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PubMedDate not supplied

[Non-convulsive epileptic status associated with Lafora disease: two case reports].

INTRODUCTION: Lafora s disease is a type of progressive myoclonic epilepsy with poor prognosis, is characterized by myoclonic crisis, tonic clonic seizures, absence or partial complex seizures and other neurological manifestations with a progressive course and a poor response to the treatment. It has not been considered as a cause of epileptic status. CASE REPORTS: Two women without important past medical history with normal psychomotor development before their suffering, with manifestations of 2 years of evolution the first one and 8 years on the second case characterized by myoclonic generalized, partial complex seizures and progressive deterioration of the mental functions that joined to our institution in a non convulsive epileptic status and they featured with a different evolution. The first patient with favorable control of the event with a single medication and functionality recover later, the second one with torpid evolution complicated with an epileptic status convulsive widespread condition and a prolonged permanency in the unit of intensive therapy. In both patients the diagnosis of Lafora s disease was established based in the findings of the skin axilar biopsy. DISCUSSION AND CONCLUSION: We believe that Lafora s disease must be suspected as a probable cause of non convulsive epileptic status in patients with myoclonic epilepsy associated with other neurological manifestations and a refractary response to the medical treatment. The evolution and clinical response will depend on the evolutionary stage of the disease.

Adolescent↗

PubMed2004

[A case of convulsion during selective intra-arterial infusion of fasudil hydrochloride for treatment of vasospasm following subarachnoid hemorrhage].

The authors report a case of convulsion during intra-arterial selective infusion of fasudil hydrochloride (FSD) for treatment of vasospasm following subarachnoid hemorrhage (SAH). A 47-year-old man (Hunt and Kosnik grade I) presented with sudden onset of headache and was diagnosed with SAH on CT, and admitted to our hospital. Digital subtraction angiography (DSA) performed on admission revealed an anterior communicating artery aneurysm. Neck clipping of the aneurysm was performed on the same day and no neurological deficits were noted postoperatively. Motor aphasia appeared on day 11 after the operation, and emergency DSA revealed vasospasm of the left middle cerebral artery and its branches. Emergency percutaneous transluminal angioplasty was performed with successful dilation of the left M1 artery, and 25 milligrams of FSD was injected into the left M1 artery selectively. During this injection, right hemifacial convulsion appeared, and three minutes later disappeared. No treatment was needed for the seizure. Additional injection of 30 milligrams of FSD into the left internal carotid artery resulted in vasodilatation of the left M1 artery and its branches, improvement of their blood flow on angiography, and recovery from motor aphasia. The patient was discharged 1 month later with no neurological deficits. Intra-arterial selective infusion of FSD plays an important role in treatment for vasospasm following SAH, however, we must be aware of risks of complications such as convulsion.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

PubMedDate not supplied

[Vein of Galen arteriovenous malformations and neonatal convulsions].

INTRODUCTION: Vein of Galen arteriovenous malformation (VGAM) appears during the embryonic period and gives rise to a complex network of arterial and venous vessels that generates a blood shift, from the brain parenchyma towards the malformation, with haemodynamic repercussions. Heart failure is the most frequent presenting symptom during the neonatal period, yet, convulsions or other neurological signs have occasionally been reported in this stage of life. CASE REPORT: A term infant with symptoms of heart failure and convulsions that began during the first 12 hours of life. CAT and magnetic resonance angiography scans revealed a vascular malformation and areas of cerebral ischaemia. CONCLUSIONS: In the case of our patient, detecting areas of ischaemia in the cerebral hemispheres suggested that the damage could be caused by a "steal" syndrome leading the blood flow away from these areas towards the malformation. This situation can occur either before or after birth and the self-limiting nature of the seizures in cerebral infarcts could lead to them going noticed because they take place inside the uterus or when the patient is not being observed directly by his or her health care providers. We suspect that the convulsions in newborn infants with this malformation may well be more frequent than is currently believed.

Bradycardia↗

PubMed1991

Hippocampus and frontal cortex are the potential mediatory sites for convulsions induced by new quinolones and non-steroidal anti-inflammatory drugs.

The combined administration of enoxacin, a new quinolone, and fenbufen, a non-steroidal anti-inflammatory drug induced convulsions in mice, but convulsion did not occur when a single administration of each drug was given. Inhibition by enoxacin of [3H]muscimol binding to mouse and human brain membranes was remarkably facilitated by fenbufen. These inhibitions were much more prominent in the hippocampus and frontal cortex than in the cerebellum of human and mouse brain. Enoxacin and fenbufen each at a high concentration produced a moderate and slight inhibition of the [3H]muscimol binding, respectively, in the hippocampus and frontal cortex but not in the cerebellum. It would thus appear that the drug interaction between enoxacin and fenbufen on the gamma-aminobutyric acidA receptor in hippocampus and frontal cortex plays a role in inducing convulsions.

Animals↗

PubMed1991

[Pathogenic role of the endogenous convulsant kynurenine in the mechanisms of development of epileptic attacks in alcoholics].

The role of the endogenous convulsant kynurenine (K) in the mechanisms of the development of epileptic seizures in alcoholic persons was studied on a clinical material of 63 patients suffering from alcoholism with the presence on the EEG of paroxysmal alterations without epileptic fits (n = 28) and alcoholic epilepsy (n = 35), epileptic patients not abusing alcohol (n = 20), and practically healthy subjects (n = 10). There was a significant increase of the K concentration in alcoholic patients with paroxysmal disturbances on the EEG or convulsive seizures. That increase directly correlated with the rate of convulsive epileptic fits. The rise of K in patients with alcoholic epilepsy was lower than in epileptic patients, being, however, significantly higher than in practically healthy subjects abusing alcohol and having but paroxysmal alterations on the EEG (without seizures).

Adult↗

PubMed1991

Histaminergic mechanisms in experimental convulsions.

Effect of some histamine (HA) agonists and antagonists were assessed on electroshock (MES) convulsions in mice and rats. In mice, pretreatment with the HA precursor, l-histidine (100, 500 and 1000 mg/kg) precipitated seizures after a subthreshold (30 mA) stimulus. Both incidence (%) and tonic hind limb extensor phase (THE) were more than that in vehicle treated controls. The H1 blockers, pheniramine (25 mg/kg) and promethazine (25 mg/kg) both protected against (60 mA) MES and both incidence of convulsions and THE were reduced. A similar protective effect was not seen with either the H2 blocker, cimetidine (up to 200 mg/kg), or atropine (1 mg/kg). In rats, both the classical antihistamines blocked MES seizures, whereas, the H2-blocker, cimetidine, and atropine were, ineffective. Further, both H1 blockers were ineffective in antagonizing seizures induced by pentylenetetrazole, INH, caffeine or strychnine. These results are discussed in light of a possible HA-ergic regulation of experimental convulsions.

Animals↗

PubMedDate not supplied

[Effect of the nature of the nutrition and of the functional state of the hypophyseal-adrenal system on the "convulsion readiness" of the body].

The effect of some amino acids, succinate and different doses of ACTH on the convulsion response readiness of the organism under the action of a strong sound stimulant was studied. With enrichment of the ration with glutamic acid and also following a parenteral introduction of large doses of succinate a definite protective effect was revealed and, conversely, administration of ACTH (intramuscularly, for 7 day in a dose of 5 Units per 100 g of body weight) increased the convulsion response readiness of the organism. A possible mechanism underlying the detected changes in the convulsion response readiness of the organism under the active factors under study are discussed.

Acoustic Stimulation↗

PubMed1991

["Fifth day fits": a syndrome of neonatal convulsions. Can this condition be defined as an independent disease entity in Denmark?].

A 12-year retrospective study to elucidate the incidence of "fifth day fits" including 127 infants with neonatal convulsions was carried out in the Randers area of Denmark. The incidence of neonatal convulsions was 8.3/1,000 live-born infants. The etiology in 74 cases of latent and 53 cases of convulsive seizures was asphyxia (38%), intracranial hemorrhage (17%), hypoglycaemia (9%), hypocalcaemia (4%), infections (6%) and developmental defects (4%). In 28 cases (22%) the etiology was unknown. In only two of these cases, the seizures started on day 4-6, and no peak incidence was found.

Denmark↗

PubMedDate not supplied

[Convulsions in neonates and early neonatal mortality].

The relationship between the early onset of convulsions in the early neonatal period and mortality was studied in 130 (0.26%) children with the birth weight exceeding 2,000 g in whom early neonatal convulsions were recorded. Early neonatal mortality in this group was very high reaching 25.4%. The peak mortality was noted in the first 12 hrs after birth (80.9%) and in the first 24 hrs (60.0%). In the cases of a postponed occurrence of convulsions, the mortality rate of neonates significantly decreases (p less than 0.01).

Humans↗

PubMed1990

Possibility for induction of convulsion by fleroxacin and its disposition in the central nervous system in animals.

Fleroxacin and its metabolites were examined for their possibility of the induction of convulsion in mice, inhibitory activity on GABA receptor binding, and disposition in the central nervous system of mice, rats and dogs. No convulsion was evoked in mice at high oral combination doses of fleroxacin and fenbufen. Brain-to-serum concentration ratios of fleroxacin after oral dose were 0.13 in mice, 0.19 in rats and 0.28 in dogs. Rats showed no accumulation of fleroxacin in brain and similar elimination from brain to that from serum after the oral dose. Dogs exhibited the similar distribution of fleroxacin into various brain regions. The inhibitory effect of fleroxacin on GABA receptor binding was relatively weak and slightly potentiated in the presence of 4-biphenylacetic acid. Demethyl fleroxacin showed more potent inhibitory activity on GABA receptor binding and potentiation with 4-biphenylacetic acid. The combination of intravenous demethyl fleroxacin and oral fenbufen showed no convulsion in mice. Fleroxacin N-oxide showed only slight inhibitory activity on GABA receptor binding, being not influenced with 4-biphenylacetic acid.

Animals↗

PubMed1990

[A spectral analysis and mathematical modelling of the brain electrical activity in normal rats and in genetically conditioned convulsibility].

Spectral signs of genetically conditioned convulsibility of rats of the Krushinskiĭ-Molodkina (KM) strain were determined when studying the background electrical brain activity. These signs were: an increase of the delta-activity power in motor and visual cortical zones; considerable increase of the hippocampal potential power; weakening of the caudate nucleus potential power. Spectra of biopotentials being approximated by theoretical spectral function, model parameters simulating physiological characteristics of neural networks were estimated (an inverse problem of modelling). Spectral signs of convulsibility were shown to reflect changes in properties of the neural network. On the basis of calculations it is supposed that genetically determined convulsibility of KM rats results from weakening of inhibitory functions of the caudate nucleus as well as from increased excitability (reactivity) of hippocampal and neocortical neurons.

Acoustic Stimulation↗

PubMed1977

[The relaxation principle in generalized convulsion (author's transl)].

According to the relaxation principle (Selbach) a phase of vagotropic preponderance is preceding to a generalized convulsion and is immediately overcome during convulsion by an increased sympathicus tonus. Conditions of generalized convulsions recently observed by animal experiments, such as high exspiratory neuronal activity and apnea a short time before the fit, and during the fit an increase of inspiratory and reticular neuronal activity as also an increased activity of the renal sympathicus, are thus attached to this two-phase-reaction.

Animals↗

PubMedDate not supplied

[Discontinuous selective prophylaxis of febrile convulsions at home with rectal diazepam].

Selective episodic prophylactic home treatment with rectal diazepam in children with febrile convulsions should reduce the risks of permanent long term anticonvulsive drug therapy. To evaluate this approach and its side effects, selective prophylaxis (rectal diazepam, 0.6 mg x kg at 8 to 12 hour intervals) was given to 15 children with previous febrile convulsions whenever their axillary temperature raised to 38 C degrees or over. They were followed up for a mean of 7.73 months (range 3 to 20 months). In a total of 27 febrile episodes only 2 seizures occurred, each to a different patient and in both cases when treatment was inadvertently withheld. No recurrences were observed in the remaining 13 patients involving 25 treated febrile crisis. The small number of patients precluded evaluation of the effects of risk factors in recurrence rates. Mild and transient collateral effects were detected in 46.6% patients and in 32.0% of the observed febrile periods. In spite of the small number of patients and short follow-up period these results suggest, that episodic, non permanent, treatment with rectal diazepam is an appropriate alternative to traditional continuous oral anticonvulsive therapy for children with febrile convulsions.

Administration, Rectal↗

PubMed1989

[Convulsions caused by psychopharmaceutical agents].

The convulsive effect of psychopharmaca depends on the 'epileptogenic' potency inherent to the substance, the sedation, the individual convulsion-threshold, epileptic disposition, paroxysmal EEG alterations, acute and chronic organic brain syndromes, alcoholism, high dosage, abrupt discontinuation of medication and forced onset of medication. The literature and the experience show convulsions to occur extremely rarely as a result of antidepressant and neuroleptic medication at standard doses. Caution is needed for patients at risk.

Antipsychotic Agents↗

PubMedDate not supplied

The effect of beta-adrenoceptor antagonists alone and in combination with a GABA-elevating agent on isoniazid-induced convulsions in rats.

A delay in the onset of isoniazid-induced convulsions was found in rats pretreated with the beta 2-adrenoceptor blocker, butoxamine and the nonspecific beta-blocker, propranolol. In these animals the convulsive responses were inhibited in a dose dependent manner. These compounds were found to be effective even after the induction of convulsions. The beta 1-blocker, acebutolol was able to protect rats only when injected prior to the challenge. The anticonvulsant effect of acebutolol and propranolol but not that of butoxamine was found to be enhanced in animals pretreated with a gamma-aminobutyric acid (GABA) elevating agent, aminooxyacetic acid (AOAA). The findings indicate that the GABA-mediated anticonvulsant action of AOAA seems to be additive with that resulting from beta 1 but not beta 2-blockade.

Acebutolol↗

PubMed1989

[Proposal for a scale for the assessment and treatment of febrile convulsions].

Prophylaxis of febrile convulsions has been very controversial. Often this prophylaxis is given based upon subjective criteria and even in the same Department of Paediatrics, criteria are not uniformly carried out. We consider of great interest to value some circumstances of the febrile convulsions, which could be worth for valorating recidives. We have quantified some parameters, that can be obtained easily. Those have systematically been used in our Department, leading us to establish and score to determine the risk factors that lead us to use or not a prophylactic treatment in children with febrile convulsions.

Anticonvulsants↗

PubMed1977

Phenobarbital in the acute management of febrile convulsions.

Blood levels of phenobarbital were determined after a single oral or intramuscular (IM) dose in children in the hospital after febrile convulsions. At a dose of 15 mg/kg, both the oral and IM routes gave therapeutic blood levels within 90 minutes. Absorption from the IM route before 90 minutes was inconsistent and would be unlikely to arrest an established convulsion within a critical time period. For use as a drug to prevent convulsions, oral phenobarbital at 15 mg/kg deserves further study.

Child, Preschool↗

PubMed1989

Characterization of convulsions induced by a hexanic extract of Spilanthes acmella var. oleracea in rats.

To characterize the convulsions induced by a hexanic extract of Spilanthes acmella var. oleracea, male Wistar rats were injected ip with 50 to 150 mg/kg of the extract and EEG and behavior were observed for periods as long as 2 h. Following the lower doses (50 and 75 mg/kg) only minor behavioral changes such as grooming and wet dog shakes were observed. Higher doses (100 to 150 mg/kg) induced full tonic-clonic convulsions in a dose-dependent manner which were accompanied by typical electrographic seizures in the EEG. These results confirm that the hexane extract of Spilanthes acmella var. oleracea is able to induce generalized convulsions in rats and can be used as a tool in the development of new models of epilepsy.

Animals↗