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At least 559 records · Page 31Linked to original sources
PubMed1996

Frontal cortex leads other brain structures in generalised spike-and-wave spindles and seizure spikes induced by picrotoxin.

Generaliszed spike-and-wave (SW) spindles (5-7 Hz) associated with myoclonic jerks precede the occurrence of regular spikes (2-3 Hz) associated with convulsive seizure induced by picrotoxin. SW spindles occur spontaneously in rodent and cat under some experimental conditions and are considered to be models of human generalised epilepsy. These spindles have been proposed as being led by a thalamic pacemaker. To examine this possibility in picrotoxin-induced SW spindles and seizure spikes, we recorded EEG using chronically implant unipolar electrodes during intravenous picrotoxin infusion in freely behaving rat. The 6 EEG signals were digitally sampled at 1000 Hz. Linear correlation, spectral, coherence and phase analyses were undertaken to determine time differences (TDs) between EEG channels and the brain structure leading seizure activity. One frontal cortex led all other structures during SW spindles. TD between SW spindles in the leading frontal cortex (Fr1) and the contralateral Fr1 was 3.6 + / - 0.5 msec. All ipsilateral structures (hippocampus, thalamus, amygdala, caudate nucleus and occipital cortex) were delayed by more than 3 msec from Fr1 (intralaminar thalamic nuclei - by 6.3 + / - 0.9 msec). TDs of SW spindles between subcortical regions were less than 1.5 msec. Similar relationships with slightly smaller TDs were found with spikes during convulsive seizure except TDs between frontal cortices did not significantly differ from zero. We suggest that seizure activity induced by picrotoxin is led by one Fr1 during SW spindles and by both frontal cortices working as one system during convulsive seizure.

Animals↗
PubMed1995

Brain processing of stimulus deviance during slow-wave and paradoxical sleep: a study of human auditory evoked responses using the oddball paradigm.

Auditory evoked potentials (AEPs) to frequent (90%) and deviant (10%) tones were recorded during both wakefulness and all-night sleep in eight drug-free volunteers. During presleep waking (10:00-11:00 p.m.), deviant stimuli elicited, in all subjects, a prominent "P300" wave of parieto-central topography, culminating at 344 ms (average), which was absent in response to frequent tones. This "presleep P300" was delayed and reduced relative to values obtained during full wakefulness (3:00-7:00 p.m.) in a control group. Passage from waking to sleep stage I was characterized by a progressive attenuation and delay of the P300 wave in response to deviant stimuli, without major changes in AEP morphology as compared to the waking state. Thus, in terms of cognitive evoked potentials (EPs), sleep stage I appeared more as a "weak" state of wakefulness than a true phase of sleep. During sleep stages II, III, and IV, both frequent and deviant tones evoked AEPs that closely resembled K-complexes. Responses to rare stimuli were four-to-five times larger than those to frequent tones, this likely being the result of K-complex habituation to monotonous stimuli. During paradoxical sleep (PS), AEP morphology again became comparable to that of wakefulness. Notably, a "P3" wave with similar topography as the waking P300 appeared in response to deviant stimuli exclusively. Thus, even though the brain seems able to detect stimulus deviance during all sleep stages, only during stage I and PS were the electrophysiological counterparts of deviance detection comparable to those of the waking state. Our results support the view that PS is not a state of "sensory isolation"; failure to respond to external stimuli during this stage may depend upon mechanisms occurring only after the sensory input has undergone cognitive analysis.

Adult↗
PubMed2002

IP3-dependent calcium-induced calcium release mediates bidirectional calcium waves in neurones: functional implications for synaptic plasticity.

IP(3)-dependent calcium-induced calcium release (ICICR) is a general mechanism of calcium release that occurs in pyramidal neurones of hippocampus, the neocortex and in Purkinje cells of the cerebellar cortex. When ICICR is initiated synaptically in dendrites of neurones from brain slices, calcium waves can propagate bidirectionally to the soma and distal dendrites. ICICR relies on the coincidence of a calcium influx triggered by the backpropagation of action potentials and the activation of cholinergic, serotoninergic or glutamatergic metabotropic receptors. The involvement of IP(3) receptors (IP(3)R) in ICICR is clearly established. In contrast, ryanodine receptors (RyR) do not seem necessary for the triggering and propagation of calcium waves, but ICICR depends on calcium stores sensitive to ryanodine. Thus, the role of RyR remains to be established. ICICR provides a mechanism for global calcium signalling in neurones that may be involved in the reinforcement of Hebbian plasticity, heterosynaptic plasticity and cell death.

Animals↗
PubMed2003

Ictal stimulus processing during spike-wave discharges in genetic epileptic rats.

In the present experiment it was investigated whether and to what extent auditory information processing is possible during the presence of spike-wave discharges in rats. To that end, WAG/Rij rats which are an animal model for absence epilepsy, were provided with cortical electrodes for the registration of the electroencephalogram (EEG). The animals were first trained in an appetitively motivated conditioning paradigm to learn to discriminate between two auditory stimuli with equal duration and frequency but with different intensities. Next, the stimuli were presented in the test phase in pseudorandom order during spike-wave discharges. The reactivity of the ongoing EEG was analysed. It was found that the presentation of the reinforced stimulus induced a larger number of aborted spike-wave discharges than the non-reinforced stimulus, regardless of the intensity of the stimuli. This implies that during generalised spike-wave discharges the brain is still capable of evaluating the meaning of an ictally presented stimulus. It also shows that sensory, attentional and mnemonic processes are at least partially intact during the occurrence of a spike-wave discharge. The results of the present study are largely in agreement with results on human spike-wave activity-related cognitive disturbances. Moreover, they may lead to a refinement of the concept of epileptic consciousness and may emphasise the heuristic value of rodent models for studying both ictal and interictal information processing.

Acoustic Stimulation↗
PubMed1994

Permeability of the blood-brain barrier induced by 915 MHz electromagnetic radiation, continuous wave and modulated at 8, 16, 50, and 200 Hz.

Biological effects of electromagnetic fields (EMF) on the blood-brain barrier (BBB) can be studied in sensitive and specific models. In a previous investigation of the permeability of the blood-brain barrier after exposure to the various EMF-components of proton magnetic resonance imaging (MRI), we found that the exposure to MRI induced leakage of Evans Blue labeled proteins normally not passing the BBB of rats [Salford et al. (1992), in: Resonance Phenomena in Biology, Oxford University Press, pp. 87-91]. In the present investigation we exposed male and female Fischer 344 rats in a transverse electromagnetic transmission line chamber to microwaves of 915 MHz as continuous wave (CW) and pulse-modulated with repetition rates of 8, 16, 50, and 200 s-1. The specific energy absorption rate (SAR) varied between 0.016 and 5 W/kg. The rats were not anesthetized during the 2-hour exposure. All animals were sacrificed by perfusion-fixation of the brains under chloral hydrate anesthesia about 1 hour after the exposure. The brains were perfused with saline for 3-4 minutes, and thereafter fixed in 4% formaldehyde for 5-6 minutes. Central coronal sections of the brains were dehydrated and embedded in paraffin and sectioned at 5 microns. Albumin and fibrinogen were demonstrated immunohistochemically. The results show albumin leakage in 5 of 62 of the controls and in 56 of 184 of the animals exposed to 915 MHz microwaves. Continuous wave resulted in 14 positive findings of 35, which differ significantly from the controls (P = 0.002).(ABSTRACT TRUNCATED AT 250 WORDS)

Albumins↗
PubMed1979

[Monitoring of intracranial pression in acute neurotrauma by extra-dural screw (author's transl)].

These data emphasize the interest of the study, in acute traumatic comatose, of the brain-stem reflexes and level of coma (Plum, Posner, Perez-Dominguez, Barge, Espagno) and the monitoring of the intracranial pression (ICP) by extra-dural screw (Vries, de Rougemont, J. Brunon). It is possible to describe: 1)The bilateral hemispherical contusions: with cortico-subcortical level and bilateral decorticate comatose. The normal brain-stem reflexes (N.B.S.R.) are presents. The monitoring of ICP allows to separate the reversible bilateral hemispherical contusions (ICP can present unstable recording during 3 days with pressure-waves--B waves--or to be stable (between 10--15 mm Hg)), from the severe bilateral contusions with rostro-caudal evolution and "plateau-waves". 2) The brain-stem contusions: the clinical level is often a mesencephalic level with decerebrate rigidity and N.B.S.R. +/- (Automatic Eye Movements). In severe injury the ICP is increased and unstable with A waves. In reversible brain-stem contusions the ICP is often stable and low with arteriography and ventriculography insignificant. 3) The associated contusions: In general, the head injuries of this group are alternatively decorticate or on decerebrate rigidity ("ambiguous reaction"). In the severe associated contusions the ICP shows A waves. In reversible contusions ICP is stable with normal supratentorial angiogramm and ventriculography.

Brain Injuries↗
PubMed1988

Effect of electroconvulsive shock on the slow components of the brain stem auditory evoked potential.

The effects of electroconvulsive shock on the slow components of the brain stem auditory evoked potential were investigated in the rat during the ictal and the immediate postictal periods. Shock did not significantly alter any aspect of the slow positive-negative complex which underlies the high-frequency waves of the brain stem auditory evoked potential. However, a succeeding potential of probable cortical origin was markedly reduced in amplitude and its peak latency was temporarily increased.

Animals↗
PubMed1993

[Effect of MHS-G, an amino acids granule, on hepatic encephalopathy in portacaval anastomosis rats].

Using portacaval anastomosis (PCA) rats as a model with or without injection of ammonium acetate, we investigated the effects of MHS-G on the abnormalities of electroencephalogram (EEG) and brain amines metabolism in comparison with those of SF-1008C, a commercial nutritional preparation for hepatic failure. MHS-G (0.68 g/kg, p.o.) clearly improved both the abnormalities of EEG (such as reduction of amplitude, increasing delta wave distribution and decreasing beta wave distribution) and brain amines metabolism (such as increasing of Trp and DOPAC content) after injection of ammonium acetate. Moreover, MHS-G significantly increased branched chain amino acid concentrations and decreased aromatic amino acid concentrations in plasma and brain in comparison with water, and it significantly decreased the ammonia level in plasma in comparison with water and SF-1008C. These results suggest that MHS-G has a positive effect on abnormalities of EEG and amino acids metabolism in the plasma and brain of PCA rats.

Acetates↗
PubMed1987

Effects of audiometric configuration on the auditory brain stem response.

Evidence reported in the literature indicates that wave I of the auditory brain stem response is influenced by cochlear contributions from a more basal area of the cochlea than is wave V. This phenomenon is invoked to explain different latency-intensity function patterns of waves I and V and the I-V interval for four types of cochlear hearing loss. In high frequency hearing losses wave V is delayed at low intensities. Wave I tends to be delayed at all intensities and by a greater amount than wave V. The I-V interval is often reduced with the effect maximal at higher intensities. Low frequency hearing losses tend to cause early wave V latencies at low intensities. Wave I latencies are normal. The I-V interval is therefore reduced at lower intensities. Flat hearing losses produce normal latency-intensity functions. High frequency notched audiograms are almost always associated with delayed wave V but early wave I latencies. The I-V interval is therefore significantly prolonged with the effect maximal at low intensities. The variability of the I-V interval as a function of audiometric configuration indicates that it is not a pure measure of central conduction time.

Adult↗
PubMed1989

[Post-tetanic potentiation of the primary response and the late negative wave in the somatosensory area of the cat brain].

A single electrical stimulus applied to the thalamic VPL nucleus or to the subcortical white matter evoked a primary response in the cat g. sigmoideus posterior followed by delayed negative wave generated in the middle layers of the cortex and not reflected on its surface. The delayed negative wave seems to reflect mainly the excitation of stellate cells. Tetanization of the VPL nucleus or the white matter evoked a sharp and long-term (several hours) potentiation of the delayed negative wave. At the same time, the changes of the primary response were not so obvious. The effect of the posttetanic potentiation, therefore, seems to be more characteristic for stellate rather than for pyramidal cells, the former being the main generators of the primary response.

Animals↗
PubMed1998

Immunohistochemical indicators of early brain injury: an experimental study using the fluid-percussion model in cats.

To detect early changes in neurons and astrocytes by immunohistochemical methods using antibodies against the neuron-specific enolase (NSE), neurofilament, glial fibrillary acid protein (GFAP), and S-100 protein, a fluid-percussion injury model in cats was chosen, in which a severe grade of injury (3.5-5.5 atm) was produced. Neuropathologic changes were produced through brain deformation by pressure gradients at the time of injury. The neuronal NSE immunoreactivity in the parietal cortex and the brain stem began to decrease at 1 to 2 hours after injury and were reduced markedly or even lost 4 hours after injury. Axons in the cerebral white matter and corpus callosum and in the hemorrhage regions at the brain stem were waved and enlarged <4 hours after injury. From 4 hours after injury, retraction balls were found after staining by antibody for the neurofilament. The GFAP-positive astrocytes appeared in the impact site in the parietal cortex and in the brain stem from 4 hours after injury, whereas S-100-positive astrocytes were not markedly changed, indicating that early after the injury, astrocytes manifested reactive hypertrophy without proliferation. These results suggest that immunochemical studies on NSE, neurofilament, GFAP, and S-100 are useful in pathologic and forensic practice in a patient who survives for a short time after a fatal head injury but without obvious focal damage.

Animals↗
PubMed1997

Frontal brain and leptomeningeal biopsy specimens correlated with cerebrospinal fluid outflow resistance and B-wave activity in patients suspected of normal-pressure hydrocephalus.

OBJECTIVE: Normal-pressure hydrocephalus (NPH) is a potentially treatable syndrome with abnormal cerebrospinal fluid dynamics. Meningeal fibrosis and/or obliteration of the subarachnoid space has been suggested as the pathoanatomic basis. The purpose of the present study was to investigate whether meningeal fibrosis causes increased resistance to cerebrospinal fluid outflow (R(out)) and/or increased B-wave activity and whether pathological changes in the brain parenchyma after brain compliance, causing increased B-wave activity. METHODS: The study involved a group of 38 consecutively studied patients with clinical and radiological evidence of idiopathic NPH, for whom a frontal brain biopsy was obtained. For 29 patients, hydrodynamic criteria of NPH were fulfilled and a ventriculoperitoneal shunt was performed. RESULTS: Meningeal fibrosis was found in 12 of 25 biopsies containing arachnoid tissue, but no correlation with R(out) or B-waves was found. Pathological parenchymal changes, most often Alzheimer's disease (10 cases) or vascular changes (10 cases), were found in 21 biopsies, but no correlation with B-waves or R(out) was found. CONCLUSION: The results suggest that leptomeningeal fibrosis is not the only pathoanatomic basis of increased R(out) and/or B-wave activity in patients with NPH and that various degenerative changes in the parenchyma may be responsible for the altered cerebrospinal fluid dynamics characteristic of NPH.

Adult↗
PubMed1996

Spike waves and synaptic ultrastructure in human epileptic brains.

OBJECTIVE: To find morphological changes of synapses related to the spike discharge by observation on ultrastructures of the EEG spike foci of cerebral cortexes. MATERIAL AND METHODS: The cerebral cortexes were obtained surgically from the EEG spike (recorded by flaky silver electrodes on the surface of cortexes) foci and nonspike areas within the limits of the brain tissue that would be removed in 20 cases of human epilepsy, and were processed for transmission electron microscopic (TEM) observation. RESULTS: In the spike foci, presynaptic terminals of axospinal asymmetric synapses were obviously swollen but postsynaptic spines were relatively unaffected. In these synapses, the synaptic vesicles remarkably decreased in number and accumulated predominantly at the presynaptic membranes or aggregated. Similar changes were observed in the presynaptic terminals of the axospinal asymmetric synapses in the nonspike areas but were of milder degree than in the spike foci. CONCLUSION: Axospinal asymmetric synapses may release a large quantity of excitatory neurotransmitters, which may result in epileptic abnormal electric activities during seizure.

Adolescent↗
PubMed1992

An immediate light microscopic response of neuronal somata, dendrites and axons to non-contusing concussive head injury in the rat.

Sixteen rats were killed by transcardial perfusion fixation 1 min after a non-contusing concussive head injury, and seven rats 1 day later. In each of the "1-min" animals Golgi-like neurons and long axonal segments scattered in various proportions among unstained neurons and axons were demonstrated by a new silver method both near to and far from the impact site in a parenchymal environment unaffected by contusion. The silver-stained neurons, dendrites and axons were considered to have been damaged by the trauma because they were consistently absent from control brains. In the "1-day" brains silver-stained dendrites and axons had a beaded appearance, indicating an advanced stage of morphopathological damage. From details of these findings the following conclusions were drawn: (1) trauma can directly induce some kind of morphopathological damage in neurons which manifests itself in shrinkage of the soma and tortuosity of appendages as well as in type III argyrophilia; (2) different vulnerability of various brain areas is likely due to the inhomogeneity of the trauma-induced pressure wave propagating through the brain; and (3) the somato-dendritic and axonal domains of the neuron are selectively vulnerable to different values of the parameters of the intracranial pressure wave.

Animals↗
PubMed1992

Normal auditory brain stem evoked responses in infants of diabetic mothers.

Auditory brain stem responses potentials were recorded from 71 newborns within the first 2 weeks after birth; conceptional age ranged from 37 to 41 weeks. Thirty-nine newborns were infants of diabetic mothers (IDMs) (17 White A, 22 White B-D) and 32 healthy term newborns served as control group. IDMs with additional high risk for cochlear or brain stem integrity were excluded. Birthweight for gestational age was significantly higher for IDMs. No differences in auditory brain stem responses wave latencies or amplitudes were observed between healthy infants of the control group and IDMs.

Birth Weight↗
PubMedDate not supplied

[Evoked potentials in a population of children below 1,500 grams at birth: a description and probabilities].

INTRODUCTION: Bioelectrical behaviour was studied in a group of low birth weight children. AIM: To evaluate whether the characteristics of the waves of the brain potentials in these children, who weighed less than 1500 g at birth and experienced anomalous circumstances and events during their perinatal period, would help reach an early diagnosis of the possible developmental disorders they might suffer later on in life. SUBJECTS AND METHODS: Both visual and auditory cerebral evoked potentials were recorded in a group of children born underweight and the results were compared with the findings from another group of healthy children who were born in normal physiological conditions and were apparently free of any kind of pathology. RESULTS: In the waves and locations that were examined, the problem group displayed latencies that were longer than those of the control group; in contrast, no statistically significant differences were found in the amplitude, regardless of the location. Low gestational age and lower weight made latencies longer, but no relationship was found between latencies and the other perinatal features that were studied. CONCLUSIONS: Children with low weight at birth have slower wave latencies than normal children. This slowing, which is inversely proportional to the weight and weeks of gestation, is considered to be an anomalous sign that could be related to brain immaturity, delayed development or to disorders affecting myelination. Moreover, the amplitude, which has received far less attention from researchers, is usually shorter in these processes, although in our study we found no differences with the group of healthy children--only very slightly in the P300, in the weeks and the weight, and the N100 only in one location with respect to weight. Since these children usually have developmental disorders, the use of evoked potentials could be a very useful tool in their detection and ensuing therapy.

Birth Weight↗
PubMedDate not supplied

Auditory brainstem response in postmenopausal women treated with hormone replacement therapy: a pilot study.

OBJECTIVE: To research the nongenital audiological target for gonadal steroids in postmenopausal women who are treated with hormone replacement therapy. DESIGN: Fifty postmenopausal volunteers were treated with hormone replacement therapy. Women with an intact uterus had sequential weekly transdermal estradiol plus nomegestrole acetate 5 mg orally for 12 days per month or a continuous daily oral dose of conjugated estrogen 0.625 mg and medroxyprogesterone acetate 5 mg tablet. Eighteen surgically postmenopausal women received a weekly transdermal estradiol system. Twenty-five postmenopausal volunteers-5 with a natural menopause and 10 with a surgical menopause-and 20 premenopausal normally cycling women were used as a control group. Each woman performed auditory brainstem response by auditory-evoked potentials for waves I, III, and V and for interpeak I-III, I-V, and III-V intervals. RESULTS: Women who were treated with hormone replacement therapy showed wave latencies and interpeak latencies shorter than those for postmenopausal women in the control group (p < or = 0.05), overlapping those of the premenopausal women (p > 0.05). Women who were treated with estrogen replacement therapy showed shorter time latencies than those treated with combined hormone replacement therapy (p < or = 0.05). CONCLUSIONS: Our data suggest that fluctuating hormone levels cause changes in auditory brain-stem response waves, even if the exact mechanism of activity of the gonadal steroids is not clear. However, we believe that estrogen may influence the neuronal plasticity, the metabolic levels of neurotransmitters, and thus the neuronal conduction time into the audiological system.

Administration, Cutaneous↗