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

A clinical, neurological and electroencephalographic investigation was undertaken in 29 previously cytogenetically verified hemizygous males with the fra(X) form of mental retardation (age range 3.5 to 59 years); in addition, 6 heterozygous females were examined. All male patients displayed the known physical aspects of this syndrome together with associated abnormalities of the palate, skeleton, connective tissue and endocrine system. The most prominent neurological features were different forms of oculomotor disturbances, minor motor and pyramidal signs, incoordination, muscle hypotonia, gait and speech abnormalities. There was no increased frequency either in seizures or in epileptic EEG discharges. Some patients had a slowing of background activity in EEG. About 50% of all patients displayed autistic-like behaviour, short attention span and/or hyperactivity. In accordance with the literature, the findings indicate that there are no neurological, electroencephalographic or neuroradiological features which occur specifically in this syndrome. The need to differentiate the findings from those resulting from encephalopathic mechanisms during the gestational and perinatal period is stressed. A distinct typing of seizures and EEG changes is needed in each patient, before definite conclusions about an association of seizures and fra(X) syndrome are drawn. In view of the lack of correlation between IQ and the clinical-neurological measures, a more practical approach to quantifying the mental impairment is proposed.
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PMID:Clinico-neurological investigations in the fra(X) form of mental retardation. 270 58

Impairment of motor coordination by the excitatory amino acid antagonists 2-amino-7-phosphonoheptanoic acid (APH) and glutamic acid diethyl ester (GDEE) was measured and compared to GABA agonists and anticonvulsants and other compounds by the Coughenour inverted screen test. The GABA agonists muscimol and imidazole acetic acid, and the GABA analogue gamma-hydroxybutyric acid were found to produce a marked impairment of motor coordination. The dosages of phenytoin and valproate which impaired motor coordination, on the other hand, were considerably above the dosages which have been reported to inhibit seizures. APH caused motor incoordination at a dosage of 125 mg/kg, and a prolonged motor impairment was present after administration of APH, 250 mg/kg. GDEE did not significantly impair motor coordination in any dosage tested up to 1920 mg/kg. These results further encourage development of more potent GDEE-like compounds as potential anticonvulsants.
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PMID:Impaired motor coordination in mice induced by 2-amino-7-phosphonoheptanoic acid (APH), glutamic acid diethyl ester (GDEE), and other compounds. 274 Apr 26

Dilazep (i.p.), a coronary vasodilator and an uptake inhibitor of adenosine, dose dependently potentiated acute ethanol-induced motor incoordination in mice. In view of peripheral cardiovascular depressive effects of dilazep, the effect of i.c.v. dilazep (25, 50 and 75 micrograms), and its metabolites, 1,4-bis(3-hydroxypropyl)perhydro-1,4-diazepine (BHPD) (15, 31 and 62 micrograms) and 1-[3-(3,4,5-trimethoxybenzoyloxy)propyl]perhydro-1,4-diazepine (TBPD) (62 and 125 micrograms) on ethanol-induced motor incoordination was studied. Dose-related potentiation of ethanol-induced motor incoordination was noted with dilazep and its metabolites. Whereas dilazep (i.p.) produced no apparent central nervous system (CNS) effects, by i.c.v. route, it caused CNS excitation including tonic-clonic seizures. Adenosine uptake inhibition, Ca2+ entry blockade or direct activation of adenosine receptors was ruled out as the possible mechanism of seizures because dipyridamole, verapamil or N6-(2-phenylisopropyl)-adenosine (R-PIA) administered i.c.v., while potentiating ethanol (i.p.)-induced motor incoordination did not produce seizures. The CNS excitation was minimal with BHPD and none with TBPD. Theophylline pretreatment partially blocked potentiation of ethanol-induced motor incoordination by dilazep and BHPD and not by TBPD. The data suggest dilazep-induced potentiation of ethanol-induced motor incoordination is partially due to central adenosine receptor mechanism and partly due to other yet unknown mechanism(s) and further supported our earlier reports about adenosine involvement in the CNS effects of ethanol. The data also suggest that dilazep (i.c.v.)-induced seizures are due to mechanism(s) other than adenosine uptake inhibition, Ca2+ entry blockade or direct adenosine receptor activation.
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PMID:Central nervous system effects and behavioral interactions with ethanol of centrally administered dilazep and its metabolites in mice. 275 78

We report our experience with 90 neurologically impaired children treated with gastrostomy and Nissen fundoplication. Malnutrition was the main problem, followed by aspiration, recurrent pneumonia, and vomiting. The symptomatology was caused by swallowing incoordination and gastroesophageal reflux. The diagnosis of gastroesophageal reflux was confirmed by upper gastrointestinal series and pH probe. Nissen fundoplication was performed following a standard technique with preservation of the vagus nerves and its branches, repair of the diaphragmatic crura, reconstruction of the angle of His, and a 360 degree wrap. A gastrostomy and pyloroplasty or pyloric dilatation were part of the operative procedure. There were no deaths and few complications related to the surgical procedure. Marked nutritional improvement was seen in most cases with an average weight gain of 3.2 kg/patient 3 months following surgery. There was also improvement in milestones and seizure control. The majority of parents were very satisfied and would recommend the procedure to other parents with similar problems.
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PMID:Gastrostomy and Nissen fundoplication in neurologically impaired children. 280 49

The behavioral and biochemical effects of ethanol in man and animals have been investigated for a long time. A role of catecholamines in the central stimulatory action and during withdrawal has been envisaged, but more recent observations have revealed the involvement of inhibitory synaptic transmitter, GABA, in the actions of ethanol. Ethanol-induced motor incoordination, hypnosedation, antianxiety, and anticonvulsant actions are reported to be GABA-mediated. Involvement of the GABA system has been implicated in ethanol withdrawal-induced seizures in animals. More direct evidences using Cl- influx studies in synaptoneurosomes and spinal neuronal culture studies confirm such a mode of action of ethanol, probably influencing the chloride channel modulation at the GABA-benzodiazepine receptor ionophore complex. RO15-4513 (ethyl-8-azido-5,6-dihydro-5-methyl-6-Oxo-4H-imidazo [1,5-alpha], [1,4] benzodiazepine-3-carboxylate), a novel imidazobenzodiazepine, an analogue of the classical benzodiazepine antagonist is reported to possess alcohol antagonistic properties. RO15-4513 reverses both the behavioral and biochemical effects of ethanol, including the action of GABA-induced Cl- fluxes. But its potential clinical application may be restricted due to its inverse agonistic property. The present review focuses on the GABA-linked behavioral and biochemical actions of ethanol and discusses the potential of RO15-4513 as an alcohol antagonist.
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PMID:Molecular interactions of ethanol with GABAergic system and potential of RO15-4513 as an ethanol antagonist. 284 47

Pharmacological activities (hypnotic activity, anticonvulsant activity against pentylenetetrazol (PTZ)-induced seizures and motor incoordination) of N-allyl substituted derivatives of barbital (B) were investigated using mice. N-Monoallylbarbital (MAB) was found to possess more potent hypnotic activity [HD50 = 146(140-152)mg/kg, i.p.] and anticonvulsant activity [PTZ-ED50 = 25.1(18.1-34.8)mg/kg, i.p.] than the parent compound, barbital [HD50 = 179(153-209)mg/kg, i.p. and PTZ-ED50 = 27.7(25.5-30.1)mg/kg, i.p.]. N,N'-Diallylbarbital (DAB) was devoid of not only the hypnotic activity, but also of anticonvulsant activity and motor incoordination. The interactions of these N-allyl derivatives with various sedative-hypnotics [B, phenobarbital (PheB), amobarbital (AB), pentobarbital (PB), thiopental (TP) or diazepam (DZ)] were studied to characterize the antagonist or agonist properties of these N-allyl compounds. MAB (50-200 mg/kg, i.p.) showed a dose-dependent potentiation of B (200 mg/kg, i.p.)-induced sleep. DAB (150-300 mg/kg, i.p.) prolonged B-induced sleeping time, but its dose-response relationship was not clearly observed. Both compounds (150 mg/kg, i.p.) also significantly prolonged PheB-, AB-, PB- and TP-induced sleeping time. Further, DAB (40 mg/kg, i.p.) enhanced DZ-induced motor incoordination. These results indicate that MAB and DAB potentiate sedative-hypnotics responses in different manner, and that the mechanism of action may be due to their different effect, each other, on the central nervous system (CNS).
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PMID:N,N'-diallylbarbital potentiation of drug-induced sleep and motor incoordination. 287 5

Neurofibromatosis (NF) is a spectrum of disorders that manifest in a variety of ways. As part of the NF spectrum, many different anatomic abnormalities can develop that cause neurologic problems. The central nervous system may be directly involved or may be affected by tumor impingement. Optic pathway gliomas may also occur. The multiple neurofibromas characteristic of the most common form of NF, Von Recklinghausen disease, have a propensity to grow anywhere along nerve pathways. Therefore, the peripheral nervous system can be extensively involved. The neurofibromas may range in size from small, circumscribed tumors to gigantic plexiform tumors that insinuate into adjacent normal tissues and may compromise their function. Other neurologic problems of a functional nature can occur as well: learning disabilities, seizures, incoordination, and sensory abnormalities, among others. Computerized tomography (CT) and magnetic resonance imaging (MRI) scans are valuable diagnostic studies for identification and follow-up of tumors and other neurologic problems that may be investigated with these techniques. Plain radiographs are useful for investigating skeletal abnormalities in the skull, the ribs, the spine, and the limbs. Neurologic studies, including electroencephalography (EEG), brain-stem evoked response (BSER) or auditory brain stem response (ABR), visual evoked response (VER), nerve conduction velocity (NCV), and electromyography (EMG) provide additional information regarding specific symptom-indicated problems.
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PMID:Neurofibromatosis. 311 1

The pharmacological actions of N-(2,6-dimethylphenyl)-8-pyrrolizidineacetamide hydrochloride hemihydrate (SUN 1165), a new antiarrhythmic agent, on the central nervous system were studied in various experimental animals as compared with those of disopyramide, mexiletine and lidocaine, and the following results were obtained. 1. Acute toxicity of SUN 1165 in mice was similar to that of mexiletine, and twice as potent as compared with that of disopyramide and lidocaine. Main acute toxic symptoms of SUN 1165 were muscle relaxation, ataxia, clonic convulsions, tremor and a decrease in spontaneous activity in mice, rats and rabbits. In addition to these symptoms, vomiting in dogs was observed. These toxic symptoms were similar to those of lidocaine. In the case of disopyramide, ataxia, tremor and a decrease in spontaneous activity were observed in mice and rats. On the other hand, mexiletine caused central nervous excitatory symptoms, that is, tremor, Straub tail, clonic convulsions, jumping, running and opisthotonus in mice and rats, and vomiting in dogs. 2. SUN 1165 even at large doses (50-100 mg/kg p.o.) exerted no significant effects on the following changes: hexobarbital-induced induced hypnosis, oxotremorine-induced tremor, apomorphine-induced hypothermia, reserpine-induced ptosis and hypothermia, 5-hydroxytryptophan syndrome and fighting behavior in mice, and conditioned avoidance response in rats. 3. An ineffective dose of SUN 1165 (12.5 mg/kg p.o.) on spontaneous locomotor activity was lower than of disopyramide and lidocaine, however, higher than that of mexiletine. 4. SUN 1165 at large doses showed antagonistic action on toxic extensor seizures induced by maximal electroshock, picrotoxin, or strychnine in mice, but anticonvulsive effects of SUN 1165 were less potent than those of mexiletine and lidocaine. SUN 1165 had no effect on clonic convulsions induced by pentetrazol and pictrotoxin in mice, while both mexiletine and lidocaine prolonged the duration of clonic convulsions. 5. The muscle relaxant effect of SUN 1165 (50%-toxic dose, TD50 = 30 mg/kg p.o.) was more marked than that of lidocaine (TD50 = 92 mg/kg p.o.) on traction test in mice. However, effect of SUN 1165 (TD50 = 62 mg/kg p.o.) on motor incoordination was similar to that of disopyramide, mexiletine and lidocaine on the rotarod test in mice. 6. The analgesic effect of SUN 1165 was as weak as that of disopyramide, mexiletine and lidocaine on chemically and mechanically-induced pain response in mice.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:General pharmacological studies on N-(2,6-dimethylphenyl)-8-pyrrolizidineacetamide hydrochloride hemihydrate. 1st communication: effect on the central nervous system. 319 80

Two unrelated females, age 15 and 5 years respectively, were studied cytogenetically because of severe mental retardation, seizures and ataxia-like incoordination. A similar deletion of the proximal long arm of chromosome 15 was found in both patients. Re-evaluation showed no voracious appetite or obesity; normal size of hands and feet, minimal to no hypotonia by history or examination and facial features not typical of the Prader-Willi syndrome. However, the facial appearance of the girls was similar to each other with mild hypertelorism. The similarity of these girls and dissimilarity to Prader-Willi syndrome suggest a different syndrome, perhaps the result of deletion of a different segment of 15q. The findings of ataxic-like movements, frequent, unprovoked and prolonged bouts of laughter and facial appearance are more compatible with the diagnosis of Angelman syndrome.
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PMID:Is Angelman syndrome an alternate result of del(15)(q11q13)? 368 21

We report two brothers with previously unexplained mental retardation and seizures who had dysmorphic facial features, macro-orchidism, and a fragile site at the X chromosome. This recently described syndrome is the second most common chromosome aberration associated with mental retardation after Down's syndrome. In order to determine the prevalence of seizures and the frequency of specific neurological features, we studied a total of 17 patients with the fragile X syndrome. 41% had grand mal seizures; 41% had extensor plantar responses; 47% had hyperactive behaviour and 65% exhibited stereotypics; 59% had incoordination and 35% had blepharospasm. We emphasise the need for chromosome analysis of patients with unexplained mental retardation, specific phenotypic abnormalities, and large testes.
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PMID:Neurological findings in patients with the fragile-X syndrome. 392 Mar 55


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