Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027066 (myoclonus)
 4,275 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Evaluation of 60% solution of Methylglucamine iocarmate (Dimer-X) for ventriculography in animal experiment and clinical cases was reported. The experimental result was compared with that of Conray 60 and Angiografin, which was reported in our previous papers. In seven intraventricular injections of 2.0 ml, administered to 6 dogs, convulsion was observed on three occasions, facial myoclonus on 1 and no symptoms on the remaining three. However, in 7 intraventricular injections of 1.5 ml for 6 dogs, 6 were symptom-free and only residual one showed convulsion. And no dog died in either experiment. No changes were seen in a subsequent ventriculogram one month after the 1st ventriculography with Dimer-X and also no histological changes of the ventricular wall were revealed one month after the first experiment. These experimental results suggested less toxicity of Dimer-X than Conray 60 or Angiografin. Clinically, in 17 neurosurgical patients, ventriculography was performed with 1-5 ml of Dimer-X. No patients showed convulsive complication, but there was one episode of vomiting in each of 2 cases and slight headache in one case. From our experimental and clinical studies, it is concluded that the Dimer-X is to be considered the best watersoluble contrast medium for ventriculography at present.
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PMID:[Ventriculography with methylglucamine iocarmate (Dimer-X). Experimental and Clinical study (author's transl)]. 108 58

Five cases are presented showing on the EEG pseudo-rhythmic discharges appearing on almost flat lines, after reanimation of a cardiac arrest. The morphology of the complexes is quite similar, except in the period immediately preceding death, where they are more disformed. All patients died within the following days, except one. In four of the five cases myoclonic jerks occurred, consisting of brief convulsions over the whole body, especially in the arms and the face. A literature survey shows that this EEG pattern after circulatory arrest, is not rare. It is almost always followed by death. Myoclonic jerks may or may not be present and are not necessarily synchronous with the EEG discharges. The electrogenetic origin is not yet elucidated, although it seems that the pattern may appear at a state of complete loss of cortical function.
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PMID:The pseudo-rhythmic electroendephalogram after cardiac arrest. 122 May 24

When human divers and experimental animals are exposed to high pressure of helium-oxygen mixture, they develop the high pressure neurological syndrome, characterized by nausea, vertigo, tremor, myoclonus, EEG modifications and convulsions. Free-moving rats were stereotaxically implanted in the anterior caudate nucleus with a microdialysis probe to measure dopamine, dihydroxyphenylacetic acid and homovanillic acid levels during different phases of a simulated dive up to 5.1 MPa. Compression was found to cause an increase in extracellular dopamine and dihydroxyphenylacetic acid concentrations, but not in homovanillic acid. This represents a specific effect of high pressure on the dopaminergic pathway. Recent findings on D2 autoreceptors, showing a decrease in receptor affinity under pressure, allow us to conclude that pressure increases dopamine synthesis through a direct action on D2 autoreceptors.
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PMID:Effects of high pressure on striatal dopamine release in freely moving rats: a microdialysis study. 149 92

A 54-year-old man who had cerebellar ataxia and pseudobulbar palsy at the age of 29 years, and soon developed dementia, myoclonus and convulsions, died after about 20 years in a vegetative state. Histological examination of the extensively atrophic and devastated brain (680 g) revealed the almost total loss of cerebral cortical neurons associated with numerous beta-protein amyloid plaques, many extracellular tangles and a large number of hypertrophic astrocytes, and prominent amyloid angiopathy. The astrocytes were frequently immunopositive for anti-human tau antibody (anti-htau) and anti-ubiquitin antibody (anti-ubi). Double immunostaining with anti-htau and anti-glial fibrillary acidic protein (GFAP) antibody clearly demonstrated htau-positive domains within the GFAP-positive perikarya/and processes of several astrocytes. Electron microscopy of the hippocampal CA1, which was completely devoid of pyramidal neurons, revealed, in astrocytes, abnormal filaments indistinguishable from the paired helical filaments (PHFs) seen in neurons. On immunoelectron microscopy, the filaments were observed to be labeled with anti-htau and anti-ubi, exhibiting the same immunohistochemical features as neuronal PHFs. This is the first demonstration of clearly constricted and both tau- and ubiquitin-positive PHFs in astrocytes, indicating that, in some special conditions like in our case, processes similar to those that attack neurons also affect astrocytes and ultimately make the latter form PHFs.
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PMID:Paired helical filaments in astrocytes: electron microscopy and immunohistochemistry in a case of atypical Alzheimer's disease. 155 54

The dose-related time course and occurrence of different seizure subtypes was examined in mice after i.c.v. administration of N-methyl-D-aspartate (NMDA), kainate (KA) or quisqualate (QA). At doses of 0.2 to 1 nmol, NMDA dose-dependently induced a single clonic-tonic seizure. Low doses (0.1 to 0.3 nmol) of KA induced only mild myoclonus and whole body clonus, which were dose-dependently replaced by short-delay clonic-tonic seizures at higher doses (0.4 to 1.2 nmol). In contrast, mice treated with 13 to 32 nmol of QA exhibited either mild myoclonus or whole body clonus as well as clonic-tonic seizures. Clonic-tonic seizures induced by NMDA or KA appeared at shorter latencies than those induced by QA, whereas whole body clonus induced by KA or QA appeared with long onset latencies. These results clearly show that i.c.v. administration of NMDA, KA and QA produces different patterns of seizures in mice. This study confirms that NMDA, KA and QA induce convulsions through different underlying mechanisms and suggests that different anatomical pathways are involved in these models.
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PMID:Comparative analysis of seizures induced by intracerebroventricular administration of NMDA, kainate and quisqualate in mice. 157 1

Three types of rat hyperthermic seizures were observed. The first comprised generalized clonic convulsions preceded by intermittent myoclonus. Ictal EEG showed diffuse intermittent spikes and sequential rapid spike-wave bursts (type 1 seizures). In the other types of seizures, the paroxysmal discharges originated in the occipital region without (type 2a seizures) or with (type 2b seizures) secondary generalization. Type 2a seizures involved no convulsive movement whereas type 2b seizures involved clonic convulsions. The threshold temperatures for type 1, 2a and 2b seizures were 44.1 +/- 0.60, 40.9 +/- 1.47 and 42.1 +/- 0.75 degrees C, respectively. Of these seizures, the type 2 seizures (2a and 2b) did not severely affect the general condition of rats and thus may be an appropriate model for the investigation of febrile seizures.
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PMID:Three types of hyperthermic seizures in rats. 159 May 28

The effects produced by IP administration of these three agents in the rat were compared because of in vitro evidence that each modulates the picrotoxinin site of the GABAA receptor. For each, hypothermia had the lowest threshold and convulsions the next, with hypophagia produced only by the highest dose of either Ro 5-4864 or lindane. Convulsant effects had a shorter latency and a shorter duration than did hypothermia. Hypophagia, when present, lasted the longest. Myoclonus was the seizure type with the lowest threshold for all three agents. At the highest dose, lindane produced a high incidence of maximal clonic (hopping) seizures, whereas Ro 5-4864 and picrotoxin produced a high incidence of maximal tonic seizures instead. On a mole/kg basis, picrotoxin was 40 times more effective than the other two agents and produced seizures which started later, peaked later, and persisted longest. Ro 5-4864 and lindane were effective at equimolar concentrations and, in combination, produced effects which suggested either dose-addition or synergism. The data are consistent with the hypothesis that the toxic effects of both Ro 5-4864 and lindane may be attributable, at least in part, to an action at a subpopulation of GABAA receptors.
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PMID:Toxicokinetics of Ro 5-4864, lindane and picrotoxin compared. 171 99

Photosensitivity has proved to be a useful model to study the acute effects of experimental antiepileptic drugs (AEDs). The photosensitivity range is usually diminished or even abolished after administration of a known or experimental AED. An increase in photosensitivity, an unexpected reaction, was found in four photosensitive epileptic patients after oral ingestion of 500, 100, or 50 mg of Org 6370. Moreover, the three patients receiving doses of 100 and 500 mg reported nausea, dizziness, restlessness, and an increase in spontaneous epileptic seizures (myoclonus and in one patient a generalized tonic-clonic convulsion). The side effects coincided with peak Org 6370 serum levels. Our findings indicate that in the photosensitivity model experimental drugs with proven anticonvulsant properties in animals may increase rather than decrease the degree of patient photosensitivity. Photosensitive patients may represent a special subgroup of epileptic patients and therefore need to be classified as such.
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PMID:Preliminary assessment of the efficacy of Org 6370 in photosensitive epileptic patients: paradoxical enhancement of photosensitivity and provocation of myoclonic seizures. 173 47

Abecarnil (ZK 112119; isopropyl-6-benzyloxy-4-methoxymethyl-beta-carboxylate) is a metabolically stable beta-carboline derivative with potent anxiolytic and few sedative and ataxic effects in rodents. The anticonvulsant and muscle relaxant actions of abecarnil have been evaluated in mice, rats, gerbils and baboons. Abecarnil raised the threshold for tonic electroconvulsions in mice after corneal but not after auricular application, had no effect on maximal electroshock-induced tonic convulsions triggered by either method, protected mice against the tonic hindlimb extension in PTZ-, picrotoxin- and 3-mercaptopropionate-induced seizures and blocked clonus after PTZ, DMCM (methyl-4-ethyl-6,7-dimethoxy-9H-pyrido-(3,4-b)-indol-3-carboxylate) and 3-mercaptopropionate. Abecarnil had no effect on convulsions induced by bicuculline and strychnine. Furthermore, abecarnil blocked kindled seizures after chronic administration of PTZ and FG 7142 (beta-carboline-3-carboxylic acid methylamide) and protected mice and rats against limbic convulsions induced by pilocarpine. Severity and afterdischarge duration of amygdala-kindled seizures were reduced in rats treated with abecarnil. Abecarnil also antagonized selectively convulsions induced by i.c.v. administration of kainate, but not those triggered by N-methyl-D-aspartate or quisqualate. In genetic models of reflex epilepsy, abecarnil was effective against sound-induced convulsions in DBA/2 mice, against air blast-induced generalized seizures in gerbils and against myoclonus in baboons Papio papio. The anticonvulsant effect of abecornil in a PTZ seizure model in mice was potentiated by ethosuximide, whereas no significant potentiation was found with diazepam, clonazepam, diphenylhydantoin, carbamazepine and phenobarbital. Electromyographic monitoring in a etorphine model of muscle rigidity in rats showed no or little muscle relaxant effect of abecarnil.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Anticonvulsant action of the beta-carboline abecarnil: studies in rodents and baboon, Papio papio. 197 Mar 62

The neurological assessment of patients admitted to the intensive care unit after successful resuscitation from cardiopulmonary arrest may be difficult. We describe the cases of two patients who developed myoclonus within 24 hours of hypoxic respiratory and cardiac arrest. Initially, the clonic movements were thought to be generalised convulsions and were treated as such, until it became evident that the patients were aware and distressed. Posthypoxic myoclonus is a rare complication of successful cardiopulmonary resusitation. Recognition depends on the awareness that the syndrome exists, and is important so that correct therapy can be instituted. There may be important prognostic implications. Both our patients had normal intellectual recovery with moderate residual neurological disability from their movement disorder.
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PMID:Posthypoxic myoclonus (the Lance-Adams syndrome) in the intensive care unit. 201 97


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