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

Utilizing in vitro autoradiographic techniques, we have studied the distribution of high affinity [3H]kainic acid ([3H]KA) binding sites in intact sections of the rat forebrain. These sites have the same kinetic and pharmacological characteristics as the [3H]KA site described in tissue homogenates. Moderate to high levels of specific binding were observed in several discrete brain regions. These include lamina I, V and VI of the neo- and cingulate cortex, superficial layers of the pyriform cortex, striatum, external plexiform and granule cell layers of the olfactory bulb, olfactory tubercle, the stratum lucidum of CA3 of the hippocampus, molecular layer of the dentate gyrus, reticular nucleus of the thalamus, the hypothalamic median eminence, and the granule cell layer of the cerebellum. Low levels of specific binding were associated with other discrete regions such as the lateral septum, bed nucleus of the stria terminalis, medial geniculate, superficial layers of the superior colliculus, nuclei of the central grey, interpeduncular nucleus and the molecular layer of the cerebellum. Moderate uniform levels of specific binding were observed over the hypothalamus, zona incerta and the amygdala. One of the important factors in KA neurotoxicity seems to be the presence of KA receptors, and regions that are susceptible to the toxic effects of KA after local administration, such as the striatum, hippocampus, amygdala and pyriform cortex, have moderate to high levels of binding. Thus, these data provide a useful map for studying the relationship between receptor-mediated and seizure-induced neuronal damage following KA administration.
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PMID:Autoradiographic localization of high-affinity [3H]kainic acid binding sites in the rat forebrain. 629 56

Electrical stimulation of the human olfactory mucosa was performed by means of an electrode attached to a rhinoscope . Stimulation of the nasal mucosa did not evoke smell sensations, but suppressed smell sensations of presented odorants. When electrical stimulation followed the exposure to an odorant within a certain interval, the stimulus recalled the already faded sensation of the preceding odorant. Electrical stimulation without prior natural stimulation produced unpleasant sensations in 3 patients with a history of temporal lobe seizures and olfactory auras , but not in patients with primary, generalized or focal epilepsy.
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PMID:Effects of electrical stimulation of the human olfactory mucosa. 642 15

Following the administration of two gamma-aminobutyric acid-(GABA) elevating drugs, namely aminooxyacetic acid (AOAA) and valproic acid (VPA), in rats, the relationship between the magnitude and the time course of increases in GABA levels of 11 brain regions and a number of pharmacological effects was studied. AOAA (30 mg/kg i.p.) caused significant GABA increases in all brain areas but the degree and time course of these increases showed considerable variation from region to region. The most marked effects were seen in the olfactory bulb, frontal cortex and hippocampus, in which maximum GABA elevations of 100-200% were reached 4-6 hr after AOAA injection. In all the other regions studied (corpus striatum, thalamus, hypothalamus, superior and inferior colliculus, substantia nigra, pons, medulla, cerebellum), increases in GABA were less marked and, at least in part, maximum increases (30-60% over control) were already reached by 1-2 hr. In contrast to AOAA, VPA (200 mg/kg i.p.) produced significant increases in GABA levels only in the cortex, olfactory bulb, corpus striatum, hypothalamus and cerebellum, maximum effects (15-35%) being already reached 5-30 min after VPA administration. As regards pharmacological effects, AOAA caused marked hypothermia, which was maximal by 1 hr and could be reversed by increasing ambient temperature, whereas effects of VPA on body temperature were only moderate. On the other hand, both drugs exerted an almost equal, pronounced antinociceptive effect in the hot plate test. Anticonvulsant efficacy was evaluated in three seizure models, namely the maximal (tonic extension) electroconvulsive threshold, and seizures induced by pentylenetetrazol and 3-mercaptopropionic acid. Anticonvulsant effects of AOAA against electroshock and pentylenetetrazol could only be determined 1 hr after injection, at which time AOAA was inactive against 3-mercaptopropionic acid-induced seizures. VPA proved to be clearly superior to AOAA in both anticonvulsant potency and duration of action. The marked differences in functional effects between VPA and AOAA could not be related to their differential effects on GABA levels in discrete brain regions. The data thus suggest that measurement of total GABA in brain regions without consideration of the compartmentalization of the neurotransmitter is only of limited value to use in an attempt to correlate elevation of GABA levels and pharmacological effects.
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PMID:Relationship between drug-induced increases of GABA levels in discrete brain areas and different pharmacological effects in rats. 642 17

We studied the effects of microinjected drugs and brainstem lesions on motor and limbic seizures in the kindling model of epilepsy. The duration of motor seizures was determined by timing the colonic and tonic movements of the extremities. The duration of limbic seizures was determined by measuring afterdischarge recorded on the electroencephalogram. Bilateral microinjection of a gamma-aminobutyric acid (GABA) agonist, muscimol, into the area of the substantia nigra (SN) markedly suppressed both motor and limbic seizures induced by stimulation of amygdala, olfactory structures, or lateral entorhinal cortex. Microinjection of saline did not suppress seizures. The suppressive effect of muscimol: (i) dissipated after several hours and was dependent on dose; (ii) was due to an elevation of the seizure threshold, since typical seizures could be elicited with electrical current far exceeding the threshold; and (iii) exhibited spatial specificity since muscimol injections 1 to 2 mm dorsal to the SN or into neocortex did not suppress the seizures. The actions of muscimol were probably mediated by its GABA agonist properties, since microinjection of an irreversible inhibitor of GABA transaminase (gamma-vinyl GABA) into the area of the SN also suppressed kindled seizures. Destruction of brainstem structures was produced by microinjection of the neurotoxin, N-methyl-D,L-aspartate. Seizures were markedly suppressed in animals with bilateral destruction of the SN but not in animals in which the SN was spared bilaterally. We interpret the data to indicate that the SN is the site at which the GABA agonists and lesions act to raise the threshold for kindled seizures. The suppression of limbic seizures indicates that this brainstem nucleus can regulate the intrinsic neuronal excitability of hemispheric sites.
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PMID:Evidence implicating substantia nigra in regulation of kindled seizure threshold. 648 54

A recently proposed diagnostic class, psychotic trigger reaction, is deduced from careful clinical studies of eight white men, who upon a very specific trigger stimulus committed murder or attempted to (and in one case also rape). The new class is defined as a sudden ego-alien, motiveless (at least with respect to aggression), motor-wise well organized, violent complex action without emotional concomitants. The action is evoked (not provoked) by an individually unique stimulus within a specific context reviving repeated past traumatic experience. Typically there is no (significant) loss of consciousness and practically full recall. Observed are first-time hallucinations (visual, auditory, tactile, somesthetic, but not olfactory as in temporal lobe epilepsy) and signs of imbalance in the autonomic nervous system (loss of bladder control, ejaculation, profuse sweating, nausea). Only four of these men had previous psychiatric diagnoses (and then various ones) or abnormal EEGs at some time in their lives. Variety in prior diagnoses would be consistent with a seizure-like disorder, here specifically implicating an imbalance in functioning between limbic and frontal lobe systems. Clinical tests for the latter were prevailingly indicative of dysfunctioning. A detailed clinical analysis of the violent acts within their context suggests behaviors are analogous to certain limbic system mechanisms, especially the kindling phenomenon.
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PMID:Specific stimulus-evoked violent action in psychotic trigger reaction: a seizure-like imbalance between frontal lobe and limbic systems? 649 48

Increasing doses of pilocarpine, 100-400 mg/kg, were given intraperitoneally to mice and the resulting behavioral, electroencephalographic and neuropathological alterations were studied. No behavioral phenomena were observed in mice treated with the lowest dose of pilocarpine. Occasional tremor and myoclonus of hindlimbs were found in animals which received pilocarpine in a dose of 200 mg/kg. At doses of 300, 325 and 350 mg/kg, pilocarpine produced a sequence of behavioral alterations including staring spells, limbic gustatory automatisms and motor limbic seizures that developed over 15-30 min and built up progressively into a limbic status epilepticus lasting for several hours. The highest dose of pilocarpine, 400 mg/kg, was generally lethal to mice. Pilocarpine produced both interictal and ictal epileptiform activity in the electroencephalogram (EEG). The earliest EEG alterations appeared in the hippocampus and then spread to cortical areas. EEG seizures started 10-15 min after injection of large doses of pilocarpine, 300-350 mg/kg. Ictal periods lasted for 1-2 min, recurred every 5-10 min and were followed by periods of depression of the EEG activity. By 30-45 min paroxysmal activity resulted in a status epilepticus. Examination of frontal forebrain sections with light microscopy revealed a widespread damage to several brain regions including the hippocampus, amygdala, thalamus, olfactory cortex, neocortex and substantia nigra. Scopolamine, 10 mg/kg, and diazepam, 10 mg/kg, prevented the development of convulsive activity and brain damage produced by pilocarpine. The results emphasize that excessive and sustained stimulation of cholinergic receptors can lead to seizures and seizure-related brain damage in mice. It is proposed that systemic pilocarpine in mice provides a useful animal model for studying mechanisms of and therapeutic approaches to temporal lobe epilepsy.
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PMID:Seizures produced by pilocarpine in mice: a behavioral, electroencephalographic and morphological analysis. 649 17

The averaged evoked potential technique was used to determine the sequence and relative effects of a single dose of trimethyltin (TMT) on the neurophysiologic functioning of two limbic system pathways, selected for study because they are known to show TMT-induced pathologic changes. Adult female rats were implanted with bipolar electrodes in the olfactory or prepyriform cortex (PPC), dentate gyrus (DG) and distal CA3 subfield of the hippocampus. Evoked potentials were elicited in the DG by stimulation of the PPC, and in CA3 by stimulation of the mossy fiber system which originates in dentate granule cells. TMT chloride was administered po in a single 7.5 mg/kg dose in water to 9 implanted rats. A parallel group of 6 implanted rats served as a control group. No changes in potentials were noted 24 hr after TMT, but some effects appeared at 48 hr. Amplitudes of potentials elicited in the DG were greatly potentiated between 2-7 days after TMT with peak effects between 4-6 days, followed by a marked decline in amplitude of the response. At the same time, recordings of spontaneous electrical activity did not reveal marked abnormalities such as electrographic seizure waves. Amplitude of the CA3 response began to decline 3 days after TMT and by 3 weeks was markedly depressed. Average amplitudes of the same responses in the control group remained within 12 percent of pretreatment values for the 20 days of the study. Tin levels in whole brain were lowest at 24 hr, doubled at 48 hr, then doubled again at 4 days when peak levels were reached. Values remained high in both blood and brain and at 20 days were still 66 percent of peak levels. Thus, the delay in onset of effects of TMT on evoked potentials may be related to the slow entry of tin into brain, presumably because of high affinity binding to hemoglobin in blood, as reported by others. Also, the time of peak potentiating effects on potentials evoked in the DG correlated well with the time of peak levels of tin in brain.
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PMID:Time course of the effects of trimethyltin on limbic evoked potentials and distribution of tin in blood and brain in the rat. 654 88

Forty-six patients were followed up after removal of an intracranial meningioma. Nine of the 46 patients in their 3rd month postoperative EEG had localised fast rhythms which remained stable. The fast rhythms appeared in small 20-25 Hz and 20-40 microV bursts; they were localised over the craniotomy flap as shown by the control X-ray of the sites of the electrodes; they were unaffected by eye-opening and slightly reduced by fist-clenching. These fast rhythms were sometimes mixed with sharp waves and theta activity and seemed to be equivalent to the 'breach rhythm' described first by Fischgold et al. (1952) and then by Cobb et al. (1979). In our study, these rhythms were more frequently observed in patients with an olfactory or sphenoidal meningioma, in patients with pre-operative seizure and in patients with an extensive post-operative intracranial atrophy (as shown by the scanner). On the other hand, incomplete removal or recurrence of the tumour or post-operative epilepsy did not seem to play a role in the appearance of these rhythms.
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PMID:[Localized fast rhythms in EEG tracings following surgery for intracranial meningioma]. 661 58

Behavioural, electroencephalographic and neuropathological responses to increasing doses of pilocarpine (100-400 mg/kg) administered intraperitoneally to rats were studied. At the dose of 400 mg/kg pilocarpine produced a sequence of behavioural alterations including staring spells, olfactory and gustatory automatisms and motor limbic seizures that developed over 1-2 h and built up progressively into limbic status epilepticus. Smaller doses showed different threshold for these behavioural phenomena but a similar time course of development. The earliest electrographic alterations occurred in the hippocampus and then epileptiform activity propagated to amygdala and cortex. Subsequently electrographic seizures appeared in both limbic and cortical leads. The ictal periods recurred each 5-15 min and were followed by variable periods of depression of the electrographic activity. The sequence of electrographic changes correlated well with the development of behavioural phenomena. Histological examination of frontal forebrain sections revealed disseminated, apparently seizure-mediated pattern of brain damage. Neuropathological alterations were observed in the olfactory cortex, amygdaloid complex, thalamus, neocortex, hippocampal formation and substantia nigra. Pretreatment of animals with scopolamine (20 mg/kg) and diazepam (10 mg/kg) prevented the development of convulsive activity and brain damage. These results show that systemic pilocarpine in rats selectively elaborates epileptiform activity in the limbic structures accompanied by motor limbic seizures, limbic status epilepticus and widespread brain damage. It is suggested that a causative relationship between excessive stimulation of cholinergic receptors in the brain and epileptic brain damage may exist.
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PMID:Limbic seizures produced by pilocarpine in rats: behavioural, electroencephalographic and neuropathological study. 663 40

Effects of intravenous cholinergic and dopaminergic agents on pre-cocaine olfactory bulb (OB) spindling and behavioral arousal, and on cocaine-induced OB-amygdala spindling and behavioral seizures were evaluated in seven cats with stereotaxically implanted electrodes. Spindle data were computer analyzed using a special program for spindle detection and averaging. The number, duration and amplitude of pre-cocaine OB spindles were increased by physostigmine and decreased by atropine. Physostigmine augmented pre-cocaine behavioral arousal levels and this effect was associated with the absence of cocaine seizures. Cocaine-induced amygdala spindle number was increased by physostigmine. Changes in seizure duration following cholinergic drugs suggest cholinergic inhibitory effects. These data, in accord with previous studies showing cholinergic effects on reticulocortical arousal and seizures, suggest a cholinergic mechanism which is excitatory on OB-amygdala arousal spindling and inhibitory on cocaine-induced seizures.
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PMID:Cholinergic effects on arousal and cocaine-induced olfactory-amygdala spindling and seizures in cats. 665 67


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