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

Neuropeptide Y (NPY)-containing neurons are known to be highly vulnerable following sustained electrical stimulation in rats and in humans suffering from temporal lobe epilepsy. This has been related to a strong excitatory input. In contrast, there is evidence that neurons containing calcium-binding proteins exhibit a high resistance under experimental seizure and hypoxia conditions. The aim of this study was to determine the coexistence of NPY and calcium-binding proteins in inhibitory neurons of the primate fascia dentata and their synaptic connections. Vibratome sections of hippocampi of African green monkeys (Cercopithecus aethiops) were immunostained with antibodies against NPY, PARV, and CB. A quantitative coexistence study was performed for NPY and PARV on consecutive semithin sections. In contrast to the rodent hippocampus, NPY-immunoreactive neurons were found exclusively in the hilus of fascia dentata with horizontally oriented dendrites which did not extend into the granular and molecular layer. Conversely, PARV-immunoreactive neurons were also present in the granular and inner molecular layer and extended their dendrites far out in the molecular layer and the hilus. Axon terminals immunoreactive for NPY were mostly concentrated in the middle and outer molecular layer and the hilar region and were rare in the granular layer. PARV-immunoreactive boutons were basically restricted to the granular layer where they formed typical baskets. The antibody against calbindin stained almost exclusively granule cells. Coexistence of NPY- and PARV-immunoreactivity was found only in hilar neurons and was rare (9 out of 152 cells analyzed). These results suggest that most NPY-immunoreactive neurons do not contain calcium-binding proteins. NPY-containing neurons exhibited ultrastructural characteristics as described for inhibitory neurons. Their dendrites were only sparsely contacted by mostly asymmetric synaptic terminals, including a very small number of mossy fiber axon terminals. In turn, numerous NPY-immunoreactive axon terminals formed symmetric synapses with spines and dendritic shafts of unlabeled neurons in the middle and outer molecular layer, whereas no contact with granule cell bodies was evident. Thus, we conclude that the vulnerability of NPY-containing inhibitory neurons may be due more to the lack of calcium-binding proteins than to a strong excitatory innervation. As their axons may contribute to the inhibitory control of the major excitatory input from the entorhinal cortex, their loss following overstimulation may play a role in perpetuating hippocampal seizure activity.
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PMID:Neuropeptide Y (NPY)-immunoreactive neurons in the primate fascia dentata; occasional coexistence with calcium-binding proteins: a light and electron microscopic study. 171 21

Barbiturates retain an important place in clinical neurological practice. They are used as both diagnostic and therapeutic drugs, their most common uses being as anticonvulsant and anaesthetic agents. This article explores the current theories explaining the mechanism of action of the barbiturates, with special emphasis on their anaesthetic and anticonvulsant effects. The primary mechanism of action of barbiturates is to increase inhibition through the gamma-aminobutyric acid (GABA) system. Anaesthetic barbiturates also decrease excitation via a decrease in calcium conductance. Phenobarbital (phenobarbitone), the primary anticonvulsant barbiturate, is effective for partial, complex partial and secondarily generalised seizures. While no longer the drug of choice for all these seizure types, it remains an important and useful agent. Mysoline has been shown to be useful in the treatment of essential tremor and several other movement disorders, and as an anticonvulsant. Barbiturates are also used for their sedative-hypnotic properties. A relatively new use is in the evaluation of patients with medically intractable seizure disorders for possible surgical therapy. The roles of methohexital and amobarbital (amylobarbitone) are discussed in the section on barbiturates used as diagnostic agents. The experimental use of barbiturates is also commented on; the most important of these is perhaps the use of barbiturates in cerebral resuscitation.
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PMID:The clinical use of barbiturates in neurological disorders. 172 Mar 79

It is well known that most patients with hypoparathyroidism have radiologically detectable basal ganglia calcification. Not as well known is that the brain calcinosis may be more extensive. We describe a 55-year-old woman with a 44-year history of symptomatic idiopathic hypoparathyroidism who has extensive calcification of her cerebrum and cerebellum as well as her basal ganglia, evident on computed tomography of the head. When first evaluated here 32 years ago, plain radiography of the skull demonstrated calcification of both caudate and lentiform nuclei (basal ganglia). Despite fair control of her serum calcium level, she has developed focal seizures, possibly related to the calcinosis of her brain.
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PMID:Case report: extensive brain calcification in hypoparathyroidism. 175 Apr 48

In order to understand the mechanisms underlying seizure generation, the present study investigated the functional and anatomical interaction between seizures and interictal bursts. Bathing rat brain slices of the hippocampus and entorhinal cortex in zero magnesium medium elicited electrographic seizures. In the later period, the electrographic seizures were eventually replaced by the interictal bursts. In this phase, lowering [K+]o and raising [Ca2+]o restored the tonic seizures by suppressing the interictal bursts. A multiple knife cut experiment revealed that the seizures arose in the entorhinal cortex and the interictal bursts originated in CA3. A selective knife cut across the subiculum showed that the interictal bursts, propagating from CA3 to the entorhinal cortex, disrupted and suppressed the electrographic seizures in standard Mg(2+)-free medium.
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PMID:Mechanism of electrographic seizure generation in the rat brain slice in low magnesium medium: modulatory effect of interictal bursting on seizure generation. 176 7

Seizure (EEG) was studied in rats unilaterally injected in the dorsal hippocampus with l-glutamate (Glu). Extracellular Ca2+ content [(Ca2+)e] in the injected area was assessed by brain microdialysis coupled to automatic atomic absorption spectrophotometry. In this experimental epileptic model, an inhibition of Glu-stimulated epileptic activity and a fall in (Ca2+)e by nimodipine (Nim, 100 micrograms.kg-1) were seen. The spike- and wave-burst frequency was reduced from 30 to 5 bursts.min-1 (P less than 0.01, n = 8). Nim 25 and 50 micrograms.kg-1, without anticonvulsant activity, did not prevent the drop in (Ca2+)e. These results indicate that Nim exerts an antiepileptic effect on Glu-induced epilepsy. The mechanisms may be involved in blocking Ca2+ influx into neurons.
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PMID:Effects of nimodipine on l-glutamate-induced seizures and Ca2+ influx in hippocampus in freely moving rats. 180 75

In freely moving rats, hippocampus neuronal extracellular calcium concentration (Ca2+)e and seizures were investigated. Application of quinolinic acid 156 nmol (exciting N-methyl-D-aspartate receptor, NMDA) to dorsal hippocampus elicited a decrease in (Ca2+)e by 48 +/- 5% in the infusion area and produced a characteristic abnormal EEG. l-Daurisoline dramatically prevented the reduction in (Ca2+)e, but not seizures (EEG). The results suggest that NMDA-operated calcium channels, but not NMDA-receptors, are involved in the effects of l-daurisoline on Ca2+ influx observed.
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PMID:Effects of l-daurisoline on quinolinic acid-induced Ca2+ influx in hippocampus neurons in freely moving rats. 180 76

There is an international consensus on the indications of electroconvulsive treatment (ECT): they result in particular from the limitations of antidepressant drug treatment. Even though the global effect of ECT is considered as satisfactory, 10 to 20% of depressed patients eligible for ECT are treatment refractory. This warrants a search for factors predicting efficacy or lack of efficacy of ECT. Predicting factors prior to ECT: Usual clinical criteria, such as the presence of delusional thoughts, are generally classified with endogenous signs of depression. Among biological criteria, EEG data, tests assessing reactivity of autonomous nervous system, plasma measures of catecholamines, calcium and cortisol do not seem relevant parameters. Dexamethasone suppression test and stimulation of TSH by TRH have no more predictive value. Predictive indices during treatment: Empirically clinicians identified a sequence in the response of depressive symptoms, although no conclusion can be drawn from these clinical impressions. Among biological factors some authors stress the importance of the epileptogenic threshold and of measuring plasma levels of peptides released by the posterior lobe of hypophysis. Such data have to be confirmed and their physiopathological value better understood. Actually some parameters representing good therapeutic practices are valued by physicians using ECT: sufficient duration of electrical crisis, total seizure time during the series of electroshocks. Those conceptions are close to the classical emphasis on the adequate number of ECTs and to the discussion on the comparative efficacy of unilateral and bilateral ECT. After ECT most authors shift to antidepressants, although data about medium and long term outcome prediction with this approach are also lacking.
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PMID:[Predictive factors of response to electronarcosis]. 180 65

1. We examined whether the three physiologically defined neuron types described for rodent neocortex were also evident in human association cortex studied in an in vitro brain slice preparation. We also examined the relationship between physiological and morphological cell type in human neocortical neurons. In particular, we tested whether burst-firing neurons were numerous in regions of human cortex that are susceptible to seizures. 2. Although we sampled regular-spiking and fast-spiking neurons, we observed no true burst-firing neurons, as defined for rodent cortex. We did find neurons that displayed a voltage-dependent shift in firing behavior. Because this behavior was due, in large part, to a low-threshold calcium conductance, we called these cells low-threshold spike (LTS) neurons. 3. Regular-spiking neurons and LTS neurons only differed in the voltage dependence of firing behavior and the first few interspike intervals (ISIs) of repetitive firing in response to small current injections (from hyperpolarized membrane potentials). Because of the general similarities between the two types, we consider the LTS cells to be a subgroup of regular-spiking cells. 4. All biocytin-filled regular-spiking neurons were spiny and pyramidal and found in layers II-VI. The lone filled fast-spiking cell was aspiny and nonpyramidal (layer V). The LTS neurons were morphologically heterogeneous. We found 80% of LTS neurons to be spiny and pyramidal, but 20% were aspiny nonpyramidal cells. LTS neurons were located in layers II-VI. 5. In conclusion, human association cortex contains two of three physiological cell types described in rodent cortex: regular spiking and fast spiking. These physiological types corresponded to spiny, pyramidal, and aspiny, nonpyramidal cells, respectively. We sampled no intrinsic burst-firing neurons in human association cortex. LTS neurons exhibited voltage-dependent changes in firing behavior and were morphologically heterogeneous: most LTS cells were spiny and pyramidal, but two cells were found to be aspiny and nonpyramidal. It is not clear whether the absence of burst-firing neurons or the morphological heterogeneity of LTS neurons are due to species differences or differences in cortical areas.
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PMID:Correlation of physiologically and morphologically identified neuronal types in human association cortex in vitro. 181 19

Seizures induced by three convulsant treatments produced differential effects on the concentration of acetylcholine in rat brain. Status epilepticus induced by (i) coadministration of lithium and pilocarpine caused massive increases in the concentration of acetylcholine in the cerebral cortex and hippocampus, (ii) a high dose of pilocarpine did not cause an increase of acetylcholine, and (iii) kainate increased acetylcholine, but the magnitude was lower than with the lithium/pilocarpine model. The finding that the acetylcholine concentration increases in two models of status epilepticus in the cortex and hippocampus is in direct contrast with many in vitro reports in which excessive stimulation causes depletion of acetylcholine. The concentration of choline increased during seizures with all three models. This is likely to be due to calcium- and agonist-induced activation of phospholipase C and/or D activity causing cleavage of choline-containing lipids. The excessive acetylcholine present during status epilepticus induced by lithium and pilocarpine was responsive to pharmacological manipulation. Atropine tended to decrease acetylcholine, similar to its effects in controls. The N-methyl-D-aspartate (NMDA) receptor antagonist, MK-801, reduced the excessive concentration of acetylcholine, especially in the cortex. Inhibition of choline uptake by hemicholinium-3 (HC-3) administered icv reduced the acetylcholine concentration in controls and when given to rats during status epilepticus. These results demonstrate that the rat brain concentrations of acetylcholine and choline can increase during status epilepticus. The accumulated acetylcholine was not in a static, inactive compartment, but was actively turning-over and was responsive to drug treatments. Excessive concentrations of acetylcholine and/or choline may play a role in seizure maintenance and in the neuronal damage and lethality associated with status epilepticus.
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PMID:Seizures increase acetylcholine and choline concentrations in rat brain regions. 181 38

The use of magnesium sulfate (MgSO4) as an anticonvulsant is controversial. Status epilepticus was induced in 0.5% halothane-anesthetized Wistar rats with a threshold (90 mg/kg) or suprathreshold (200 mg/kg) dose of intravenous (i.v.) pentylenetetrazol (PTZ) under stereotactic hippocampal depth electrode monitoring. Fifteen minutes after seizure induction, the maximum hemodynamically tolerated dose of MgSO4 (10 mg/kg/min in 22 min) was administered i.v. MgSO4 was ineffective in altering seizure discharge. A subgroup of nine animals received hypertonic mannitol before MgSO4 to open the blood-brain barrier (BBB) to facilitate Mg2+ CNS penetration. Again MgSO4 was ineffective in attenuating epileptic activity. These results support the contention that MgSO4 is not an effective treatment for status epilepticus. We hypothesize that because Mg2+ blocks Ca2+ influx into the neuron through the N-methyl-D-aspartate (NMDA) receptor-operated calcium channel in a voltage-dependent manner it would be ineffective in neurons that are continuously depolarizing as in status epilepticus.
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PMID:Effects of magnesium sulfate on pentylenetetrazol-induced status epilepticus. 183 Nov 20


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