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At least 811 records · Page 45Linked to original sources
PubMed1982

Participant of serotonin turnover rate in the brain on barbital withdrawal convulsion.

The correlation between the development of barbital (B)-withdrawal signs and alterations in the metabolism of brain 5-hydroxytryptamine (5-HT) was studied. Barbital (B)-dependent rats were prepared by the B-Admixed Food method (DAF method). The B-dependent rats were grouped according to the following 5 states: G-I, B-dependent state; G-II, B-withdrawn state; G-III, cross-administration of nitrazepam (NZP) following B-withdrawal; G-IV, cross-administration of chlorpromazine (CPZ) following B-withdrawal; and G-V, cross-administration of phenytoin following B-withdrawal. The controls were comprised of naive rats (G-VI) and naive rats dosed in the same manner as the dependent rats. The brain 5-HT synthesis rate and the brain 5-hydraxyindole acetic acid (5-HIAA) elimination were measured at 44 to 48 hr after B-withdrawal in all groups (when withdrawal convulsion was still persisting in the B-withdrawn rats of the G-II group). The brain 5-HT synthesis rate was elevated significantly (P less than 0.001) in the rats with persistent B-withdrawal convulsion (G-II) as compared with that in the B-dependent rats (G-I). Cross-administration of nitrazepam caused the elevation of 5-HT synthesis rate with B-withdrawal to be inhibited to the dependent level in parallel with the inhibition of B-withdrawal signs. On the other hand, CPZ and phenytoin, which inhibit B-withdrawal convulsion slightly, failed to recover completely the 5-HT turnover rate during B-withdrawal. From these results, it is obvious that the elevation of the brain 5-HT synthesis rate with B-withdrawal plays an important role in eliciting B-withdrawal convulsion.

Animals↗
PubMed2001

The role of nitrergic system in lidocaine-induced convulsion in the mouse.

The effects of N-nitro-L-arginine-methyl ester (L-NAME) a nitric oxide (NO) synthase inhibitor and L-arginine, a NO precursor, were investigated on lidocaine-induced convulsions. In the first experiment, four groups of mice received physiological saline (0.9%), L-arginine (300 mg/kg, i.p.), L-NAME (100 mg/kg, i.p.) and diazepam (2 mg/kg), respectively. Thirty minutes after these injections, all mice received lidocaine (50 mg/kg, i.p.). In the second experiment, four groups of mice received similar treatment in the first experiment, and 30 min after these injections, all mice received a higher dose of lidocaine (80 mg/kg). L-NAME (100 mg/kg, i.p.) and diazepam (2 mg/kg) significantly decreased the incidence of lidocaine (50 mg/kg)-induced convulsions. In contrast, the L-arginine treatment increased the incidence of lidocaine (80 mg/kg, i.p.)-induced convulsions significantly. These results may suggest that NO is a proconvulsant mediator in lidocaine-induced convulsions.

Anesthetics, Local↗
PubMed1995

Spontaneous convulsions in Charles River Wistar rats.

Spontaneous clonic convulsions in the Charles River Wistar rat have been observed at an incidence of 1.5%. Females (2.3%) are more susceptible than males (0.7%). These convulsions are not seen in rats of less than approximately 16 weeks of age. Some animals have exhibited single convulsions whilst others have convulsed on numerous occasions. No histopathological abnormalities of the brain have been recorded for these animals following routine examination.

Aging↗
PubMed2004

Effect of bis(acetato)tetrakis(imidazole) copper(II) in delaying the onset and reducing the mortality rate of strychnine- and thiosemicarbazide- induced convulsions.

The anticonvulsant activity of bis(acetato)tetrakis(imidazole) copper(II), Cu(OAc)2(Im)4, was studied in normal mice using chemical convulsions induced by strychnine, thiosemicarbazide, picrotoxin, and pentelenetetrazol. Intraperitoneal administration of Cu(OAc)2(Im)4, 50 mg/kg body mass, has delayed the onset of strychnine (3 mg/kg)-induced convulsion by 204% (p < or = 0.005) and thiosemicarbazide (20 mg/kg)-induced convulsant by 61% (p < or = 0.005). The changes in the onset of picrotoxin- (6 mg/kg) and pentelenetetrazol (50 mg/kg)-induced convulsions were not significant. The same dosage of the copper compound was effective in delaying the lethal time and reducing the mortality rate of treated animals. The anticonvulsant activity of Cu(OAc)2(Im)4 complex against strychnine was not related to its constituents because the inorganic form of copper such as copper chloride, copper acetate, and the parent imidazole has no anticonvulsant activity. Other copper(II) complexes like copper(II)aspirinate and bis(acetato)bis(2-methyl imidazole) copper(II) were less effective.

Animals↗
PubMed1978

A newly designed method for removal of the pineal body, and depression of convulsions and enhancement of exploratory movements by pinealectomy in mice.

We designed a simple technique for surgical excision of the pineal body in mice. Such can be accomplished in 10 min by a skilled worker and there are no lesions whatever. In pinealectomized El-strain mice the appearance of convulsions was inhibited up to 30 days, while intact El-mice were all fallen into convulsions by being shaken up and down on a flat carton. Pentazole-induced convulsions propagate from one dd-mouse to another in an aggregated state, but such propagation did not occur in pinealectomized animals. Exploratory movements of pinealectomized dd-mice increased as compared to intact animals and the increase was always more extensively observed in El-mice in which, even in the intact animals, the exploratory movements were much more than those of dd-mice. From the above-mentioned experiment, it is considered that the pineal body plays a role not only in initiating but also in propagating convulsions, and that it may have a depressive action on motor activities in mice.

Animals↗
PubMed1982

Flurothyl-induced convulsions delay the onset of sexual maturation in the female rat.

We have investigated whether sexual maturation in female rats is affected by repeated flurothyl-induced convulsions. This treatment had no effect on the normal age-related increase in body weight though puberty (vaginal opening) was significantly delayed when compared with non-convulsed control rats. In an attempt to probe the mechanism of this delaying effect we observed that (1) anterior pituitary response to gonadotrophin releasing hormone in vitro was normal in terms of LH release but FSH secretion was impaired and (2) progesterone injection in oestrogen-primed convulsed rats failed to generate an ovulatory-type surge of LH or FSH. Basal serum levels and basal in-vitro secretion of LH and FSH were normal. We conclude that repeated convulsions adversely affect the hypothalamo-pituitary-gonadotrophin system of immature female rats.

Animals↗
PubMed1985

Atropine sulfate and 2-pyridine aldoxime methylchloride elicit stress-induced convulsions and lethality in mice and guinea pigs.

The present study demonstrates that dose combinations of atropine sulfate and 2-pyridine aldoxime methylchloride (2-PAM), which do not produce any overt toxic effects on the behavior of mice or guinea pigs in a stable environment, elicit clonic-tonic convulsions and death when the animals are physically stressed by cold water swimming. Phenoxybenzamine (1-6 mg/kg), diazepam (0.625 and 1.25 mg/kg) and pilocarpine (2.5 and 5 mg/kg) significantly decreased (or abolished) the occurrence of atropine and 2-PAM stressed-induced convulsions and/or lethality. In contrast, propranolol (20 mg/kg), was ineffective in preventing either convulsions or lethality. Changes in plasma glucose levels and internal body temperature did not appear to explain the precipitation of convulsions or ensuing death. These results suggest that during acute physical stress, relatively low doses of atropine and 2-PAM produce toxic and lethal effects due to the activation of alpha-adrenergic mechanisms along with a concomitant inactivation of cholinergic mechanisms.

Animals↗
PubMed1982

Neonatal convulsions treated with continuous, intravenous infusion of diazepam.

Eight patients born at term in the years 1974-76, with neonatal convulsions due to severe perinatal asphyxia, were treated for 6-11 days with continuous intravenous infusion of diazepam. Doses of 1.0-1.5 mg per hour (mg/h) were usually required to stop the convulsions. In one infant 2.75 mg/h was needed. During the treatment, all infants had measurable serum concentrations of diazepam, half of them above 35 mumol/1. The convulsions stopped in all eight infants, and did not return after discontinuation of the infusion. Side-effects were noted in all infants, but they were all able to breathe adequately. At follow-up the psychomotor development was normal in all cases and there were no signs of neurological disorders, except in one patient, in whom mild epilepsy was observed. Continuous infusion of diazepam should be given in doses of at least 1 mg/h (corresponding to around 0.3 mg/kg h) to stop convulsions in full-term infants efficiently and should be increased under close supervision and with monitoring of respiration and heart rate until treatment is effective.

Diazepam↗
PubMed1979

Release of gamma-aminobutyric acid from isolated brain synaptosomes during semicarbazide-induced convulsions.

The in vivo effect of semicarbazide (SC) and aminoxyacetic acid (AOAA) upon gamma-aminobutyric acid (GABA) levels in the synaptosomal fraction, and GABA release from the same fraction were studied in the mouse. The convulsive dose of SC reduced the GABA content in synaptosomes, and when the convulsions were protected by pretreatment with AOAA, the reduced GABA content in synaptosomes rose to or above the normal level. Moreover, the SC treatment decreased the GABA releases from synaptosomes both in a Ca2+-free Ringer's solution and in a high K+ Ringer's solution. When the convulsions were protected by pretreatment with AOAA, the decreased GABA releases in both the conditions rose to or above the normal levels. Therefore, it is suggested that the decrease in GABA release from the nerve endings, because of the decrease of GABA content in the same compartment, is possibly an important factor in the onset of some kinds of convulsions.

Aminooxyacetic Acid↗
PubMed1990

Unsuspected bacterial infections in febrile convulsions.

In a 12-month prospective study in 1984, blood and urinary cultures were obtained as a routine from 307 children who presented with fever and convulsions to the Mater Misericordiae Children's Hospital, Brisbane, and the results were compared with data from 1981-1983 when cultures were not taken as a routine. In the prospective study, bacteraemia was found in 12 (4.3%) of 282 patients but was not suspected clinically in half of these; urinary-tract infection was found in seven (2.6%) of 272 patients and in six of these it was not suspected clinically. All 12 patients with unsuspected bacteraemia or urinary-tract infection had persistent fever; of these, nine patients suffered simple convulsions and all cases of urinary-tract infection occurred in female patients. Bacteraemia was significantly more common in patients of less than two years of age, in children who were selected for lumbar puncture and in the study period compared with the retrospective period, 1981-1983. Leukocytosis (white-cell count, more than 15.0 X 10(9)/L) was a sensitive (75%) diagnostic aid but was poorly specific (59%) for bacteraemia. Bacterial meningitis was not diagnosed initially in four of the nine cases which occurred among children who presented with fever and convulsions between 1981 and 1984; in all four children, the cerebrospinal fluid appeared normal at hospital admission. We conclude that bacteraemia and urinary-tract infections are detected more frequently in children who are admitted to hospital with febrile convulsions when cultures are performed as a routine. In the at-risk group (children of less than two years of age), the prevalence of urinary-tract infection is increased in female patients and the prevalence of bacteraemia is increased in those patients who are selected for lumbar puncture. The use of leukocytosis as a criterion to determine the need for blood cultures improves the diagnostic yield but would result in increased costs and additional venepuncture. Bacterial meningitis was rare in our case series and the performance of a lumbar puncture as a routine at admission to hospital would not have led to its earlier diagnosis.

Acute Disease↗
PubMed1999

[Convulsion in two non-epileptic patients following induction of anesthesia with propofol].

Two non-epileptic patients developed convulsions immediately after induction of anesthesia with propofol. Their vital signs were stable during operation and they recovered from convulsion promptly. Case 1: A 25-year-old man was scheduled for lumbar herniectomy. Anesthesia was induced with propofol 200 mg (2 mg.kg-1). On termination of propofol administration, he developed generalized shivering like movements. Although tracheal intubation was performed with suxamethonium 100 mg, he showed no fasciculations. Vital signs and Spo2 were stable except increase of pulse rate from 70 to 116.min-1 for a few minutes. Case 2: A 75-year-old female was scheduled for cholecystectomy for cholelithiasis. Immediately after induction with propofol 60 mg (1.5 mg.kg-1), she developed generalized tonic-clonic convulsion, and she had her trachea intubated with aid of vecuronium 6 mg. Propofol-related convulsion may occur in non-epileptic patients.

Adult↗
PubMed1999

Independent and combined effects of L-arginine and diazepam on ammonium chloride-induced convulsions in rats.

The independent and combined effects of L-arginine (840 mg/kg) and diazepam (0.75 mg/kg) pretreatment (30 min) were tested on ammonium chloride (400 mg/kg)-induced convulsions in rats. Ammonia concentrations were determined in blood and brain regions (cerebral cortex, brain stem and cerebellum) 30 min after L-arginine or diazepam treatment. Ammonia concentrations were measured at the time of induction of convulsions by ammonium chloride in L-arginine, diazepam or saline pretreated animals. L-arginine and not diazepam decreased ammonia concentrations in control as well as in ammonium chloride-treated animals. However, both the compounds suppressed convulsions elicited by ammonium chloride. Protection produced concurrently by these agents was much greater than that produced by them independently. It is concluded that convulsions caused by hyperammonemic condition can be suppressed either by preventing a rise in brain ammonia to toxic level or by anticonvulsant agents having a GABA potentiating action. A much greater protection can be achieved if agents having these properties are administered concurrently.

Ammonia↗
PubMed1975

Neuropathology of the convulsive foal syndrome.

Brains from eighteen Thoroughbred foals suffering from the convulsive foal syndrome were examined neuropathologically and compared with brains from nine foals dying from different causes. In the brains of nine convulsive foals there was necrosis of the cerebral cortex, accompanied in three by severe necrosis of the diencephalon and brain stem; haemorrhage into the cerebral cortex was also present in most of this group. In the other nine brains from convulsive foals there was haemorrhage, often severe, especially in the white and grey matter of the cerebral cortex and in the cerebellum. Minimal haemorrhage occurred in the brains of the control group of animals, except in that from one Caesarian-delivered premature foal that suffered severe haemorrhage into the brain stem and cerebellum. Both types of lesion in the convulsive foal appeared to be related to events occurring just before, during or after birth.

Animals↗
PubMed1998

[Convulsive status epilepticus--clinical analysis of patients treated iin the Neurological Clinics, Medical Academy in Lublin in the years 1986-1995].

The authors reviewed clinical records of 57 consecutive adults (age: 17-78, 63%--men) treated in the intensive care unit to convulsive SE that was refractory to first-line medication (BDZ,PB). They were divided into three groups: up to 30 (mean 21 years, 28%), between 31-50 (43 y, 32%) and above 50 (59 y, 40%), 58% had previously had epilepsy with prevalence in the youngest (85%). Among the oldest in whom epilepsy occurred de novo as much as 42% experienced it in the form of convulsive SE. Generalized SE was observed in 83% of cases; exclusively in patients up to 50 and in 61% of the oldest. The identifiable precipitating causes of SE were determined in 72% cases but in 25% there were two or more of them. Among previously epileptics leading etiologies for SE were: alcohol abuse, infection or drug withdrawal. Recent brain injury (stroke, neuro-infection, trauma) accelerated refractory seizures in epilepsy-free cases. Time to recovery varied from 0.5-2 (6%) to 2-6 or above 6 hrs (46% each) after continuous i.v. administration of BZD or chlormethiazole (53%) when ineffective. No side effects were noted. The commonest complications during SE were hyperthermia and transient dysregulation of circulatory or/and respiratory systems. Everyone was led out of SE. Overall mortality amounted to 12%. Among the deceased 71% were in the oldest group and everyone with recent brain lesion. This study highlights differences in the course of convulsive SE according to age and underlying etiology and the importance of intense care in therapeutic schedule. A more common chlormethiazole administration, a useful therapeutic tool in management of convulsive SE in adults had been discussed.

Adolescent↗
PubMed1999

Effects of L-arginine on picrotoxin-induced increase in brain ammonia concentrations and convulsions in rats.

The effect of L-arginine (840 mg/kg) pre- (30 min before challenge) and post-treatment (5 min after challenge) period was tested on picrotoxin-induced increase in ammonia concentrations in brain regions (cerebral cortex, brain stem and cerebellum) and the accompanying convulsive responses in adult male rats. The combined effect of L-arginine and diazepam was also tested against picrotoxin-induced convulsions. Picrotoxin-induced increase in ammonia was reverted partially by L-arginine pretreatment. However, L-arginine pretreatment did not show anticonvulsant effect independently or concurrently with diazepam. On the other hand, L-arginine post-treatment reverted ammonia to control level in all brain regions. A partial but significant inhibition of convulsion responses was found in these animals. The combined effect of diazepam and L-arginine post-treatment was much greater than that produced by these agents independently. These findings suggest that ammonia has a partial but significant participation in the convulsant action of picrotoxin. L-arginine has a potential to revert brain ammonia to control level in picrotoxin-treated animals and thereby it has produced a partial protection. The data further indicate that the duration of action of L-arginine is considerably short and has an additive anticonvulsant action with diazepam.

Ammonia↗
PubMedDate not supplied

Effect of sigma ligands on the cocaine-induced convulsions in mice.

It has been hypothesized that some of negative effects exerted by cocaine are mediated via sigma (sigma) receptors. This report demonstrates the effects of selective sigma ligands, panamesine, DTG, rimcazole and SA 4503, on the cocaine-induced convulsions in mice and locomotor hyperactivity in rats. Only panamesine decreased both these effects of cocaine, whereas DTG and rimcazole increased the total time of cocaine-evoked convulsions and locomotor activity. SA 4503 slightly enhanced and prolonged cocaine-induced convulsions but it was ineffective in locomotor hyperactivity test. Moreover, the increase in cocaine-induced locomotor hyperactivity evoked by DTG was antagonized by panamesine. The obtained results indicate that panamesine, a selective sigma ligand with a preference for sigma1 receptor subtype and potential antagonistic activity, decreased the effects of cocaine. DTG and rimcazole (potential sigma1/sigma2 sites agonists) as well as SA 4503 (potential sigma1 site agonist) showed rather opposite effects. These findings support the idea that sigma2 receptor subtype is involved in psychomotor stimulant effects of cocaine while sigma1 receptor subtype participates in the cocaine-induced convulsions. In addition, sigma receptor antagonists (especially sigma1 ones) are able to antagonize toxic effects of cocaine while sigma agonists facilitate them.

Animals↗
PubMed1999

Clonic convulsion caused by epileptic discharges arising from the human supplementary motor area as studied by subdural recording.

In order to help clarify the mechanism of tonic convulsion, which is commonly seen in supplementary motor area (SMA) seizures, we investigated the temporal relationship between ictal discharges arising from the SMA and the associated EMG discharges in the foot, in a patient with SMA seizures, prior to surgical treatment. The patient's intractable seizures consisted of tonic followed by clonic convulsion of the left foot also involving at times, the left hand. Ictal EEGs were investigated by subdural electrodes placed on the SMA-proper and pre-SMA, which were defined by cortical stimulation and by recording cortical-evoked potentials. Interictally, repetitive spike discharges were seen at the pre-SMA. Each seizure initially had a tonic phase associated with an electrodecremental EEG pattern. It was followed by clonic convulsion as shown by clonic EMG discharges of the left tibialis anterior (TA) muscle. It had a duration of 300 to 500 msec, and on each occasion a positive cortical activity at the pre-SMA preceded the EMG onset by 110 msec, and a negative spike at the SMA-proper preceded the EMG onset by 50 to 60 msec. Epileptic discharges originating from the pre-SMA spread to the SMA-proper and possibly also to the primary motor cortex (MI) in this patient. Since both SMA-proper and MI could elicit EMG discharges through the independent corticospinal tracts having different conduction velocities, even a single spike arising from the SMA could give rise to a long EMG burst, which may play some role in the tonic convulsion which characterizes SMA seizures.

Adult↗
PubMed2001

Generalized convulsions after consuming a large amount of gingko nuts.

We report a 36-year-old woman, without any past or family histories of epilepsy, who presented frequent vomiting and generalized convulsions. About 4 h before the convulsion, she had consumed approximately 70-80 gingko nuts, seeds of Gingko biloba, in an attempt to improve her health. It is important to know that convulsion may be induced if a large amount of gingko nuts is consumed. The neurotoxicity of gingko nuts, particularly their convulsion-inducing effect, should be recognized.

Adult↗