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PubMed2006

Seizure outcome after surgery for epilepsy due to focal cortical dysplastic lesions.

Neocortical development is a highly complex process encompassing cellular proliferation, neuronal migration and cortical organization. At any time this process can be interrupted or modified by genetic or acquired factors causing malformations of cortical development (MCD). Epileptic seizures are the most common type of clinical manifestation, besides developmental delay and focal neurological deficits. Seizures due to MCD are frequently pharmacoresistant, especially those associated to focal cortical dysplasia (FCD). Surgical therapy results have been reported since 1971, however, currently available data from surgical series are still limited, mainly due to small number of patients, distinct selection of candidates and surgical strategies, variable pathological diagnosis and inadequate follow-up. This study addresses the possibilities of seizure relief following resection of focal cortical dysplasia, and the impact of presurgical evaluation, extent of resection and pathological findings on surgical outcome. We included 41 patients, 22 adults and 19 children and adolescents, with medically intractable seizures operated on from 1996 to 2002. All were submitted to standardized presurgical evaluation including high-resolution MRI, Video-EEG monitoring and ictal SPECT. Post-surgical seizure outcome was classified according to Engel's schema. Univariate and multivariate analysis were performed. Fifteen patients had temporal and 26 extratemporal epilepsies. Of the total 26 patients (63.4%) reached seizure-free status post-operatively. There was no correlation between outcome and age at surgery, duration of epilepsy, frequency of seizures, and pathological findings. There was, however, a clear correlation with topography of FCD (temporal versus extratemporal) and regional ictal EEG onset, on univariate as well as multivariate analysis.

Adolescent↗
PubMedDate not supplied

The role of cortical geometry in the nuclear development of Tetrahymena thermophila.

Vegetative cells were subjected to electrofusion and the resulting heteropolar doublets were then mated to normal single cells and followed throughout conjugation using cytological and genetic techniques. The unique cyto-geometry created in a heteropolar doublet--a continuous cytoplasmic compartment bounded by two anterior poles and sharing a fused posterior pole at midbody, and the potential for two conjugal exchange junctions--resulted in instructive perturbations of nuclear behavior. Our results indicate that the course of nuclear development is strongly dependent on the cortical geometry of conjugating cells. Specifically, 1) continuation of development after meiosis requires an established conjugal junction; 2) after pronuclear exchange, pronuclei are subjected to attractive forces; and 3) products of the second postzygotic division are actively positioned near the posterior region of the cell cortex where they develop into micronuclei.

Animals↗
PubMedDate not supplied

Glutamate-like immunoreactivity and fate of Cajal-Retzius cells in the murine cortex as identified with calretinin antibody.

Cortical layers VI to II develop between two layers of older neurons, the marginal and subplate zones, which are believed to have unique roles in cortical development. While subplate cells have been found essential for the establishment of thalamocortical relationships, the function of the marginal zone and in particular of the neurons of Cajal-Retzius has not been elucidated. Here we show that an antibody against the calcium-binding protein calretinin labels the population of Cajal-Retzius cells throughout their life in the murine cerebral cortex. In prenatal and early postnatal stages, Cajal-Retzius cells were found evenly distributed throughout the murine cerebral cortex. Cajal-Retzius-like neurons were also found in the developing hippocampus and dentate gyrus, which indicates that they may have a general function in cortical development. From P8 onward Cajal-Retzius cells disappeared from the neocortex and hippocampus, at the same time as degenerating immunoreactive neurons were observed. Calretinin-positive Cajal-Retzius cells were glutamate immunoreactive and their presumed axon terminals formed asymmetric synapses. These observations indicate that Cajal-Retzius cells may provide a tonic excitatory input, essential for the maturation of cortical neurons. Furthermore, since neuronal migration has been shown to be dependent on glutamate receptors, we propose that Cajal-Retzius cells releasing glutamate may direct migrating neuroblasts toward the marginal lamina, therefore creating the "inside-out" sequence of cortical development.

Animals↗
PubMed1983

Correlation of brain glucose utilization and cortical electrical activity during development of brain oxygen toxicity.

Central nervous system (CNS) oxygen toxicity in rats is characterized by the appearance of alterations in electrical cortical activity (ECoG), followed by the appearance of paroxysmal electrical discharges and finally the onset of clinical convulsions. The correlation between the changes in ECoG and the regional cerebral metabolic rate for glucose (rCMRgl) during progressive oxygen toxicity was studied. Cortical electrodes for ECoG recording and venal arterial cannula for autoradiographic measurement of rCMRgl were chronically implanted. Using [14C]2-deoxyglucose (2-DG), the rCMRgl was measured in conscious unrestrained rats during different periods of exposure to 5 atmospheres absolute oxygen as well as an equivalent normoxic high pressure, while ECoG was continuously recorded and analyzed. A statistically significant increase in rCMRgl in 13 out of 24 investigated brain structures was found during the pre-paroxysmal electrical discharge period. This increase was accompanied by an elevation in slow and a reduction in fast ECoG frequency bands. The largest increase in rCMRgl was found in cerebellar and cerebral cortices, limbic, auditory and visual structures. Following the appearance of the first paroxysmal electrical discharge (FED) some limbic structures and cerebellar cortex showed further increases in rCMRgl, while several auditory and visual structures exhibited a significant decrease. Five atmospheres normoxic pressure had no effect on rCMRgl in any of the brain structures examined. It is concluded that pre-paroxysmal electrical discharge ECoG changes and the onset of the FED during progressive oxygen toxicity are not due to inhibition of brain energy metabolism. The possible mechanisms leading to alterations in rCMRgl during hyperbaric oxygenation are discussed.

Animals↗
PubMed1998

The role of the first postmitotic cortical cells in the development of thalamocortical innervation in the reeler mouse.

In the mutant mouse reeler, the tangential distribution of thalamocortical fibers is essentially normal, even though neurons of the cortical plate accumulate below the entire early-born preplate population (Caviness et al., 1998). This seems incompatible with the hypothesis that cells of the subplate (the lower component of the preplate in normal mammals) form an axonal scaffold that guides thalamic fibers and act as temporary targets for them (Blakemore and Molnár, 1990, Shatz et al., 1990). We used carbocyanine dyes to trace projections in wild-type and reeler mice between embryonic day 13 and postnatal day 3. Preplate formation and early extension of corticofugal fibers to form a topographic array are indistinguishable in the two phenotypes. So too are the emergence of thalamic axons in topographic order through the primitive internal capsule, their meeting with preplate axons, and their distribution over the preplate scaffold. Distinctive differences appear after the cortical plate begins to accumulate below the preplate of reeler, causing the preplate axons to form oblique fascicles, running through the cortical plate. Thalamic axons then pass through the plate within the same fascicles and accumulate in the "superplate" layer for approximately 2-3 d, before defasciculating and plunging down to terminate deep in the cortical plate, creating the curious "looping" pattern seen in the adult. Thus, thalamocortical innervation in reeler follows the same algorithm of development but in relation to the misplaced population of early-born neurons. Far from challenging the theory that preplate fibers guide thalamic axons, reeler provides strong evidence for it.

Animals↗
PubMed1996

Nitric oxide in cortical map formation.

We analyse the possible role of nitric oxide in the early development of cortical maps. A mathematical analysis shows that with the aid of the diffusing messenger NO, cortical maps can develop without the need for lateral-inhibitory interactions. We derive that the maps that NO can set up depend on the stimulus environment in a way that is similar to lateral-inhibitory models of map formation but that they also have properties that depend specifically on the parameters of the diffusion process. These dependencies have not before been extracted and can be used to test the involvement of NO in cortical map formation.

Brain Mapping↗
PubMed1984

Amelioration of ischaemic cerebral oedema by a free radical scavenger, AVS: 1,2-bis(nicotinamido)-propane. An experimental study using a regional ischaemia model in cats.

The effect of a free radical scavenger, AVS: 1,2-bis(nicotinamido)-propane, on the blood flow, oedema, and energy metabolites in the cortical area rendered ischaemic by the occlusion of the middle and the internal cerebral arteries was studied using cats. The development of cortical oedema was assessed by the changes in the specific gravity as well as the water and electrolyte contents of the cortical samples obtained 4 h after the arterial occlusion. Compared to the control group receiving saline, the AVS group exhibited a significant amelioration of cortical oedema, whereas no effect of AVS on the cortical blood flow was observed. The decrease of the energy charge and the increase of lactate in the ischaemic cortical area were less pronounced in the AVS groups. These data indicate that AVS possesses an action to mitigate the development of cortical oedema following regional ischaemia. The possible mechanism of action of AVS is discussed in reference to the free radical hypothesis.

Animals↗
PubMed1975

[Postnatal development of Rattus norvegicus B. cortical neurons and the influence of trauma].

The differentiation of the pyramid neurons during ontogenesis and the effects of a trauma on the process of neuron differentiation and synaptogenesis were investigated in the rat cerebral cortex after Golgi-impregnation. 1. There are temporal differences in the differentiation of the processes of cortical neurons. Axons differentiate earlier than dendrites, apical dendrites earlier than basal ones. 2. Varicosities in the processes of cortical neurons during the early postnatal period are regarded as a feature of growth processes. 3. The appearance of the dendritic spines is an important process in the ontogenetic and phylogenetic development of cortical neurons. 4. The different cortical layers show a different degree of differentiation during development. The deeper layers precede the upper layers in the process of differentiation. 5. Ingrowing afferents have an essential influence on the differentiation - especially on the differentiation of the dendritic postsynaptic structures. 6. The cortex of 6 month old rats shows no principle differences in comparison with 24 days old animals. It is concluded that the visible differentiation processes of cortical neurons are nearly finished 24 days post partum. 7. As an effect of the trauma a considerable loss of dendritic spines of layer III and V pyramid cells is found in addition to general degeneration features. 8. The following factors are thought to be responsible for the loss of spines: (i) transneuronal processes with spine degeneration and subsequent phagocytosis of the synaptosome. (ii) destruction of differentiation furthering afferents results in differentiation defects of the neuron with the failure of further postsynaptic differentiation (spines).

Animals↗
PubMed1994

Development pattern of the GABAA-benzodiazepine receptor ionophore complex in primary cultures of cortical neurons.

The development pattern of the GABAA/benzodiazepine (BZ) receptor ionophore complex was characterized in mammalian cortical cultured neurons utilizing radioligand binding and GABA-induced 36Cl-influx. The specific binding of [3H]flunitrazepam, [3H]Ro15-1788 and [3H]Ro15-4513 increased with time from day 3 to day 21. The EC50 value and Emax of the GABA, muscimol and pentobarbital to enhance [3H]-flunitrazepam binding did not change during the development. Furthermore, GABA-induced 36Cl- influx also did not change during development from day 3 to day 21. However, the potency of ligands that bind to type-1 BZ receptors (alprazolam, zolpidem and C1218,872) to inhibit [3H]flunitrazepam binding increased from day 7 to day 21. Taken together, these data suggest the presence of type-II BZ receptors in early stages of the development which appears to change to type-I BZ receptors with age in the cortical neurons in culture.

Affinity Labels↗
PubMed2006

Cortical ventricular zone progenitors and their progeny maintain spatial relationships and radial patterning during preplate development indicating an early protomap.

The graded expression of transcription factors by progenitors in the ventricular zone (VZ) confers positional or area identity that is inherited by subplate (SP) neurons and governs their expression of guidance molecules for thalamocortical axons and other properties required for cortical area specification. This mechanism would be most efficient if VZ progenitors and their SP neuronal progeny maintain neighbor relationships during the generation of the preplate (PP), the precursor of the SP. Therefore, a major goal of this study is to determine whether progenitors in the cortical VZ and their progeny maintain neighbor relationships during the genesis of the neocortical PP. We used time-lapse video microscopy to follow the movements of VZ progenitors and the radial movement of their progeny and distribution in the PP in whole-mount or slice cortical explants from embryonic rats at stages when PP neurons are generated. We show that labeled VZ cells proliferate and have a strong tendency to retain neighbor relationships within the VZ and that their neuronal progeny move superficially along a radial column to form the overlying PP; during this process, their neuronal progeny also retain neighbor relationships and thereby form the PP in spatial register with the VZ progenitors that generate them. This behavior differs from that reported at later stages of cortical development, when cortical plate (CP) neurons are generated, and considerable dispersion is evident among both cells within the VZ and neuronal progeny as they migrate from the VZ to the CP. However, our findings show that at the early stage of cortical development, when PP/SP neurons are generated, the VZ is, at a cellular level, a "protomap" of the PP/SP.

Animals↗
PubMed2003

ERK5 activation of MEF2-mediated gene expression plays a critical role in BDNF-promoted survival of developing but not mature cortical neurons.

Extracellular signal-regulated kinase 5 (ERK5) is a member of the mitogen-activated protein kinase family whose biological function in the CNS has not been defined. In contrast to ERK1 and ERK2, which are activated by neurotrophins (NTs), cAMP, and neuronal activity in cortical neurons, ERK5 is activated only by NTs. Here, we report that ERK5 expression is high in the brain during early embryonic development but declines as the brain matures to almost undetectable levels by postnatal day (P) 49. Interestingly, expression of a dominant-negative ERK5 blocked brain-derived neurotrophic factor protection against trophic withdrawal in primary cortical neurons cultured from embryonic day (E) 17 but not P0. Furthermore, expression of a dominant-negative ERK5 induced apoptosis in E17 but not P0 cortical neurons maintained in the presence of serum. We also present evidence that ERK5 protection of E17 cortical neurons may be mediated through myocyte enhancer factor 2-induced gene expression. These data suggest that ERK5 activation of myocyte enhancer factor 2-induced gene expression may play an important and novel role in the development of the CNS by mediating NT-promoted survival of embryonic neurons.

Animals↗
PubMed1995

Seizures associated with stroke in childhood.

Seventy-three consecutive children younger than 17 years of age seen from 1978 to 1992 with acute hemiplegia from stroke, were retrospectively reviewed to evaluate the incidence of seizures and the risks of recurrent seizures after stroke. The population consisted of 56 children with cerebral infarction, 12 with intracranial hemorrhage, and 5 with transient ischemic attack. Children whose strokes occurred in the neonatal period and those secondary to trauma, malignancy, or infection were excluded. Mean follow-up time was 43.5 months (range: 12-156 months). At least 1 seizure occurred in 36 patients (49.3%) and recurrent seizures occurred in 21 patients (28.8%). Recurrent seizures developed more often among patients who had initial seizures with delayed onset (P < .05). In 56 patients with cerebral infarction, 16 of 31 patients (51.6%) with cortical involvement documented by neuroradiologic studies and 1 of 25 patients (4%) without cortical involvement developed recurrent seizures (P < .01). In 12 patients with intracranial hemorrhage, 3 of 10 patients with cortical involvement and none of 2 patients without cortical involvement developed recurrent seizures. It is concluded that seizures commonly occur in childhood stroke. Risk factors for recurrent seizures include later onset of initial seizures and presence of cortical involvement.

Adolescent↗
PubMed1982

The processing of speech sounds in a patient with cortical auditory disorder.

A 56-yr old woman developed a cortical auditory disorder after two successive strokes involving the temporal lobes. Dichotic listening tests did not show a left car advantage with right ear suppression, as shown in other cases with similar disorders. Tasks exploring phonological analysis showed an impairment limited to the stop consonants. Within this framework, processing of feature place was selectively disturbed, while voicing was normally analysed. The possible role of psychoacoustic deficits in the pathogenesis of cortical auditory disorders is discussed. Some general considerations on cortical auditory disorders are also made.

Auditory Cortex↗
PubMedDate not supplied

Concurrent generation of subplate and cortical plate neurons in developing trisomy 16 mouse cortex.

During embryonic development of the mammalian cerebral cortex, the generation of the marginal zone (MZ) and subplate (SP) precedes that of the cortical plate (CP). MZ and SP neurons are believed to play a 'pioneering' role in directing the organization of the CP and the specificity of connections between the CP and other brain regions. Here we report that this sequential order of neurogenesis is disrupted in the trisomy 16 (Ts16) mouse, a potential animal model of Down syndrome. Bromodeoxyuridine labeling was used to establish the date of generation of postmitotic SP and CP neurons in the somatosensory cortex. As has been previously reported, most SP neurons in euploid (control) cortex were generated on embryonic day 12.5 (E12.5), and production of CP neurons began a day later. In contrast, in the Ts16 cortex, few SP neurons were born on E12.5 and most were generated on E13.5 and E14.5 when CP neurons were also being produced. Thus, in the Ts16 cortex, many CP neurons are born and arrive at their destinations before the normal complement of SP neurons is present. This disruption of the temporal sequence of SP and CP generation may, therefore, interfere with the pioneering functions of the SP during cortical neurogenesis and may alter the connectivity of the cortex. Indeed, using lipophilic membrane tracers to label axonal projections, we found very little thalamocortical innervation of the Ts16 SP at an age when there is extensive innervation of the euploid SP.

Animals↗
PubMed1980

[Use of gentamycin and furosemide in acute pyelonephritis (an experimental morphological study)].

The favourable effect of gentamicin and its combination with furosemid was shown in treatment of rats with experimental pyelonephritis. However, alongside the favourable effect, a danger of the gentamicin nephrotoxic effect, especially in combination with furosemid was noted. The nephrotoxic effect was evident from foci of distrophic and necrobiotic changes in the epithelium of the convoluted tubules, impairment of the cortical hemodynamics and development of the cortical hypoxia of the kidneys resulting in severe renal insufficiency. Gentamicin had no direct inhibitory effect on the tissue respiration, did not block the oxygen uptake and oxidative phosphorilation in isolated mitochondria. To prevent the development of the nephrotoxic effect of gentamicin and its combination with furosemid strict and effective control of the antibiotic plasma levels is necessary. Informative tests for the control of the renal function are the concentration parameters of creatinine and urea, especially at the beginning of the pathological state when the level of hyperazotemia is still of a low informative value. The diurnal urine excretion is not an important informative index of renal function.

Acute Disease↗
PubMed1998

Modification of parallel activity elicited by propagating bursts in developing networks of rat cortical neurones.

Networks of cultured cortical neurones exhibit regular, synchronized, propagating bursts which are synaptically mediated, and which are hypothesized to play a part in activity-dependent formation of connections during development in vivo. The relationship between the strength of synaptic connections and the characteristics of synchronized propagating bursting, however, is unclear. Modification of synchronized activity in cortical cultures in response to electrical stimulation was examined using multisite electrode array recording. By measuring the response of the network to weak, localized, test stimulation (TS), we observed a potentiation of activity following a relatively stronger inducing stimulation (IS). This potentiation was evident as an increased probability of eliciting bursts by TS, an increased frequency of spontaneous bursts and number of spikes per burst, and increased speed of burst propagation, and it lasted for at least 20 min. Changing the parameters of IS revealed that high frequency tetanic stimulation is not necessary to induce potentiation, while it is essential for IS to produce a regeneratively propagating burst. The results provide a direct demonstration of modification of both the spatial and temporal characteristics of synchronized network activity, and suggest an important physiological role for propagating synchronized bursting, as a mechanism for inducing plastic modifications in the developing cortex.

Animals↗
PubMed1994

The effects of epileptic cortical activity on the development of callosal projections.

The effect of epileptic neural activity on the postnatal development of the corpus callosum was studied. Epileptiform activity was induced in the visual cortex of postnatal rabbits by continuous infusion of penicillin. Callosal projections of the occipital cortex were studied in rabbits aged at least 4 weeks. In these penicillin-exposed rabbits, the visual callosal projections extended through most of area 17 in a projection pattern characteristic of neonatal rabbits, rather than being restricted to a narrow callosal zone at the lateral border of area 17, as they usually are by this age. The results indicate that epileptic cortical activity stabilizes immature callosal projections which are normally eliminated during development. The maintenance of such immature and non-specific projections in the mature CNS may interfere with normal cortical functions and could underlie the cognitive deficits which have been observed following childhood epilepsy.

Animals↗