrease of ADC in the striatum of rats pretreated with nitro-L-arginine was significantly smaller (P < .05) than in the control group at 30 minutes and 1 and 2 hours of ischemia. The ADC in the injured cortex of nitro-L-arginine-treated rats did not differ significantly from the ADC value measured in the contralateral cortex until 3 hours after the occlusion. However, at 3 hours of ischemia the percentage decrease of ADC in both the striatum and the cortex of either group of rats was similar. This transient attenuation of ADC drop during ischemia after nitro-L-arginine pretreatment occurred concurrently with a transient improvement of blood supply to the ischemic regions. The percentage of hemispheric area with abnormal TTC staining after 3 hours of ischemia did not differ between control and nitro-L-arginine-treated rats. CONCLUSIONS: Nitro-L-arginine delays the development of ischemic injury by retarding cytotoxic brain edema. This effect is, at least partially, mediated by an improvement in blood supply to the ischemia tissues.

Animals↗
PubMed1996

Differential temporal evolution of post-training changes in regional brain glucose metabolism induced by repeated spatial discrimination training in mice: visualization of the memory consolidation process?

The present study analyses the effects of the stage of learning on the spatial patterns and time-course of [14C]glucose uptake in BALB/c mice brain regions produced by spatial discrimination training in an eight-arm radial maze. Our particular approach was designed to follow, during the post-training period, the level of functional activity in individual brain areas which may underlie the memory consolidation process. Regional mapping of relative [14C]glucose uptake was assessed at three post-training time intervals (5 min, 1 and 3 h) after either the first (Day 1), the fourth (Day 4) or the last (Day 9) daily training session of the discrimination task and compared with sham-conditioned animals placed in the same experimental environment. The results indicated that numerous subcortical and cortical brain regions exhibit metabolic alterations following the acquisition of the spatial discrimination task. These alterations, which were specifically related to learning since they did not appear in sham-conditioned animals, were functions both of the post-training interval studied and of the degree of mastery of the task. On Day 1, a progressive, time-dependent and sequential increase in labelling was found from subcortical (5 min post-training) to cortical regions (3 h post-training). On Day 4, a peak of cortical metabolic activation was identified at 1 h post-training. In contrast, on Day 9, maximum labelling was found 5 min post-training in all subcortical and cortical regions followed by a general monotonic decline at 1 and 3 h post-training. These findings, which show widely distributed changes of metabolic activity in the brain, are consistent with the hypothesis that learning involves distributed neural networks. The sequential activation from subcortical to cortical regions seems to indicate a general mechanism whose function would ultimately be to store cortical memory representations. The acquisition-dependent shifts in the patterns of post-training metabolic labelling observed as a function of task mastery may be taken to represent a visualization of the spatio-temporal evolution of the networks of brain structures actively engaged in the memory consolidation process. In particular, the present data suggest that the duration of post-acquisition memory processing is a function of the quantity of new information which has to be dealt with by the central nervous system.

Animals↗
PubMed2026

WWOX-related developmental and epileptic encephalopathy (WOREE): A case series of seven patients from Argentina.

PURPOSE: WWOX-related developmental and epileptic encephalopathy (WOREE) is a rare autosomal recessive disorder caused by biallelic pathogenic WWOX variants, characterized by very early-onset epilepsy, profound developmental delay, and progressive brain abnormalities. Detailed electroclinical descriptions remain limited. METHODS: We conducted a retrospective study of seven patients with pathogenic/likely pathogenic WWOX variants. Clinical features, seizure evolution, EEG findings, brain MRI, and genetic data were reviewed. Epilepsy syndromes were classified according to International League against Epilepsy (ILAE) criteria. Variants were identified through next-generation sequencing and interpreted following American College of Medical Genetics and Genomics (ACMG) guidelines. RESULTS: Median seizure onset was 3 months (range 2-6). Five patients presented with focal seizures evolving to infantile epileptic spasms syndrome (IESS), while two had IESS at onset. Epilepsy was drug-resistant in all. Developmental delay was evident from birth with generalized hypotonia, acquired microcephaly, and impaired visual attention. Four patients had dysmorphic features. During the IESS period, EEG showed hypsarrhythmia in six patients and a severely disorganized encephalopathic background that did not strictly fulfill the criteria for hypsarrhythmia in one. Brain MRI revealed abnormalities in all patients, including frontotemporal atrophy and corpus callosum hypoplasia; delayed myelination was observed in one case. Eight pathogenic/likely pathogenic WWOX variants were found; including one novel variant (NM_016373.4:c.571C>T, p.(Gln191*)). The recurrent splice-site variant NM_016373.4:c.107+1G>A was identified in five patients, suggesting a possible regional founder effect. CONCLUSION: WOREE shows a recognizable electroclinical and neuroimaging profile with early drug-resistant epilepsy and profound developmental delay. Recognition of this pattern may facilitate early diagnosis and targeted genetic testing, particularly in populations with recurrent variants.

Developmental and epileptic encephalopathy↗
PubMed2003

Sexual dimorphism and asymmetries in the gray-white composition of the human cerebrum.

Using high resolution MRI scans and automated tissue segmentation, gray and white matter (GM, WM) volumes of the frontal, temporal, parietal, and occipital lobes, cingulate gyrus, and insula were calculated. Subjects included 23 male and 23 female healthy, right-handed subjects. For all structures, male volumes were greater than female, but the gray/white (G/W) ratio was consistently higher across structures in women than men. Sexual dimorphism was greater for WM than GM: most of the G/W ratio sex differences can be attributed to variation in WM volume. The corpus callosum, although larger in men, is less sexually dimorphic than the WM as a whole. Several regions demonstrate pair-wise asymmetries in G/W ratio and WM volume. Both the cingulate gyrus and insula exhibit strong asymmetries. The left cingulate gyrus is significantly larger than the right, and the G/W ratio of the left insula is significantly greater than that of the right. Although statistically significant sex differences and asymmetries are present at this level of analysis, we argue that researchers should be wary of ascribing cognitive functional significance to these patterns at this time. This is not to say, however, that these patterns are not important for understanding the natural history of the human brain, and its evolution and development.

Adult↗
PubMed2006

DNA sequence and analysis of human chromosome 8.

The International Human Genome Sequencing Consortium (IHGSC) recently completed a sequence of the human genome. As part of this project, we have focused on chromosome 8. Although some chromosomes exhibit extreme characteristics in terms of length, gene content, repeat content and fraction segmentally duplicated, chromosome 8 is distinctly typical in character, being very close to the genome median in each of these aspects. This work describes a finished sequence and gene catalogue for the chromosome, which represents just over 5% of the euchromatic human genome. A unique feature of the chromosome is a vast region of approximately 15 megabases on distal 8p that appears to have a strikingly high mutation rate, which has accelerated in the hominids relative to other sequenced mammals. This fast-evolving region contains a number of genes related to innate immunity and the nervous system, including loci that appear to be under positive selection--these include the major defensin (DEF) gene cluster and MCPH1, a gene that may have contributed to the evolution of expanded brain size in the great apes. The data from chromosome 8 should allow a better understanding of both normal and disease biology and genome evolution.

Animals↗
PubMed1996

The Agnathan ark: the origin of craniate brains.

An outgroup analysis of head organization of tunicates, lancelets and craniates indicates that the origin of craniates involved the development of a new muscular pharyngeal pump, which was a key innovation underlying the evolution of a more metabolically active group of chordates. This innovation involved the genesis of new embryonic tissues, neural crest and neurogenic placodes, whose derivatives formed skeletal elements of the new pump as well as new receptors advantageous to the more mobile craniates. These changes also involved the evolution of a more complex brain by elaboration and reorganization of a lancelet-like cephalic neural tube. All of these events appear to be linked to a number of homeobox genes that were duplicated in the ancestral chordates leading to craniates. An outgroup analysis of the life histories of lancelets, hagfishes and lampreys suggests that hagfishes and lampreys have life histories that are substantially derived in comparison to that of ancestral craniates and that the highly derived features of the brain of hagfishes evolved in conjunction with their invasion of a bathyal benthic environment.

Anatomy, Comparative↗
PubMed1991

Evolution of technetium-99m-HMPAO SPECT and brain mapping in a patient presenting with echolalia and palilalia.

A 78-yr-old woman presented with transient echolalia and palilalia. She had suffered from Parkinson's disease for 2 yr. Routine laboratory examination showed hypotonic hyponatremia, but was otherwise unremarkable. Brain mapping revealed a bifrontal delta focus, more pronounced on the right. Single photon emission computed tomography (SPECT) of the brain with technetium-99m labeled d,l hexamethylpropylene-amine oxime (99mTc-HMPAO), performed during the acute episode showed relative frontoparietal hypoactivity. Brain mapping performed after disappearance of the echolalia and palilalia, which persisted only for 1 day, was normal. By contrast, SPECT findings persisted for more than 3 wk. Features of particular interest in the presented patient are the extensive defects seen on brain SPECT despite the absence of morphologic lesions, the congruent electrophysiologic changes and their temporal relationship with the clinical evolution.

Aged↗
PubMed2006

Costs of encephalization: the energy trade-off hypothesis tested on birds.

Costs and benefits of encephalization are a major topic of debate in the study of primate and human evolution. Comparative studies provide an opportunity to test the validity of a hypothesis as a general principle, rather than it being a special case in primate or hominid evolution. If a population evolves a larger brain, the metabolic costs of doing so must be paid for by either an increased energy turnover (direct metabolic constraint) or by a trade-off with other energetically expensive costs of body maintenance, locomotion, or reproduction, here referred to as the energy trade-off hypothesis, an extension of the influential Expensive Tissue Hypothesis of Aiello and Wheeler (1995, Curr. Anthropol. 36, 199-221). In the present paper, we tested these hypotheses on birds using raw species values, family means, and independent contrasts analysis to account for phylogenetic influences. First, we tested whether basal metabolic rates are correlated with brain mass or any other variable of interest. This not being the case, we examined various trade-offs between brain mass and the mass of other expensive tissues such as gut mass, which is approximated by gut length or diet quality. Only weak support was found for this original Expensive Tissue Hypothesis in birds. However, other energy allocations such as locomotor mode and reproductive strategy may also be reduced to shunt energy to an enlarged brain. We found a significantly negative correlation between brain mass and pectoral muscle mass, which averages 18% of body mass in birds and is indicative of their relative costs of flight. Reproductive costs, on the other hand, are positively correlated with brain mass in birds. An increase in brain mass may allow birds to devote more energy to reproduction, although not through an increase in their own energy budget as in mammals, but through direct provisioning of their offspring. The trade-off between locomotor costs and brain mass in birds lets us conclude that an analogous effect could have played a role in the evolution of a larger brain in human evolution.

Animals↗
PubMed1982

Brain abscess and its surgical management.

A series of 56 patients with brain abscesses who were treated over a period of 23 years is reviewed. Patients with posttraumatic infections were not included. The operative mortality was 11%. Aspiration of purulent material, radical excision of the abscess, drainage of pus, or a combination of these procedures was used according to the patient's condition and the location of the abscess. The relatively low mortality may be related to the preoperative condition of these patients, who were operated upon in the subacute or chronic stage of their disease. Conservative surgery, especially when functionally important parts of the brain are involved, helps to keep the postoperative neurological deficit as low as possible. Computerized tomography is of primary importance in localizing, diagnosing, and following the evolution of a brain abscess.

Brain Abscess↗
PubMed2006

Aspm specifically maintains symmetric proliferative divisions of neuroepithelial cells.

The ASPM (abnormal spindle-like microcephaly-associated) protein has previously been implicated in the determination of human cerebral cortical size, but the cell biological basis of this regulation has not been studied. Here we investigate the role of Aspm in mouse embryonic neuroepithelial (NE) cells, the primary stem and progenitor cells of the mammalian brain. Aspm was found to be concentrated at mitotic spindle poles of NE cells and to be down-regulated with their switch from proliferative to neurogenic divisions. Upon RNA interference in telencephalic NE cells, Aspm mRNA is reduced, mitotic spindle poles lack Aspm protein, and the cleavage plane of NE cells is less frequently oriented perpendicular to the ventricular surface of the neuroepithelium. The alteration in the cleavage plane orientation of NE cells increases the probability that these highly polarized cells undergo asymmetric division, i.e., that apical plasma membrane is inherited by only one of the daughter cells. Concomitant with the resulting increase in abventricular cells in the ventricular zone, a larger proportion of NE cell progeny is found in the neuronal layer, implying a reduction in the number of NE progenitor cells upon Aspm knock-down relative to control. Our results demonstrate that Aspm is crucial for maintaining a cleavage plane orientation that allows symmetric, proliferative divisions of NE cells during brain development. These data provide a cell biological explanation of the primary microcephaly observed in humans with mutations in ASPM, which also has implications for the evolution of mammalian brains.

Animals↗
PubMedDate not supplied

Alzheimer's disease as a loss of differentiation control in a subset of neurons that retain immature features in the adult brain.

Degeneration in AD primarily occurs in a subset of neurons that in the adult brain retain a high degree of structural plasticity and in these neurons is associated with the activation of mitogenic pathways and a cell cycle re-entry. Brain areas affected by AD pathology are those structures involved in the regulation of "higher brain functions" that become increasingly predominant as the evolutionary process of encephalization progresses, such as hippocampus, neocortical association areas and the cholinergic basal forebrain neurons. The functions these areas subserve such as learning, memory, perception, self-awareness, and consciousness require a life-long re-fitting of synaptic contacts that allows for the acquisition of new epigenetic information. This adaptive reorganization of neuronal connectivity in the mature brain is based upon the strengthening of existing synapses, the formation of new synapses and the destabilization of previously established synaptic contacts. With the increasing need during evolution to organize brain structures of increasing complexity, these processes of dynamic stabilization and de-stabilization become more and more important but might also provide the basis for an increasing rate of failure. A hypothesis is proposed that it is the 'labile state of differentiation' (G0-arrest) of a subset of neurons in the adult brain that allows for ongoing morphoregulatory processes after development is completed but at the same time renders these neurons particularly vulnerable. The delicate balance between G0-arrest and G1-entry might be prone to a variety of potential disturbances during the lifetime of an individual. Morphodysregulation in AD, accompanied by an activation of intracellular mitogenic signaling might, thus, be a slowly progressing dysfunction that eventually overrides the differentiation control and results in dedifferentiation, a condition in conflict with the otherwise 'mature' background of the nervous system. Cell-cycle and differentiation control might thus provide the link between structural brain self-organization and neurodegeneration that both are unique to human.

Adult↗
PubMed1999

MR line-scan diffusion-weighted imaging of term neonates with perinatal brain ischemia.

BACKGROUND AND PURPOSE: MR diffusion-weighted imaging provides early demonstration of neonatal brain infarction. The evolution and limitations of diffusion-weighted imaging findings in newborns, however, have not been evaluated. Using line-scan diffusion imaging (LSDI), we investigated perinatal ischemic brain injury. METHODS: Nineteen term newborns (age, 9 hours to 8 days; mean age, 2.6 days) with perinatal brain ischemia were evaluated using LSDI (1520/62.5/1 [TR/TE/excitations]) (b maximum = 750 s/mm2) and T1- and T2-weighted spin-echo (conventional) MR imaging. Follow-up examinations were performed in seven patients and autopsy in one. Apparent diffusion coefficients (ADCs) were measured in deep gray matter, white matter, the cortex, and focal lesions. RESULTS: Based on conventional MR imaging or pathologic findings, patients were divided into two groups. Group 1 (n = 12) had symmetric/diffuse injury consistent with global hypoperfusion. Group 2 (n = 7) had focal/multifocal injury suggesting cerebrovascular occlusion. ADCs were abnormal at initial examination in 10 newborns in group 1 and in all newborns in group 2. The results of LSDI were abnormal before conventional MR imaging was performed in three newborns in group 1. ADCs were maximally decreased between days 1 and 3 in deep gray matter, perirolandic white matter, and focal lesions. Delayed decreases in ADCs were observed in subcortical white matter from days 4 through 10 in three patients in group 1. CONCLUSION: After global hypoperfusion, LSDI showed deep gray matter and perirolandic white matter lesions before conventional MR imaging. LSDI may underestimate the extent of injury, however, possibly because of variations in the compartmentalization of edema, selective vulnerability, and delayed cell death. Differences in LSDI of symmetric/diffuse and focal/multifocal lesions may reflect differences in pathophysiology or timing of the injury. These findings may have implications for acute interventions.

Asphyxia Neonatorum↗
PubMed1993

Temporal evolution of NMDA-induced excitoxicity in the neonatal rat brain measured with 1H nuclear magnetic resonance imaging.

The aim of this study is to characterize the evolution of excitotoxic damage in neonatal rat brain by diffusion-weighted and T2-weighted magnetic resonance imaging. Results are compared with histological findings. Magnetic resonance imaging was performed at various times (15 min, 24 h, 3 days and 5 days) after intrastriatal microinjection of N-methyl-D-aspartate (NMDA) at postnatal day 8. The transverse relaxation time (T2) and apparent diffusion coefficient of water were determined. The results show an acute reduction of the apparent diffusion coefficient, reflected by an ipsilateral hyperintensity in the diffusion-weighted images, within 15 min after intrastriatal NMDA injection. At this time no changes in the T2-weighted images were apparent. The volume of the hyperintensity was relatively large with a radius of approximately 2 mm and coincided with histological signs of pronounced karyo-dendritic swelling. Subcutaneous administration of MK-801 25 min after the intracerebral NMDA injection readily reversed the hyperintensity and resulted in complete protection as verified by histology. Areas with increased T2 values were observed 1 day after NMDA microinjection and corresponded to regions with obvious cell necrosis. Five days after NMDA injection the lesion was evident using both diffusion- and T2-weighted images and coincided with an overt lesion comprising areas of cell loss and dilatation of the ipsilateral ventricle. In conclusion, this study illustrates the possibility of using diffusion-weighted imaging as a tool to monitor efficacy of treatment strategies at an early stage of excitotoxic injury.

Animals↗
PubMed1987

Focal protein synthesis inhibition in a model of neonatal hypoxic-ischemic brain injury.

Cerebral hypoxia-ischemia was produced in 1-week-old rats by exposing them to 8% O2-92% N2 commencing 4 to 6 h after unilateral carotid artery ligation. Protein synthesis rates were measured in cerebral cortex, caudate-putamen, thalamus, and lateral septal nuclei during 2 h of hypoxia and at three times (15 min, 10 h, and 18 h) after a 3.5-h hypoxic exposure. Protein synthesis was inhibited in the ipsilateral but not contralateral forebrain during the brief hypoxic exposure, and in both hemispheres during early recovery after a 3.5 h exposure, which was sufficient to produce brain injury in the ipsilateral hemisphere. At 10 h after hypoxia, protein synthesis rates in the contralateral forebrain had recovered to control values, but in vulnerable structures of the ipsilateral forebrain, recovery of protein synthesis was transient and incomplete (cerebral cortex) or remained at the low values found immediately after hypoxia (caudate-putamen). The early development of abnormal patterns of protein synthesis in vulnerable brain regions during hypoxia and its persistence in some rats during recovery when irreversible cell injury becomes manifest suggests a possible role for abnormal protein metabolism in the evolution of irreversible brain cell damage.

Animals↗
PubMed2006

Differential modulation of estrogen receptors (ERs) in ischemic brain injury: a role for ERalpha in estradiol-mediated protection against delayed cell death.

Estradiol enhances plasticity and survival of the injured brain. Our previous work demonstrates that physiological levels of estradiol protect against cerebral ischemia in the young and aging brain through actions involving estrogen receptors (ERs) and alterations in gene expression. The major goal of this study was to establish mechanisms of neuroprotective actions induced by low levels of estradiol. We first examined effects of estradiol on the time-dependent evolution of ischemic brain injury. Because estradiol is known to influence apoptosis, we hypothesized that it acts to decrease the delayed phase of cell death observed after middle cerebral artery occlusion (MCAO). Furthermore, because ERs are pivotal to neuroprotection, we examined the temporal expression profiles of both ER subtypes, ERalpha and ERbeta, after MCAO and delineated potential roles for each receptor in estradiol-mediated neuroprotection. We quantified cell death in brains at various times after MCAO and analyzed ER expression by RT-PCR, in situ hybridization, and immunohistochemistry. We found that during the first 24 h, the mechanisms of estradiol-induced neuroprotection after MCAO are limited to attenuation of delayed cell death and do not influence immediate cell death. Furthermore, we discovered that ERs exhibit distinctly divergent profiles of expression over the evolution of injury, with ERalpha induction occurring early and ERbeta modulation occurring later. Finally, we provide evidence for a new and functional role for ERalpha in estradiol-mediated protection of the injured brain. These findings indicate that physiological levels of estradiol protect against delayed cell death after stroke-like injury through mechanisms requiring ERalpha.

Animals↗
PubMed1992

Distribution of tyrosine hydroxylase, serotonin, and leu-enkephalin immunoreactive cells in the brainstem of a shark, Squalus acanthias.

The central nervous system location of neurochemicals that are widely distributed among extant animals may give us clues to changes that occurred in the brains of these animals during evolution. We have been studying the brains of cartilaginous fishes, a heterogeneous group whose central nervous system varies considerably. Squalus acanthias, the spiny dogfish shark, was chosen to represent the squalomorphs, a group of living sharks known to possess many primitive characters. The distribution of tyrosine hydroxylase (TH+), serotonin (5-HT+), and leu-enkephalin (LENK+) positive cells within the brainstem of Squalus was determined by use of antibodies to these substances. All the major raphe groups described for mammals were found in Squalus. The 5-HT+ cells in raphe nuclei were more uniformly distributed in Squalus than in Heterodontus, the horn shark. Other nuclei that were 5-HT+ and LENK+, and that have been identified in mammals, included reticularis paragigantocellularis lateralis, a B9 cell group, and reticularis magnocellularis. The postcommissural nucleus and pretectal area contained 5-HT+ and LENK+ cells. These cells have been described in a holocephalian, in teleosts, and in reptiles but not in other elasmobranchs or in mammals. Cells that were TH+ were located in prominent A1/A2, A6 (locus coeruleus), A9 (substantia nigra), and A10 (ventral tegmental area) cell groups, and in a very small A5 group. We conclude that the variation in chondrichthian brainstems exceeds that in mammals, and we suggest that this variation is related to life-style and the long evolutionary history of these fishes.

Animals↗