Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “CONVULSIONS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 829 records · Page 46Linked to original sources

[In vivo and in vitro production of interleukin-1 after febrile convulsions].

Pathogenesis of febrile convulsions (FC) is still unknown, suggested causes include the role of antidiuretic hormone (ADH). ADH is an endogenous antypyretic and his excessive production of the consequent hyponatraemia may be the cause of FC in children with susceptibility to this type of seizure. Whereas, interleukin-1 (IL1) is a pyrogenic substances and is involved in the release of AVP. Helminen et al. have reported a significantly higher production of IL1 in culture of peripheral blood monocytes stimulated with lipopolysaccharide (LPS) of children with FC than in the others with fever but without convulsions. More recently Lahat et al. have compared plasma and cerebrospinal fluid ILI levels of children with FC with those of children with fever but without convulsions, but they did not find significant differences. The aims of this study were to determine the IL1 levels in vivo and in the supernatants of cultures of peripheral blood mononuclear cells (PBMC) stimulated or not with LPS in children with FC and in children with fever without FC and to evaluate the influence of ADH and diazepam (DZ) on IL1 production. Blood samples for PBMC cultures were obtained from 11 children with FC on the hospital admission, (group 1) and after 48 hours from treatment with DZ (group 2). The production of IL1 was measured by RIA in the supernatants of the PBMC stimulated with LPS, LPS + DDAVP (synthetic vasopressin), LPS + DZ and in vivo in plasma samples. The control groups were constituted by 9 children with fever and without convulsions (group 3), 4 of them were studied at the end of fever too (group 4), and finally by 9 children in good health (group 5). No significant differences were observed. These results do not support the hypothesis that increased production of IL1 is involved in the pathogenesis of FC in children.

Child, Preschool↗

[The effect of propanidid in patients with an increased tendency to cerebral convulsions (author's transl)].

In view of the observation of tonic-clonic convulsions after the use of Propanidid in certan patients, a study was undertaken of the effects of this drug (7 mg/kg) on the EEG of 2 volunteers with a known history of epilepsy. Both subjects developed tonic-clonic convulsions and showed typical alterations of the EEG pattern even before the onset of hyperventilation. These EEG alterations were producible also during complete relaxation. The convulsions were easily stopped by the administration of short-acting barbiturates. Similar observations reported in the literature are briefly discussed. The conclusion is drawn that Propanidid should not be given to patients with a known history of epilepsy or any other convulsive disease.

Electroencephalography↗

High oxygen pressure-induced convulsions in suckling mice.

Two hundred suckling mice from 20 litters were used for determining their functional development of the hyperoxic convulsion mechanism. It was found that 1 to 12-day-old mice did not develop convulsion when they were subjected to oxygen under high pressure. The hyperoxic convulsion was observed in 1 of 10 13-day-old (10%), 3 of 10 14-day-old (30%), 16 of 20 15-day-old (80%) and all of 16-day-old mice (100%). This finding indicates that the hyperoxic convulsion mechanism of the young mice takes 13-16 days for functional maturation. Besides, it was shown that hyperoxia could cause pulmonary damage, the incidence of which also increased with age of suckling mice.

Age Factors↗

[Propofol was useful for intractable convulsion in a patient with tetanus: a case report].

An 82-year-old woman with severe tetanus was admitted to our ICU. Anti-convulsive treatment was started by continuous intravenous administration of midazolam followed by thiamylal. On day 15, thiamylal became insufficient to manage the spastic convulsion without frequent intravenous administration of other sedative and muscle relaxants. On day 16, intravenous infusion of propofol was started at the rate of 1 mg.kg-1.h-1. Propofol was more effective than thiamylal to treat convulsion and to stabilize the sympathetic nerve activity. Propofol was also effective to achieve the better general condition in which enteral nutrition could be started. In this case, propofol was apparently more suitable than thiamylal to manage a patient with tetanic convulsion.

Aged↗

[The seasonal characteristics of the circadian rhythm of hypoxic resistance and convulsive resistance].

Hypoxic and convulsive resistances have daily rhythms, the pattern of which depends on the year season. Latent period of occurrence of epileptic seizures and time of life at the "height" of 11,000 m above the sea level undergo similar changes in autumn and spring. In winter minimal similarity between daily dynamics of each of these resistances and analogous ones in other seasons is observed, but rhythms of tolerance to hypoxia are maximally synchronized with the rhythms of convulsive resistance. In autumn hypoxic and convulsive resistances are minimal. Maximums of these indices are observed in different seasons: for tolerance to hypoxia it is summer, for convulsive resistance--spring.

Animals↗

Antidepressants and convulsions.

We reviewed available computer records and clinical charts in an estimated 42,000 recipients of antidepressant drugs. The study was restricted to persons with no known condition predisposing to convulsions. Only 16 study subjects developed a convulsive disorder that we judged could have been caused by an antidepressant. We conclude that the frequency of convulsions caused by these drugs used at usual prescribed doses in the settings studied is substantially less than one per 1,000 recipients who have no conditions predisposing to convulsions.

Adult↗

[Five single nucleotide polymorphisms of casein kinase I gamma 2 gene in children with familial febrile convulsions].

OBJECTIVE: To investigate the association between single nucleotide polymorphisms (SNPs) of casein kinase I gamma 2 (CSNK1G2) gene and children with familial febrile convulsions. METHODS: The study samples were collected from unrelated Chinese Han population of Hebei province, including a cohort of 53 children with familial febrile convulsions(FC) and a control cohort of 101 individuals. Genotypes of SNPs rs2074882, rs740423, rs2277737, rs4806825, rs1059684 were typed by polymerase chain reaction-restriction fragment length polymorphism. RESULTS: The frequencies of the five SNPs complied well with the Hardy-Weinberg equilibrium in FC group and normal group. The distribution of genotype and frequencies of alleles of the SNPs rs740423, rs2277737, rs1059684 in familial febrile convulsions group was significantly different from that in control group. No significant difference was observed in the distribution of genotypes and frequencies of alleles at SNP rs2074882 between two groups. Analysis on rs4806825 was not made owing to its less allele frequency. CONCLUSION: These data indicate that SNPs rs740423, rs2277737, rs1059684 of CSNK1G2 gene may contribute to familial febrile convulsions in children.

Casein Kinase I↗

Cerebral arteriovenous malformation diagnosed during labor induction with headache and convulsions as presentations--a case report.

The occurrence of complications of intracranial arteriovenous malformation (AVM) during labor induction is relatively uncommon. Intracranial AVM can cause convulsions, headache, focal neurological deficits and intracranial hemorrhage if ruptures. We present a 33-year-old parturient with history of paroxysmal supraventricular tachycardia, who was admitted for labor induction. She experienced a bout of convulsion following a 30-min oxytocin infusion, by which time it was three and half hours since she was given the test dose of epidural analgesic. She also denied having history of convulsions or preeclampsia. Magnetic resonance imaging (MRI) of brain demonstrated a cerebral AVM in the left frontal base without signs of intracranial hemorrhage or brain edema. The obstetrician opted for Cesarean section in order to avoid stress during vaginal delivery. The surgery was successfully performed under general anesthesia without hemodynamic fluctuations or neurological complications. We discuss the possible mechanisms of the convulsions attack in this patient and the ensuring anesthetic management for the Cesarean section she sustained.

Adult↗

[Convulsive conditions in somatic pathology of infectious etiology in children with perinatal brain injury].

Convulsive conditions account for 69.8% out of the total number of patients admitted to the department of intensive care of the children's neurological hospital. In 25.3% (348 children) they first developed in the presence of somatic pathology of the infectious inflammatory genesis in children with perinatal brain injury. Acute somatic pathology (acute respiratory diseases, pneumonia, intestinal infections) dominated (n = 318). In all the children, convulsive seizures occurred in hyperthermia largely in early childhood. Apparently, in the majority of cases, perinatal injury alone was insufficient to precipitate seizures. However, the combined perinatal brain injury and an infectious disease form favourable conditions for the appearance of convulsive conditions in children. Therefore, to prevent them, of importance is the prophylaxis of both perinatal pathology and infectious diseases. The patients with convulsive conditions should be given combined treatment including anticonvulsants, antiinflammatory, antibacterial, detoxication and other drugs.

Adolescent↗

Convulsive status epilepticus in Thai children at Ramathibodi Hospital.

BACKGROUND: Convulsive Status Epilepticus (SE) is an emergency neurological condition with high morbidity and mortality. The outcome of this condition in children depends on the etiology and the duration of convulsion. There is no report of this condition in Thai children. OBJECTIVE: To study the etiology, clinical course and outcome in children with convulsive SE in a referral hospital in Thailand. MATERIAL AND METHOD: The medical records of infants and children aged between one month and 15 years with the diagnosis of SE who were admitted to the Department of Pediatrics, Ramathibodi Hospital, Bangkok from January 1st, 1981 to December 31st, 2000 were retrospectively reviewed. The demographic data, types of seizure, duration of seizure, underlying diseases, precipitating factors, laboratory results, treatment, clinical course and outcomes were collected for descriptive analysis. RESULTS: Thirty-two patients (15 boys, 17 girls) whose ages ranged from 2 months to 14.4 years (mean 6.5 years) were included Twenty-four patients had underlying epilepsy. Twelve patients had prior diagnosis of symptomatic and idiopathic/cryptogenic epilepsy. Seven patients had acute insults to the central nervous system leading to SE. One patient with acute lymphoblastic leukemia presented with SE without association to either the underlying disease or the treatment. Fever with or without specific infection was the most common precipitating factor observed in these patients. The mean duration of SE was 64.4 minutes. The mean duration from initiation of treatment to the cessation of seizure was 41.4 minutes. Twelve patients were lost to follow up. Of the two patients who died, one had severe infection and the other had renal failure. Twelve patients had severe neurological deficits and six had mild neurological deficits. Among the thirteen patients who had > or = 1 hour of convulsion, eleven had severe neurological deficits or died. CONCLUSION: Infantile SE occurred more frequently in children with pre-existing epilepsy or neurological disorder Acute febrile illness and infection were the most common precipitating causes in the present study. Early recognition and treatment of fever and infection in conjunction with prompt and appropriate termination of seizure in epileptic children may prevent the occurrence of SE and its morbidity.

Adolescent↗

The Thai Anesthesia Incidents Study (THAI Study) of perioperative convulsion.

OBJECTIVES: To identify the incidence of perioperative convulsion within 24 hours, outcome, predisposing risk factors, contributing factors related to anesthesia and corrective strategies. MATERIAL AND METHOD: The prospective cohort study enrolled all anesthetics from twenty eligible hospitals in Thailand between March 1, 2003, and February 28, 2004. Postoperative convulsion incidents were extracted from the Thai Anesthesia Incidents Study (THAI Study) database in terms of demographic data, details of events, outcome, contributing factors related to anesthesia and corrective strategies. RESULTS: The incidence of perioperative convulsion was 3.1 per 10,000 from all 172,592 anesthetics. Most patients (73.59%) recovered in 24 hours. The majority of risk factors were related to surgery (67.92%) and patient factors (54.72%) while anesthesia was the minor factor (30.19%). The contributing factors related to anesthesia were medication error (route, type, time) 43.75% and human error (inadequate care, inadequate knowledge, inadequate communication) 43.75%. The important corrective strategies included improved supervision and clinical practice guideline. CONCLUSION: The incidence of postoperative convulsion was 3.1 per 10000. Anesthesia was the minor contributing factor. The most important risk factors included medication error and human error.

Adolescent↗

[Acute renal failure following convulsion-induced myoglobinuria].

A 75-year-old female with history of putamenal hemorrhage 8 years earlier was admitted to our hospital with generalized convulsion lasting 40 minutes. Convulsion responded quickly to intravenous administration of diazepam, but deep coma persisted thereafter. Although renal function had normalized before this episode, urinary output was immediately estimated to be limited. Drip-infusion of Ringer's solution and the combined administration of furosemide and mannitol were started. The laboratory values 6 hours after admission demonstrated extremely elevated GOT, GPT, CPK, BUN and Cr levels, suggesting rhabdomyolysis. Urinalysis confirmed myoglobinuria. Despite massive diuretic therapy, renal dysfunction did not improve and she died on hospital day 4. The treatment outcome was probably influenced by her general condition of dehydration and acidosis at admission, as well as muscle damage caused by convulsion. Myoglobinuria can induce life-threatening renal failure, and may be caused by convulsion.

Acute Kidney Injury↗

[Correlations of convulsive and hypoxic resistance in rats at different stages of ontogenesis].

Hypoxic and convulsive resistances were studied in 3, 7, 14, 21, 40-day-old rats and in adults. Susceptibility to hypoxia was determined in pressure chamber by "lifting" the animals to the altitude of 12,000 metres. Convulsions were caused by intraabdominal injections of corazol. A correlation between hypoxic and convulsive resistances was found from 3 day after the birth. Their indexes were maximum at this period. Similar decrease of hypoxic and convulsive resistances was observed with the growth of the animals. Moreover the reduction in hypoxic resistance was more dramatic and reached its minimum on the 40th day. In grown up animals, resistance to hypoxia was higher, than in 40-day-old rats. Minimum latency period for development of status epilepticus was detected in 21-day-old rats.

Age Factors↗

[A case of cerebrotendinous xanthomatosis with convulsive seizures].

A 35 year-old male was admitted to our hospital because of convulsive seizures. His parents are first cousins. No other members of his family have similar symptoms. He showed mental retardation since childhood. At age 14, he had generalized convulsive seizures that were intractable. Bilateral cataracts were found and extracted at age 18. He noticed bilateral swellings at Achilles tendons at around 25 years of age. Physical examination revealed bilateral swellings of Achilles tendons. Neurologically, he showed poor intellectual ability, hyperreflexia with positive Babinski's sign and cerebellar ataxia. Marked elevations of cholestanol level (53.84 micrograms/ml; normal: 2.71 +/- 0.81, n = 17) and cholestanol/cholesterol ratio (2.20%; normal: 0.16 +/- 0.05, n = 17) were detected in serum. EEG showed abnormal background activities with bursts of high voltage slow theta activities. MRI study showed high intensity lesions in globus pallidus and multiple lesions in white matter with long spin echo sequence. Oral administration of chenodeoxycholic acid improved EEG findings, serum cholestanol level and convulsive seizures. However, the MRI abnormalities remained unchanged, which suggested irreversible brain damage. We reviewed the previous reports of 144 cases of CTX. Fourteen cases had convulsive seizures. We stress that CTX is one the causes of symptomatic epilepsy.

Adult↗

Comparative systemic toxicity of convulsant and supraconvulsant doses of intravenous ropivacaine, bupivacaine, and lidocaine in the conscious dog.

This study evaluated the systemic toxicity, arrhythmogenicity, and mode of death of convulsant and supraconvulsant doses of lidocaine, bupivacaine, and ropivacaine. Experiments in awake dogs were designed to mimic the clinical situation of an accidental intravenous (IV) injection of local anesthetics. On the first experimental day, lidocaine (8 mg.kg-1.min-1), bupivacaine (2 mg.kg-1.min-1), and ropivacaine (2 mg.kg-1.min-1) were infused intravenously until seizures occurred (n = 6 for each group). The average dose and arterial plasma concentration at seizure onset was 20.8 +/- 4.0 mg/kg and 47.2 +/- 5.4 micrograms/mL for lidocaine, 4.31 +/- 0.36 mg/kg and 18.0 +/- 2.7 micrograms/mL for bupivacaine, and 4.88 +/- 0.47 mg/kg and 11.4 +/- 0.9 micrograms/mL for ropivacaine. The margin of safety between the convulsive and lethal doses was determined by administering two times the convulsive dose 24 h later. Two dogs given lidocaine died because of progressive hypotension, respiratory arrest, and finally cardiovascular collapse with an average peak plasma concentration (Cmax) of 469 micrograms/mL. No ventricular arrhythmias were observed in this group. Ventricular arrhythmias occurred in five of six dogs receiving bupivacaine. Four animals died because of hypotension, respiratory arrest, and cardiovascular collapse. One additional animal died because of ventricular fibrillation. The Cmax for bupivacaine was 70.1 +/- 14.6 micrograms/mL in nonsurvivors. In the ropivacaine group one animal died because of hypotension, respiratory arrest, and cardiovascular collapse (Cmax = 72.4 micrograms/mL). A surviving dog had transient premature ventricular contractions. Twenty-four hours later three times the convulsive dose was administered to the survivors.(ABSTRACT TRUNCATED AT 250 WORDS)

Amides↗

Anti-convulsant therapy in eclampsia.

Seventy four patients presented with eclampsia at N.W.M. Hospital. Bombay. Among the patients with eclampsia, 64.9% were primis, 29.7% were gravida II-IV and 5.4% were grand multis. As many as 40.5% patients were less than 20 years of age, while 2.7% were over 30 years of age. 48.7% had antepartum convulsions, 40.5% had intrapartum convulsions, while 8 patients convulsed in the postpartum period. Besides standard management of eclamptic patients, 3 protocols of anticonvulsant therapy were utilised. 27% were managed with diphenyl hydantoin sodium, 43% with magnesium sulphate, and 30% by combination of diazepam and pentazocine. The maternal and perinatal outcome was evaluated. Control of convulsions was superior with magnesium sulphate while perinatal outcome was best with diphenyl hydantoin.

Adult↗

[Effect of GABA-linoleamide and glycine linoleamide on pentamethylenetetrazole convulsions].

We have studied the effect of GABA-linoleamide (GL) (100 mg/kg i.p.) and glycine-linoleamide (LG) (70 mg/kg i.p.), on the pentamethylenetetrazole (PTZ) (82 mg/kg i.p.) convulsions and lethality of rats. LG antagonize more efficiently than GL the PTZ convulsions and lethality. In another experiment, rats have received haloperidol (2 mg/kg i.p.) for 12 days. Four days after the last administration of haloperidol, rats received as previously GL (100 mg/kg i.p.) or LG (70 mg/kg i.p.) and PTZ (82 mg/kg i.p.). GL only antagonized the PTZ convulsions and lethality. The above results seem to demonstrate the importance of GABA-ergic and glycinergic receptors in the control of PTZ convulsions and they are supported by the recent data on the role of the inhibiting neuromediators, GABA and glycine, in the substantia nigra.

Animals↗

Modification of electroshock convulsive responses and thresholds in neonatal rats after brain monoamine reduction.

Modification of electroshock (60 Hz; a.c.) convulsive responses and thresholds by monoamine-reducing drugs was investigated in developing rats. Throughout postnatal development, tetrabenazine (TBZ) reduced brain monoamines and increased the severity of motor responses to electroshock. The predominant maximal response in control pups progressed from hyperkinesia (day 1) to clonic convulsions (day 3) and tonic forelimb (day 7) and hindlimb (day 19) extension. The pattern in TBZ-treated pups progressed from tonic forelimb extension (day 1) to tonic hindlimb extension (day 7). On day 7, TBZ reduced the thresholds for clonic (CT) and tonic convulsions (TT) to 41 and 24% of control, respectively. Reserpine (1.25 mg/kg, 24 hours) decreased the TT but not the CT; TBZ, 4 hours before reserpine, prevented this decrease. A higher dose of reserpine (2.5 mg/kg) decreased both the CT and TT. On day 8, TBZ (25 mg/kg, 4 hours) decreased the TT (46% control); L-dihydroxyphenylalanine, but not 5-hydroxytryptophan prevented this decrease. Intracisternal 6-hydroxydopamine reduced the TT on day 8, while intracisternal 5,7-dihydroxytryptamine had no effect despite a 46% reduction in serotonin. The results indicate that in the neonatal rat brain, monoaminergic systems are sufficiently mature to attenuate electroshock convulsive responses, perhaps by limiting propagation of seizure discharge.

5,7-Dihydroxytryptamine↗