Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied a 59-year-old man with transient paroxysms of hypertension, tachycardia, and flushing in whom pheochromocytoma was excluded. Although catecholamine excretion was normal, plasma catecholamine levels rose from normal basal levels (282 +/- 14 pg/ml) to increased levels (585 +/- 67 pg/ml; x +/- SEM; n = 4) at the peak of spells. Other hormones or substrates expected to rise with nonspecific "stress" did not increase after paroxysms. Therapy with clonidine (0.2 to 0.4 mg/day) suppressed basal catecholamines to undetectable levels and markedly reduced peak levels during spells (80 pg/ml). An epileptic pathogenesis was suggested by stereotypic olfactory and epigastric prodromata before spells, and abolition of paroxysms with the anticonvulsant carbamazepine. This patient represents a rare case of autonomic epilepsy with the seizure focus in the temporal lobe.
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PMID:Autonomic epilepsy: clonidine blockade of paroxysmal catecholamine release and flushing. 62 48

A case history is reported of a 44-year-old man with a 6-year history of psychomotor seizures. For the past year he had described persistent olfactory hallucinations of an unpleasant nature which he referred to himself. In many respects these symptoms conform to the pattern observed in the olfactory reference syndrome, a recently described but apparently quite discrete psychiatric disorder; there were, however, certain atypical features. At a later stage unilateral anosmia was noted. Radiological examination then demonstrated an arterio-venous malformation in the right frontal lobe. The relationship between the malformation and the psychomotor seizures, and the implications that each has for the development of an olfactory reference syndrome are fully discussed.
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PMID:Psychomotor seizures, arterio-venous malformation and the olfactory reference syndrome. A case report. 69 78

A 37-year-old woman had bilateral anygdalotomy for psychomotor and minor motor seizures and long periods of very pronounced mental depression. The patient has been seizure-free for four years postoperatively. A preoperative left temporal spike focus disappeared after extensive left anygdalotomy. Of particular interest in this case is the recovery of olfactory and memory functions which were partially impaired by the bilateral lesions. Bilateral anygdalotomy is effective in relieving temporal lobe seizures without the complications and deficits that usually occur with resections of the bilateral temporal lobe.
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PMID:Amygdalotomy for bilateral temporal lobe seizures. 80 18

Sustained seizure activity can be induced in rabbit olfactory bulb by application of brief low-level current via chronically implanted micro-electrodes. Sensitivity to such stimulation is markedly augmented by prior surgical isolation of the ipsilateral or contralateral bulb. The isolated rabbit olfactory bulb apparently possesses an intrinsic system sufficient to acquire and retain altered neuronal excitability of an epileptiform kind. The preparation described here offers promise as a model for further studies of electrophysiological plasticity in a simple cortical system.
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PMID:Electrically-induced epileptogenesis in rabbit olfactory bulb: electrophysiological plasticity in a simple cortical system. 114 70

Previous studies have demonstrated regional variation in the anatomical organization and physiological properties of the hippocampus along its septotemporal (dorsoventral) axis. In this study, regional variation of the supragranular projection of the mossy fiber pathway in the dentate gyrus of normal and kindled rats was characterized with a scoring method for assessment of the distribution of mossy fiber synaptic terminals detected by Timm histochemistry. In normal rats, there was a sparse projection of the mossy fiber pathway into the supragranular region near the tips and crest of the dentate gyrus along the entire septotemporal axis, and a prominent projection into the supragranular region at the temporal pole. Kindling of the perforant path, amygdala, and olfactory bulb induced synaptic reorganization of the mossy fiber pathway into the supragranular region along the entire septotemporal axis of the dentate gyrus. There was regional variation of the seizure-induced synaptic reorganization along this axis, and distinct septotemporal patterns were observed as a function of the site of kindling stimulation. Kindling of the perforant path induced mossy fiber synaptic reorganization that was relatively more prominent in the septal pole than in the temporal pole of the dentate gyrus. In contrast, rats that received kindling stimulation of the amygdala had a more uniform distribution of synaptic reorganization along the septotemporal axis. As there is regional variation of the anatomical and physiological properties of the human epileptic hippocampus, these observations could be pertinent to human epilepsy.
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PMID:Septotemporal variation of the supragranular projection of the mossy fiber pathway in the dentate gyrus of normal and kindled rats. 130 94

Basic fibroblast growth factor (bFGF) is a trophic factor synthesized in the central nervous system (CNS), where it is believed to play a role in neuronal maintenance and repair. Little is known about the regulation of this growth factor in the CNS. To determine whether the expression of the bFGF gene in the brain of adult animals changes in response to alterations of neuronal activity, we examined bFGF mRNA levels in several brain regions of rats experiencing focally-evoked convulsive seizures. Seizures were induced by microinjecting bicuculline unilaterally into an epileptogenic site within the deep prepiriform cortex, area tempestas (AT). By 5 h after initiation of brief limbic motor seizures from AT, there was a four fold increase in the levels of bFGF mRNA in the entorhinal cortex, hippocampus and olfactory bulb, but not in the caudate-putamen. The maximal expression of bFGF mRNA was reached by 10 h after seizure onset. In the same animals, the mRNA encoding nerve growth factor (NGF) was increased in entorhinal cortex and hippocampus, but not in the olfactory bulb. Our results demonstrate that neuronal activity can influence bFGF expression in an anatomically selective fashion and that acute changes in bFGF can occur in the uninjured mature brain. The increase in bFGF expression in response to excessive activation of specific neuronal circuitry may represent an adaptive response to protect against potential injury in those circuits.
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PMID:Basic fibroblast growth factor mRNA increases in specific brain regions following convulsive seizures. 133 86

The seizure-modulating role of N-methyl-D-aspartate (NMDA) receptors located in several limbic areas was investigated. Amygdala-kindled rats were microinfused with the selective NMDA-receptor antagonist 2-amino-5-phosphonovalerate (APV, 1 microliter, 70 nmol) or artificial cerebrospinal fluid (ACSF) applied through a cannula located in either the amygdala or perirhinal, pyriform or deep prepyriform cortices. APV infused into the stimulation site raised the threshold for seizure generation. Surprisingly, APV infused into perirhinal cortex, but not into other regions, also dramatically suppressed behavioural seizures and afterdischarges (AD) elicited 5 min after the infusion. If stimulus intensities were markedly elevated however, the seizure suppression was overcome. This latter effect was reversible and repeatable, as seizures and AD were reliably reinstated when these animals were stimulated after infusion with ACSF. A similar effect, whereby perirhinal infusions blocked seizure activity, was also demonstrated in an animal kindled from the olfactory bulb and in one kindled from the perforant path. These results suggest that NMDA receptors located in the perirhinal cortex may play a major role in the modulation of AD activity elicited from more distal brain regions. Furthermore, activation of perirhinal cortex may be a critical requirement for the generation of amygdala-stimulated AD in the kindled animal.
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PMID:The infusion of an NMDA antagonist into perirhinal cortex suppresses amygdala-kindled seizures. 135 65

The involvement of synaptosomal neurotransmitter amino-acids in seizure susceptibility and seizure severity was explored. The amino-acid contents of brain synaptosomes were determined in three sublines of Rb mice differing in their response to an acoustic stimulus: Rb1, clonic-tonic seizure-prone, Rb2, clonic seizure-prone, and Rb3, seizure-resistant. Synaptosomes were prepared from 6 brain areas considered to be involved in seizure activity: olfactory bulbs, amygdala, inferior colliculus, hippocampus, cerebellum, pons-medulla. The steady-state levels of GABA and glycine (Gly), inhibitory amino-acids, of taurine (Tau), an inhibitory neurotransmitter of neuromodulator, of aspartate (Asp) and glutamate (Glu), excitatory amino-acids, as well as of serine (Ser) and glutamine (Gln), two precursors of neurotransmitter amino-acids, were determined by HPLC. Low levels of Tau, GABA, and Ser in hippocampus, Gly in amygdala, Glu in hippocampus, inferior colliculus and pons, Gln and Asp in inferior colliculus appeared to correlate with seizure-susceptibility. GABA and Asp in olfactory bulb, Gln in amygdala, hippocampus and pons, ser in olfactory bulb and pons, appeared to be associated either with seizure-severity or -diversity. A strong involvement of hippocampus (Tau, GABA, Ser, Glu, and Gln) and inferior colliculus (Asp, Glu, Gln) in audiogenic seizure-susceptibility, and of olfactory bulb (GABA, Asp) in seizure-severity and/or -diversity is suggested.
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PMID:Involvement of synaptosomal neurotransmitter amino acids in audiogenic seizure-susceptibility and -severity of Rb mice. 135 66

It is now a recognized principle that various neuropeptides are neuronally co-localized with biogenic amine or aminoacid neurotransmitters. In the rat CNS it has previously been shown that TRH is co-localized with 5-HT (and also with substance P) in cell bodies of the posterior raphe that project to the spinal cord. Although TRH cell bodies are known to be widely distributed throughout the forebrain there is no other known co-localization with 5-HT. In this study we further specify the forebrain there is no other known co-localization with 5-HT. In this study we further specify the anatomical relationship of TRH with 5-HT by use of surgical and neurotoxic lesioning with reference to limbic forebrain regions wherein TRH is greatly increased following seizures. In groups of rats, the fimbria-fornix was lesioned alone, or combined with a lesion of the dorsal perforant path or the ventral perforant path. There was a sham lesioned control group. Additional groups were lesioned with 5,7 dihydroxytryptamine, 100 micrograms i.v.t., 45 min. after i.p. desipramine, 25 mg/kg. All rats were sacrificed three weeks after lesions. Indoleamines were determined by HPLC in left anterior cortex, left pyriform/olfactory cortex, left dorsal hippocampus and left ventral hippocampus. TRH was determined by specific RIA in the corresponding right brain regions. The modal n was 7 rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Some regional anatomical relationships of TRH to 5-HT in rat limbic forebrain. 138 39

Recent studies in this laboratory have demonstrated that intramuscular injection of the irreversible acetylcholinesterase (AChE) inhibitor, soman (pinacolylmethylphosphonofluoridate), produces a rapid (1-2 h) and profound depletion (70% of control) of norepinephrine (NE) in the olfactory bulb and forebrain. NE is decreased only in convulsing animals. As NE-containing locus coeruleus (LC) neurons provide the only NE input to the olfactory bulb and the major NE innervation of the forebrain, the reduction of NE suggests that soman may cause tonic activation of LC neurons leading to rapid depletion of NE. Activation of LC may result from: (i) facilitation of cholinergic transmission in LC; (ii) soman-induced activation of excitatory inputs to LC; or (iii) generalized activation of LC neurons due to seizures. The present experiments were designed to assess these alternatives. We examined whether LC neuronal activity, c-fos expression, and AChE staining are altered after peripheral (systemic) or direct intracoerulear injection of soman in anesthetized rats. Both modes of soman administration rapidly and potently increase the spontaneous discharge rate of LC neurons. This activation was associated with a desynchronization of the electroencephalogram, but not with seizures. The discharge of LC neurons remained elevated at all postsoman intervals examined (up to 2 h) and was rapidly and completely reversed by systemic injection of the muscarinic receptor antagonist scopolamine hydrochloride, but not by the nicotinic receptor antagonist mecamylamine. Both systemic and intracoerulear soman administration completely inhibited AChE staining in LC and rapidly induced the expression of c-fos in LC neurons. These results demonstrate that soman potently and tonically activates LC neurons. This effect appears to be mediated by direct inhibition of AChE in LC leading to a rapid accumulation of ACh. Unhydrolyzed ACh tonically activates LC neurons via muscarinic receptors. Soman-induced activation of LC neurons does not require seizures. We conclude that depletion of forebrain and olfactory bulb NE after systemic administration of soman results from tonic hypercholinergic stimulation of LC.
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PMID:Tonic activation of locus coeruleus neurons by systemic or intracoerulear microinjection of an irreversible acetylcholinesterase inhibitor: increased discharge rate and induction of C-fos. 138 4


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