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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-five head-injured patients with localized theta bursts on standard or 24 h ambulatory EEG were administered a standardized interview for neuropsychiatric symptoms associated with complex partial seizures (e.g. olfactory hallucinations, memory gaps) and a battery of neuropsychological tests. Although the formal neuropsychological test performances of these patients were relatively normal they reported an abundance of seizure-like behavioural symptoms. While the frequency of these symptoms was high, they did not occur in a stereotyped complex or sequence. These findings suggest that localized theta bursts may be diagnostic of an underlying neuroelectrical disorder.
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PMID:Neuropsychiatric correlates of theta bursts in patients with closed head injury. 139 81

The organophosphate chemical nerve agent, soman, causes convulsions, neuropathology, and, ultimately, death. A major problem in treating soman intoxication is that peripherally acting pharmacological agents which prevent death do not prevent seizures. Although a primary cause of these symptoms is the excess of acetylcholine which follows acetylcholinesterase (AChE) inhibition, centrally acting muscarinic blockers, such as atropine, alleviate, but do not block, the convulsive actions of soman. Moreover, there is a relatively weak relationship between CNS reductions of AChE and the incidence of convulsions. There is evidence suggesting that soman intoxication stimulates the release of norepinephrine (NE) in the brain. Recent evidence has implicated NE in the induction and/or maintenance of seizures. Thus, in the present study the relations among soman-induced convulsions, AChE inhibition, and brain NE and other monoamine changes were examined. The time course of brain NE recovery was also determined. Rats were injected (im) with a single dose (78 micrograms/kg) of soman. At this dose 68% of the injected rats developed convulsions. Both convulsive and nonconvulsive rats were sacrificed between 1 and 96 h following soman injection and NE levels in the rostral forebrain and olfactory bulb were determined by HPLC with electrochemical detection. In all convulsive rats NE levels declined substantially. Forebrain NE levels were decreased by 50% at 1 h and 70% at 2 h following soman injection. Recovery of NE began at 8 h and was complete by 96 h following soman administration. Although nonconvulsive rats showed other signs of intoxication, NE levels in these rats were unchanged. Dopamine (DA) and serotonin (5-HT) levels were not significantly affected in either convulsive or nonconvulsive rats. However, 5-hydroxyindoleacetic acid, the major metabolite of 5-HT, and homovanillic acid and 3,4-dihydroxyphenylacetic acid, the two major metabolites of DA, were increased significantly in the forebrain of convulsive, but not nonconvulsive rats, indicating an increase in 5-HT and DA turnover. However, in contrast to the abrupt decline in NE, these increases in DA and 5-HT metabolites were slow and progressive. Taken together, the present results and other recent findings suggest that rapid, sustained NE release could play a role in the induction and/or maintenance of soman-induced convulsions, whereas increased release of 5-HT and DA may be a consequence of seizures. Further investigation of the role of NE in soman-induced convulsions may lead to improved treatment of soman intoxication and a better understanding of the role of NE in other forms of seizures, including human epilepsy.
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PMID:Brain norepinephrine reductions in soman-intoxicated rats: association with convulsions and AChE inhibition, time course, and relation to other monoamines. 142 25

Chaos theory is a rapidly growing field. As a technical term, "chaos" refers to deterministic but unpredictable processes being sensitively dependent upon initial conditions. Neurobiological models and experimental results are very complicated and some research groups have tried to pursue the "neuronal chaos". Babloyantz's group has studied the fractal dimension (d) of electroencephalograms (EEG) in various physiological and pathological states. From deep sleep (d = 4) to full awakening (d > 8), a hierarchy of "strange" attractors paralles the hierarchy of states of consciousness. In epilepsy (petit mal), despite the turbulent aspect of a seizure, the attractor dimension was near to 2. In Creutzfeld-Jacob disease, the regular EEG activity corresponded to an attractor dimension less than the one measured in deep sleep. Is it healthy to be chaotic? An "active desynchronisation" could be favourable to a physiological system. Rapp's group reported variations of fractal dimension according to particular tasks. During a mental arithmetic task, this dimension increased. In another task, a P300 fractal index decreased when a target was identified. It is clear that the EEG is not representing noise. Its underlying dynamics depends on only a few degrees of freedom despite yet it is difficult to compute accurately the relevant parameters. What is the cognitive role of such a chaotic dynamics? Freeman has studied the olfactory bulb in rabbits and rats for 15 years. Multi-electrode recordings of a few mm2 showed a chaotic hierarchy from deep anaesthesia to alert state. When an animal identified a previously learned odour, the fractal dimension of the dynamics dropped off (near limit cycles).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:On the existence and the role of chaotic processes in the nervous system. 146 29

In situ hybridization for c-fos mRNA was performed on brain sections (a) from rats after an acute cocaine-induced seizure or from saline-injected controls and (b) from rats after their first cocaine-kindled seizure, as well as from rats that had not yet developed cocaine-kindled seizures (but were exposed to the same amount of cocaine as those that did exhibit convulsions) and from saline-injected controls. Increased expression of c-fos mRNA was observed in animals demonstrating cocaine-induced seizures acutely or following pharmacological kindling. Rats that experienced acute seizures after cocaine (65 mg/kg) showed pronounced increase in expression of c-fos mRNA in the dentate gyrus of the hippocampus and olfactory bulb. Increases were also observed in several other limbic cortical regions, as well as the striatum and ventromedial hypothalamic nucleus (VMH). In rats that were injected daily with an initially subconvulsive dose of cocaine-HCl (40 mg/kg), the cocaine-kindled seizures induced elevations in c-fos mRNA in the same brain regions as with an acute cocaine-induced seizure with the single exception of the VMH. These findings not only suggest the involvement of limbic, cortical and striatal structures in the cocaine-induced seizure, but also raise the possibility that alterations in the proto-oncogene c-fos and its subsequent impact on gene expression could play a role in the changes in neural excitability associated with cocaine-induced kindling.
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PMID:Expression of c-fos mRNA in acute and kindled cocaine seizures in rats. 149 73

Four patients had prolonged, sensory, simple partial seizures (SPS), lasting up to several days, without associated behavioural impairment. In three patients, the SPS often occurred as a prolonged "aura" before a more overt seizure. Descriptions included: "butterflies", rising epigastric sensation; "a thought in the stomach", and an olfactory sensation. Seizure localisation was frontal in one case, temporal in two cases and uncertain in one case. These sensations may represent an under-reported form of continuous, focal seizure activity, which arises from various cerebral regions.
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PMID:Prolonged sensory or visceral symptoms: an under-diagnosed form of non-convulsive focal (simple partial) status epilepticus. 152 44

Recent studies with kindling and convulsant drug models of epilepsy suggest that the piriform (primary olfactory) cortex may be particularly susceptible to generation of epileptiform activity. The present study has examined the generation of interictal epileptiform events in the piriform cortex of kindled rats in vivo, taking advantage of special features of this system that facilitate physiological analysis. The investigation included analysis of extracellular and intracellular potentials, and membrane currents computed by current source density (CSD) analysis. In pyramidal cells, epileptiform events consisted of an initial EPSP that occurred in all-or-none fashion and a long-lasting IPSP with Cl(-)- and K(+)-mediated components. Onset of the IPSP was sufficiently fast that firing evoked by the EPSP was consistently limited to single action potentials. CSD analysis revealed the presence of two distinctly different excitatory epileptiform currents: an initial inward current of unknown origin that is widely distributed over depth, and a second much larger inward current at the depths of proximal apical and basal dendrites of pyramidal cells. It was concluded that this second component is mediated by the associational projections of pyramidal cells excited by the first component. Since these heavy associational projections also extend to neighboring areas including the amygdala, entorhinal cortex, and insular and orbitofrontal areas of neocortex, this second component could be widely propagated within the basal forebrain. An important finding was that the EPSP generated by this associational pathway was completely blocked in cell bodies of pyramidal cells in piriform cortex by the IPSP during most events. This IPSP may therefore play a critical role in limiting seizure activity by preventing reverberating positive feedback in the pyramidal cell population. It can be speculated that compromise of this IPSP, as by repetitive activation by the shock trains used for kindling, leads to prolonged epileptic activity in the piriform cortex and the many limbic structures to which it projects.
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PMID:Neuronal processes that underlie expression of kindled epileptiform events in the piriform cortex in vivo. 160 37

A total of 33 patients with brain tumors and 22 patients with temporal epilepsy were compared. The differential diagnostic signs at the initial stages were revealed. In tumors, the disease starts most commonly from paroxysms of the isolated aura or complex absence epilepsy types. At the disease onset, the olfactory auras were recorded 6 times more frequently than in temporal epilepsy. The gustatory and vestibular auras also turned out more typical for epileptic onset . The psychomotor, psycho-sensory , ideational, and emotional paroxysmal manifestations were found to predominate at the onset of temporal epilepsy. As compared to epilepsy, the tumorous process leads much more swiftly to the development of pleomorphism and aggravation of the seizures, progress of the neurological symptomatology. The aggravated pre-epileptic anamnesis and hereditary as well as typical pointed wave epileptic activity on the EEG were demonstrable much more rarely in tumors.
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PMID:[Early differential diagnosis of brain tumors with temporal epileptic syndrome and temporal epilepsy]. 166 75

The existence of long-lasting (15-18 h) alterations of neurotransmitter amino acid levels following a single or repeated acoustic stimulations in audiogenic seizure-prone Rb1 and Rb2 mice and seizure-resistant Rb3 mice were investigated. The levels of glutamate, aspartate, glycine, taurine, and of some of their precursors: glutamine and serine were determined. Fourteen brain areas were examined. Alterations were found only in 6 brain areas (pons, olfactory bulbs, superior colliculus, inferior colliculus, olfactory tubercles and raphe). Most frequent occurring changes were observed in pons and olfactory tubercles. These changes concerned mainly the excitatory amino acids, glutamate, and aspartate. Alterations of taurine, glycine and serine were also recorded.
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PMID:Long-lasting effects of audiogenic seizures on neurotransmitter amino acids in Rb mice. 168 75

The influence of kainic acid (KA)-induced limbic seizure activity on the expression of mRNA for nerve growth factor (NGF) in adult rat brain was studied using in situ hybridization and S1 nuclease protection techniques with RNA probes complementary to murine and rat NGF mRNA. Within hippocampus, intracerebroventricular injection of 0.5 microgram KA caused a dramatic bilateral increase in hybridization of the 35S-labeled cRNA within stratum granulosum. This increase was first evident 1 h post-KA, appeared maximal at approximately 20-fold control levels at 2-3 h post-injection, and declined to control levels by 48 h post-injection. During the period of maximal hybridization, all but the deepest cells within stratum granulosum appeared to be autoradiographically labeled. Hybridization of the NGF cRNA probe was also increased within superficial layers of piriform and entorhinal cortex and, to much lesser extent, within scattered neurons of layers II and III of neocortex in KA-treated rats. In olfactory cortical areas, hybridization was maximally elevated 15.5-24.5 h after KA injection. In contrast to these effects, KA treatment did not consistently influence the density of hybridization, or number of neurons labeled, within the dentate gyrus hilus or the hippocampus proper (CA1-CA3). In agreement with the in situ hybridization results, S1 nuclease protection assay detected KA-induced increases in hybridization within pooled dentate gyrus/CA1 samples, but not hippocampal CA3 samples. These data support the conclusion that seizure activity stimulates a transient increase in NGF expression by select populations of forebrain neurons and indicates that experimental seizure paradigms might be further exploited for analyses of the mechanisms of NGF regulation and processing in the adult brain.
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PMID:Kainic acid-induced seizures stimulate increased expression of nerve growth factor mRNA in rat hippocampus. 170 74

Expression of the proto-oncogene c-fos is known to increase in rat brain following various types of seizures. Measuring c-fos mRNA or protein levels was shown to be a good cellular marker for neurons activated during central nervous system (CNS) excitation. In this study, we used in situ hybridization analysis of c-fos mRNA to determine brain regions activated by a peptide that has been closely linked to stress responsivity and kindling-like seizure activity. Corticotropin-releasing hormone (CRH) was injected into the left lateral ventricle of rats and produced the late onset of seizures between 1.5-5 h after its administration. Rats were sacrificed at various time points after the administration of CRH or sterile water, and c-fos mRNA levels were determined. In the preseizure state, CRH increased c-fos unilaterally in several cerebral cortical structures (most prominently in the dorsal endopiriform nucleus and in the piriform and insular cortices). CRH-induced seizures increased c-fos bilaterally in the same cortical regions, and in addition, in the hippocampus and olfactory bulb. The data are congruous with the hypothesis that intracerebroventricularly (i.c.v.) administered CRH elicits a rapid kindling-like response.
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PMID:Expression of c-fos mRNA in rat brain after intracerebroventricular administration of corticotropin-releasing hormone. 178 25


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